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1
Matuschak, G. M., M. R. Pinsky, and M. Klain. "Hemodynamic effects of synchronous high-frequency jet ventilation during acute hypovolemia." Journal of Applied Physiology 61, no. 1 (July 1, 1986): 44–53. http://dx.doi.org/10.1152/jappl.1986.61.1.44.
Повний текст джерелаАнотація:
We studied the effects of synchronous cardiac cycle-specific high-frequency jet ventilation (HFJV) in pentobarbital-anesthetized, splenectomized, closed-chest dogs to test the hypothesis that phasic inspiratory increases in intrathoracic pressure (ITP) selectively timed to specific periods of the cardiac cycle have different hemodynamic effects during both hypovolemia (acute hemorrhage, 20 ml/kg) and neurogenic vasomotor shock (hexamethonium, 10 mg/kg) than those observed during normovolemic control conditions. Ventricular stroke volumes (SV) were measured by electromagnetic flow probes. The influence of changes in venous return (VR) on the subsequent hemodynamic response to synchronous HFJV was analyzed using instantaneous VR curves (M. R. Pinsky, J. Appl. Physiol. 56:765–771, 1984). During hemorrhage the VR curve was shifted leftward with concomitant reductions in apneic SV (15.4 +/- 3.8 to 11.2 +/- 3.6 ml, mean +/- SD), (P less than 0.01) that were accentuated by HFJV (P less than 0.01), except when the phasic inspiratory increases in ITP during HFJV were timed to occur during late diastole (-4% apneic SV, NS). SV was greater with late diastolic pulses than with other timed synchronous ITP pulses during hypovolemia (P less than 0.01). During ganglionic blockade, arterial pressure decreased (139 +/- 14 to 76 +/- 18 Torr, P less than 0.001), but VR was preserved at control levels, and no significant cardiac cycle-specific HFJV effects occurred. We conclude that SV reductions associated with positive-pressure ventilation during acute hypovolemia are minimized by HFJV synchronized to late diastole but that this effect is preload dependent.
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Raza, Sheharyar, Andre C. Amaral, Jeffrey Pang, Fuad Moussa, Dominick Shelton, Lowyl Notario, Heather Harrington, Jeannie L. Callum, and Paul M. Yip. "Reducing redundant creatine kinase testing in cardiac injury." BMJ Open Quality 9, no. 4 (December 2020): e001182. http://dx.doi.org/10.1136/bmjoq-2020-001182.
Повний текст джерелаАнотація:
BackgroundCreatine kinase (CK) testing in the setting of suspected cardiac injury is commonly performed yet rarely provides clinical value beyond troponin testing. We sought to evaluate and reduce CK testing coupled with troponin testing by 50% or greater.MethodsWe performed root cause analysis to study prevailing processes and patterns of CK testing. We developed new institutional guidelines, removed CK from high-volume paper and electronic order bundles and conducted academic detailing for departments with highest ordering frequency. We evaluated consecutive patients at Sunnybrook Health Sciences Centre between 1 January 2018 and 31 March 2020 who had either a CK or troponin level measured. We prespecified successful implementation as a reduction of 50% in total CK orders and a decrease in the ratio of CK-to-troponin tests to one-third or less. We retained additional data beyond our study period to assess for sustained reductions in testing.ResultsTotal CK tests decreased over the study period from 3963 to 2111 per month, amounting to a 46.7% reduction (95% CI 33.2 to 60.2; p<0.001) equalling 61 fewer tests per hospital day. Troponin testing did not significantly change during the intervention. Ratio of CK-to-troponin tests decreased from 0.91 to 0.49 (p<0.001). The reduction coincided with changes to order-sets, was observed across all clinical units and was sustained during additional months beyond the study period. These reductions in testing resulted in a projected annual cost savings of C$28 446.ConclusionsWe demonstrate that a low-cost and feasible quality improvement initiative may lead to significant reduction in unnecessary CK testing and substantial savings in healthcare costs for patients with suspected cardiac injury.
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Van De Borne, Philippe, Martin Hausberg, Robert P. Hoffman, Allyn L. Mark, and Erling A. Anderson. "Hyperinsulinemia produces cardiac vagal withdrawal and nonuniform sympathetic activation in normal subjects." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 276, no. 1 (January 1, 1999): R178—R183. http://dx.doi.org/10.1152/ajpregu.1999.276.1.r178.
Повний текст джерелаАнотація:
The exact mechanisms for the decrease in R-R interval (RRI) during acute physiological hyperinsulinemia with euglycemia are unknown. Power spectral analysis of RRI and microneurographic recordings of muscle sympathetic nerve activity (MSNA) in 16 normal subjects provided markers of autonomic control during 90-min hyperinsulinemic/euglycemic clamps. By infusing propranolol and insulin ( n = 6 subjects), we also explored the contribution of heightened cardiac sympathetic activity to the insulin-induced decrease in RRI. Slight decreases in RRI ( P < 0.001) induced by sevenfold increases in plasma insulin could not be suppressed by propranolol. Insulin increased MSNA by more than twofold ( P < 0.001), decreased the high-frequency variability of RRI ( P< 0.01), but did not affect the absolute low-frequency variability of RRI. These results suggest that reductions in cardiac vagal tone and modulation contribute at least in part to the reduction in RRI during hyperinsulinemia. Moreover, more than twofold increases in MSNA occurring concurrently with a slight and not purely sympathetically mediated tachycardia suggest regionally nonuniform increases in sympathetic activity during hyperinsulinemia in humans.
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Hu, Min, Shen Wang, Dan Wang, Qinhao Lai, Xiaoying Chen, Shiwei Duan, Mengke Zhao, and Junhao Huang. "Combined moderate and high intensity exercise with dietary restriction improves cardiac autonomic function associated with a reduction in central and systemic arterial stiffness in obese adults: a clinical trial." PeerJ 5 (October 5, 2017): e3900. http://dx.doi.org/10.7717/peerj.3900.
Повний текст джерелаАнотація:
Objective The present study aimed to assess the effects of exercise with dietary restriction on cardiac autonomic activity, arterial stiffness, and cardiovascular biomarkers in obese individuals. Methods Seventeen obese adults completed an 8-week exercise and dietary program. Anthropometry, body composition, and multiple biochemical markers were measured. We used carotid-femoral pulse wave velocity (cfPWV), brachial-ankle pulse wave velocity (baPWV), central blood pressure, and augmentation index (AIx) to assess arterial stiffness. To determine cardiac autonomic activity, heart rate variability (HRV) was analyzed by standard deviation of normal-to-normal intervals (SDNN), square root of the mean squared differences of successive normal-to-normal intervals (RMSSD), total power (TF), low-frequency power in normalized units (LFnu), high-frequency power in normalized units (HFnu), and low-frequency power/high-frequency power (LF/HF). Results Following the exercise and diet intervention, obese subjects had significant reductions in body weight, body mass index, body fat percentage, brachial systolic blood pressure, and resting heart rate, and they had shown improvements in blood chemistry markers such as lipid profiles, insulin, and high-sensitivity C-reactive protein. There was a significant reduction in both cfPWV and baPWV following the intervention when compared to baseline levels. Moreover, the AIx and aortic systolic blood pressure were significantly reduced after the intervention. The diet and exercise intervention significantly increased cardiac autonomic modulation (determined by improved SDNN, RMSSD, TP LF, HF, and LF/HF), which was partly due to changes in heart rate, insulin resistance, and the inflammatory pattern. Furthermore, we observed a correlation between enhanced cardiac autonomic modulation (LF/HF) and decreased arterial stiffness, as measured by central cfPWV and systemic baPWV. Discussion An 8-week combined intervention of diet and exercise is effective in improving cardiac autonomic function in obese adults, with an associated decrease in central and systemic arterial stiffness.
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Howden, Reuben, Eva Gougian, Marcus Lawrence, Samantha Cividanes, Wesley Gladwell, Laura Miller-DeGraff, Page H. Myers, et al. "The Influence ofNrf2on Cardiac Responses to Environmental Stressors." Oxidative Medicine and Cellular Longevity 2013 (2013): 1–10. http://dx.doi.org/10.1155/2013/901239.
Повний текст джерелаАнотація:
Nrf2protects the lung from adverse responses to oxidants, including 100% oxygen (hyperoxia) and airborne pollutants like particulate matter (PM) exposure, but the role ofNrf2on heart rate (HR) and heart rate variability (HRV) responses is not known. We hypothesized that genetic disruption ofNrf2would exacerbate murine HR and HRV responses to severe hyperoxia or moderate PM exposures.Nrf2-/-andNrf2+/+mice were instrumented for continuous ECG recording to calculate HR and HRV (low frequency (LF), high frequency (HF), and total power (TP)). Mice were then either exposed to hyperoxia for up to 72 hrs or aspirated with ultrafine PM (UF-PM). Compared to respective controls, UF-PM induced significantly greater effects on HR (P<0.001) and HF HRV (P<0.001) inNrf2-/-mice compared toNrf2+/+mice.Nrf2-/-mice tolerated hyperoxia significantly less thanNrf2+/+mice (~22 hrs;P<0.001). Reductions in HR, LF, HF, and TP HRV were also significantly greater inNrf2-/-compared toNrf2+/+mice (P<0.01). Results demonstrate thatNrf2deletion increases susceptibility to change in HR and HRV responses to environmental stressors and suggest potential therapeutic strategies to prevent cardiovascular alterations.
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Iwasaki, Ken-Ichi, Rong Zhang, Julie H. Zuckerman, James A. Pawelczyk, and Benjamin D. Levine. "Effect of head-down-tilt bed rest and hypovolemia on dynamic regulation of heart rate and blood pressure." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 279, no. 6 (December 1, 2000): R2189—R2199. http://dx.doi.org/10.1152/ajpregu.2000.279.6.r2189.
Повний текст джерелаАнотація:
Adaptation to head-down-tilt bed rest leads to an apparent abnormality of baroreflex regulation of cardiac period. We hypothesized that this “deconditioning response” could primarily be a result of hypovolemia, rather than a unique adaptation of the autonomic nervous system to bed rest. To test this hypothesis, nine healthy subjects underwent 2 wk of −6° head-down bed rest. One year later, five of these same subjects underwent acute hypovolemia with furosemide to produce the same reductions in plasma volume observed after bed rest. We took advantage of power spectral and transfer function analysis to examine the dynamic relationship between blood pressure (BP) and R-R interval. We found that 1) there were no significant differences between these two interventions with respect to changes in numerous cardiovascular indices, including cardiac filling pressures, arterial pressure, cardiac output, or stroke volume; 2) normalized high-frequency (0.15–0.25 Hz) power of R-R interval variability decreased significantly after both conditions, consistent with similar degrees of vagal withdrawal; 3) transfer function gain (BP to R-R interval), used as an index of arterial-cardiac baroreflex sensitivity, decreased significantly to a similar extent after both conditions in the high-frequency range; the gain also decreased similarly when expressed as BP to heart rate × stroke volume, which provides an index of the ability of the baroreflex to alter BP by modifying systemic flow; and 4) however, the low-frequency (0.05–0.15 Hz) power of systolic BP variability decreased after bed rest (−22%) compared with an increase (+155%) after acute hypovolemia, suggesting a differential response for the regulation of vascular resistance (interaction, P < 0.05). The similarity of changes in the reflex control of the circulation under both conditions is consistent with the hypothesis that reductions in plasma volume may be largely responsible for the observed changes in cardiac baroreflex control after bed rest. However, changes in vasomotor function associated with these two conditions may be different and may suggest a cardiovascular remodeling after bed rest.
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Saul, J. P., R. F. Rea, D. L. Eckberg, R. D. Berger, and R. J. Cohen. "Heart rate and muscle sympathetic nerve variability during reflex changes of autonomic activity." American Journal of Physiology-Heart and Circulatory Physiology 258, no. 3 (March 1, 1990): H713—H721. http://dx.doi.org/10.1152/ajpheart.1990.258.3.h713.
Повний текст джерелаАнотація:
Low-frequency (less than 0.15 Hz) fluctuations of heart rate are increased by maneuvers, such as standing or hemorrhage, that increase sympathetic outflow to the heart and vasculature. To test the hypothesis that low-frequency heart rate fluctuations provide an index of sympathetic efferent activity, we compared power spectral measures of heart rate variability with two measures of sympathetic outflow, peroneal nerve sympathetic activity and antecubital vein plasma norepinephrine concentrations. Autonomic outflow was varied with graded stepwise infusions of nitroprusside and phenylephrine, which lowered or raised average diastolic pressures by approximately 15 mmHg. Before vasoactive drug infusions, no spectral measure of heart rate variability correlated significantly with muscle sympathetic activity, plasma norepinephrine concentration, average heart rate, or arterial pressure. During increases of muscle sympathetic activity and probable reductions of cardiac vagal activity induced by nitroprusside, the fraction of heart rate spectral power at low frequencies, but not the absolute value, correlated significantly with muscle sympathetic activity and plasma norepinephrine. However, during reductions of muscle sympathetic activity and probable elevations of cardiac vagal activity induced by phenylephrine, no measure of heart rate variability correlated significantly with muscle sympathetic activity. These findings can be explained by a model of heart rate control in which low-frequency heart rate fluctuations result from changing levels of both the sympathetic and parasympathetic inputs to the sinoatrial node.
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Kukielka, Monica, Douglas R. Seals, and George E. Billman. "Cardiac vagal modulation of heart rate during prolonged submaximal exercise in animals with healed myocardial infarctions: effects of training." American Journal of Physiology-Heart and Circulatory Physiology 290, no. 4 (April 2006): H1680—H1685. http://dx.doi.org/10.1152/ajpheart.01034.2005.
Повний текст джерелаАнотація:
The present study investigated the effects of long-duration exercise on heart rate variability [as a marker of cardiac vagal tone (VT)]. Heart rate variability (time series analysis) was measured in mongrel dogs ( n = 24) with healed myocardial infarctions during 1 h of submaximal exercise (treadmill running at 6.4 km/h at 10% grade). Long-duration exercise provoked a significant (ANOVA, all P < 0.01, means ± SD) increase in heart rate (1st min, 165.3 ± 15.6 vs. last min, 197.5 ± 21.5 beats/min) and significant reductions in high frequency (0.24 to 1.04 Hz) power (VT: 1st min, 3.7 ± 1.5 vs. last min, 1.0 ± 0.9 ln ms2), R-R interval range (1st min, 107.9 ± 38.3 vs. last min, 28.8 ± 13.2 ms), and R-R interval SD (1st min, 24.3 ± 7.7 vs. last min 6.3 ± 1.7 ms). Because endurance exercise training can increase cardiac vagal regulation, the studies were repeated after either a 10-wk exercise training ( n = 9) or a 10-wk sedentary period ( n = 7). After training was completed, long-duration exercise elicited smaller increases in heart rate (pretraining: 1st min, 156.0 ± 13.8 vs. last min, 189.6 ± 21.9 beats/min; and posttraining: 1st min, 149.8 ± 14.6 vs. last min, 172.7 ± 8.8 beats/min) and smaller reductions in heart rate variability (e.g., VT, pretraining: 1st min, 4.2 ± 1.7 vs. last min, 0.9 ± 1.1 ln ms2; and posttraining: 1st min, 4.8 ± 1.1 vs. last min, 2.0 ± 0.6 ln ms2). The response to long-duration exercise did not change in the sedentary animals. Thus the heart rate increase that accompanies long-duration exercise results, at least in part, from reductions in cardiac vagal regulation. Furthermore, exercise training attenuated these exercise-induced reductions in heart rate variability, suggesting maintenance of a higher cardiac vagal activity during exercise in the trained state.
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White, JM. "Effects of relaxing music on cardiac autonomic balance and anxiety after acute myocardial infarction." American Journal of Critical Care 8, no. 4 (July 1, 1999): 220–30. http://dx.doi.org/10.4037/ajcc1999.8.4.220.
Повний текст джерелаАнотація:
BACKGROUND: Acute myocardial infarction places additional demands on an already compromised myocardium. Relaxing music can induce a relaxation response, thereby reversing the deleterious effects of the stress response. OBJECTIVES: To compare the effects of relaxing music; quiet, uninterrupted rest; and "treatment as usual" on anxiety levels and physiological indicators of cardiac autonomic function. METHODS: A 3-group repeated measures experimental design was used. Forty-five patients, 15 per group, with acute myocardial infarction were assigned randomly to 20 minutes of (1) music in a quiet, restful environment (experimental group); (2) quiet, restful environment without music (attention); or (3) treatment as usual (control). Anxiety levels and physiological indicators were measured. RESULTS: Immediately after the intervention, reductions in heart rate, respiratory rate, and myocardial oxygen demand were significantly greater in the experimental group than in the control group. The reductions in heart rate and respiratory rate remained significantly greater 1 hour later. Changes in heart rate, respiratory rate, and myocardial oxygen demand in the attention group did not differ significantly from changes in the other 2 groups. The 3 groups did not differ with respect to systolic blood pressure. Increases in high-frequency heart rate variability were significantly greater in the experimental and attention groups than in the control group immediately after the intervention. State anxiety was reduced in the experimental group only; the reduction was significant immediately and 1 hour after the intervention. CONCLUSIONS: Patients recovering from acute myocardial infarction may benefit from music therapy in a quiet, restful environment.
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Barrios, Vivencio, and Carlos Escobar. "Canagliflozin: metabolic, cardiovascular and renal protection." Future Cardiology 17, no. 3 (May 2021): 443–58. http://dx.doi.org/10.2217/fca-2020-0192.
Повний текст джерелаАнотація:
Patients with Type 2 Diabetes (T2D) are at risk of developing macrovascular (cardiac, cerebrovascular, peripheral arterial disease) and microvascular (nephropathy, neuropathy, retinopathy) complications. Glycemic control improves only microvascular outcomes. However, some SGLT-2 inhibitors and GLP1-R agonists have proven beneficial in macrovascular conditions. Canagliflozin is an SGLT2 inhibitor that provides sustained reductions in HbA1c, blood pressure and weight. Remarkably, as CANVAS program and CREDENCE trial demonstrated, canagliflozin promotes significant reductions in the frequency of atherosclerotic cardiovascular events, hospitalizations for heart failure and renal outcomes. In addition, real-world studies have confirmed the results of clinical trials in clinical practice. Therefore, canagliflozin should be considered a first-line therapy in the management of T2D patients in order to reduce both micro- and macrovascular complications.
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Marshall, Erica M., Jason C. Parks, Emily K. Erb, Stacie M. Humm, and J. Derek Kingsley. "Cardiac Autonomic Function Following Bilateral and Unilateral Upper Body Acute Resistance Exercise." International Journal of Environmental Research and Public Health 19, no. 10 (May 17, 2022): 6077. http://dx.doi.org/10.3390/ijerph19106077.
Повний текст джерелаАнотація:
The purpose of this study was to compare cardiac autonomic responses following bilateral and unilateral upper-body (UB) acute resistance exercise (ARE). In total, 14 individuals were assessed for markers of cardiac autonomic responses via heart rate variability (HRV) and baroreflex sensitivity (BRS) at rest and at 10- and 30-min following ARE. Logarithmically transformed (ln) HRV measures included: total power (ln TP), high-frequency power (ln HF power), low-frequency power (ln LF power), sympathovagal balance (ln LF: HF), and the square root of the mean squared differences of successive R-R intervals (ln RMSSD). BRS was assessed using the sequence method. Two-way repeated measures ANOVAs were used to analyze effects of UB ARE (bilateral, unilateral) across time (Rest, 10, and 30 min). There were no significant (p > 0.05) interactions. However, there were significant (p ≤ 0.05) main effects of time such that ln TP, ln HF power, ln RMSSD, and BRS decreased and did not recover within 30 min compared to Rest for both conditions. Collectively, this study suggests that bilateral and unilateral UB ARE yielded similar reductions, for at least 30 min, in respect to vagal measures of HRV and BRS.
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Kenney, Michael J., Dale E. Claassen, Richard J. Fels, and Cristina S. Saindon. "Cold stress alters characteristics of sympathetic nerve discharge bursts." Journal of Applied Physiology 87, no. 2 (August 1, 1999): 732–42. http://dx.doi.org/10.1152/jappl.1999.87.2.732.
Повний текст джерелаАнотація:
Frequency-domain analyses were used to determine the effect of cold stress on the relationships between the discharge bursts of sympathetic nerve pairs, sympathetic and aortic depressor nerve pairs, and sympathetic and phrenic nerve pairs in chloralose-anesthetized, baroreceptor-innervated rats. Sympathetic nerve discharge (SND) was recorded from the renal, lumbar, splanchnic, and adrenal nerves during decreases in core body temperature from 38 to 30°C. The following observations were made. 1) Hypothermia produced nonuniform changes in the level of activity in regionally selective sympathetic nerves. Specifically, cold stress increased lumbar and decreased renal SND but did not significantly change the level of activity in splanchnic and adrenal nerves. 2) The cardiac-related pattern of renal, lumbar, and splanchnic SND bursts was transformed to a low-frequency (0–2 Hz) pattern during cooling, despite the presence of pulse-synchronous activity in arterial baroreceptor afferents. 3) Peak coherence values relating the discharges between sympathetic nerve pairs decreased at the cardiac frequency but were unchanged at low frequencies (0–2 Hz), indicating that the sources of low-frequency SND bursts remain prominently coupled during progressive reductions in core body temperature. 4) Coherence of discharge bursts in phrenic and renal sympathetic nerve pairs in the 0- to 2-Hz frequency band increased during mild hypothermia (36°C) but decreased during deep hypothermia (30°C). We conclude that hypothermia profoundly alters the organization of neural circuits involved in regulation of sympathetic nerve outflow to selected regional circulations.
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Ibragimov, I. F., T. S. Vlasova, A. M. Sadykova, and R. I. Sungatullin. "CHANGE IN THE FREQUENCY OF CARDIAC REDUCTIONS IN CALM, IN BOYS OF 8-14 YEARS, REGULARLY DEPENDING GREEK-ROMAN FIGHT." SCIENTIFIC NOTES KAZAN BAUMAN STATE ACADEMY OF VETERINARY MEDICINE 237, no. 1 (March 5, 2019): 77–82. http://dx.doi.org/10.31588/2413-4201-1883-237-1-77-82.
Повний текст джерела
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Van Lieshout, Johannes J., Wouter Wieling, John M. Karemaker, and Niels H. Secher. "Syncope, cerebral perfusion, and oxygenation." Journal of Applied Physiology 94, no. 3 (March 1, 2003): 833–48. http://dx.doi.org/10.1152/japplphysiol.00260.2002.
Повний текст джерелаАнотація:
During standing, both the position of the cerebral circulation and the reductions in mean arterial pressure (MAP) and cardiac output challenge cerebral autoregulatory (CA) mechanisms. Syncope is most often associated with the upright position and can be provoked by any condition that jeopardizes cerebral blood flow (CBF) and regional cerebral tissue oxygenation (cO2Hb). Reflex (vasovagal) responses, cardiac arrhythmias, and autonomic failure are common causes. An important defense against a critical reduction in the central blood volume is that of muscle activity (“the muscle pump”), and if it is not applied even normal humans faint. Continuous tracking of CBF by transcranial Doppler-determined cerebral blood velocity ( Vmean) and near-infrared spectroscopy-determined cO2Hb contribute to understanding the cerebrovascular adjustments to postural stress; e.g., MAP does not necessarily reflect the cerebrovascular phenomena associated with (pre)syncope. CA may be interpreted as a frequency-dependent phenomenon with attenuated transfer of oscillations in MAP to Vmeanat low frequencies. The clinical implication is that CA does not respond to rapid changes in MAP; e.g., there is a transient fall in Vmeanon standing up and therefore a feeling of lightheadedness that even healthy humans sometimes experience. In subjects with recurrent vasovagal syncope, dynamic CA seems not different from that of healthy controls even during the last minutes before the syncope. Redistribution of cardiac output may affect cerebral perfusion by increased cerebral vascular resistance, supporting the view that cerebral perfusion depends on arterial inflow pressure provided that there is a sufficient cardiac output.
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Hogue, Charles W., Pekka Talke, Phyllis K. Stein, Charles Richardson, Peter P. Domitrovich, and Daniel I. Sessler. "Autonomic Nervous System Responses during Sedative Infusions of Dexmedetomidine." Anesthesiology 97, no. 3 (September 1, 2002): 592–98. http://dx.doi.org/10.1097/00000542-200209000-00012.
Повний текст джерелаАнотація:
Background The purpose of this study was to determine the effects of dexmedetomidine on systemic and cardiac autonomic reflex responses during rest and during thermal stress. Methods Volunteers received either placebo or low- or high-dose dexmedetomidine (target plasma concentrations 0.3 or 0.6 ng/ml, respectively) infusions in a prospectively randomized, double-blinded crossover study design. After 1 h, baroreflex sensitivity was assessed, and then core body temperature was raised to the sweating threshold and then lowered to the shivering threshold. Plasma catecholamines and blood pressure were measured, and cardiac autonomic responses were assessed by analysis of heart rate variability. Results Compared with placebo, plasma norepinephrine concentrations, blood pressure, heart rate, and some heart rate variability measures were lower after 1-h infusion of dexmedetomidine, but baroreflex responses did not differ significantly. Dexmedetomidine blunted the systemic and cardiac sympathetic effects of sweating observed during placebo infusion but had no effect on parasympathetic measures. Increases in blood pressure, and systemic catecholamines due to shivering were observed during placebo and dexmedetomidine, but these responses were less with dexmedetomidine. During shivering, dexmedetomidine infusion was associated with higher low-frequency and high-frequency heart rate variability power but lower heart rate compared with the sweating threshold and with the control period, suggesting nonreciprocal cardiac autonomic responses. Conclusions Infusion of dexmedetomidine results in compensated reductions in systemic sympathetic tone without changes in baroreflex sensitivity. Dexmedetomidine blunts heart rate and the systemic sympathetic activation due to sweating, but it is less effective in blunting cardiac sympathetic responses to shivering. During dexmedetomidine infusion, cardiac sympathetic and parasympathetic tone may have nonreciprocal changes during shivering.
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Davy, Kevin P., Christopher A. Desouza, Pamela P. Jones, and Douglas R. Seals. "Elevated Heart Rate Variability in Physically Active Young and Older Adult Women." Clinical Science 94, no. 6 (June 1, 1998): 579–84. http://dx.doi.org/10.1042/cs0940579.
Повний текст джерелаАнотація:
1. Low heart rate variability is associated with an increased risk of cardiac sudden death, coronary heart disease and all-cause mortality. We have previously shown that physically active postmenopausal women demonstrate higher levels of heart rate variability and cardiac baroreflex sensitivity compared to their sedentary peers. The purpose of the present prospective study was to test the hypothesis that heart rate variability and cardiac baroreflex sensitivity would be reduced with age in sedentary but not physically active women. To accomplish this, we measured heart rate variability (both time and frequency domain) and spontaneous cardiac baroreflex sensitivity (SBRS, sequence method) in the sitting posture in 23 sedentary women [11 premenopausal and 12 postmenopausal (age, 28 ± 1 and 61 ± 2 years; Vo2max, 35.3 ± 1.4 and 21.7 ± 1.5 ml · min−1 · kg−1 respectively] and in 22 physically active women [12 premenopausal and 10 postmenopausal (age, 31 ± 1 and 59 ± 2 years; Vo2max, 52.5 ± 1.4 and 39.7 ± 1.8 ml · min−1 · kg−1)]. 2. The S.D. of the R—R interval (time domain) was reduced (P < 0.05) with age in both sedentary (52 ± 6 versus 33 ± 4 ms) and physically active women (72 ± 8 versus 49 ± 9 ms). The high-frequency power (3740 ± 1527 versus 915 ± 188 and 9516 ± 2849 versus 2803 ± 1083 ms2/Hz), total power of heart rate variability and SBRS (11 ± 2 versus 7 ± 2 and 19 ± 3 versus 13 ± 2 ms/mmHg) also demonstrated similar age-related reductions in sedentary and physically active women, respectively (all P < 0.05). The S.D. of the R—R interval, high-frequency and total power of heart rate variability, and SBRS were higher (all P < 0.05) in the physically active compared with the sedentary women at any age. There was no significant influence of age or physical activity status on the low-frequency power of heart rate variability. In addition, no significant differences in any of the time or frequency domain measures of heart rate variability or SBRS were observed in users compared with non-users of hormone replacement therapy. 3. The results of the present study suggest that heart rate variability and cardiac baroreflex sensitivity decline similarly with age in healthy sedentary and physically active women. However, physically active women demonstrate higher levels of heart rate variability and cardiac baroreflex sensitivity compared with their sedentary peers, regardless of age.
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Iwasaki, Ken-ichi, Rong Zhang, Merja A. Perhonen, Julie H. Zuckerman, and Benjamin D. Levine. "Reduced baroreflex control of heart period after bed rest is normalized by acute plasma volume restoration." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 287, no. 5 (November 2004): R1256—R1262. http://dx.doi.org/10.1152/ajpregu.00613.2002.
Повний текст джерелаАнотація:
Adaptation to spaceflight or head-down-tilt bed rest leads to hypovolemia and an apparent abnormality of baroreflex regulation of cardiac period. In a previous study, we demonstrated that both chronic (2 wk) head-down-tilt bed rest and acute induced hypovolemia led to similar impairments in spontaneous baroreflex control of cardiac period, suggesting that a reduction in plasma volume may be responsible for this abnormality after bed rest. Therefore we hypothesized that this reduced “baroreflex function” could be restored by intravenous volume infusion equivalent to the reduction in plasma volume after bed rest. Six healthy subjects underwent 2 wk of −6° head-down bed rest. Beat-by-beat arterial blood pressure and ECG were recorded during 6 min of spontaneous respiration and fixed-rate breathing (0.2 Hz), and transfer function analysis between systolic blood pressure and R-R interval was performed. Plasma volume was measured with Evans blue dye, and cardiac filling pressures were directly measured (Swan-Ganz catheter). After bed rest, studies were repeated before and after plasma volume restoration, with which both plasma volume and left ventricular end-diastolic pressure were restored to pre-bed rest levels by intravenous dextran40 infusion (288 ± 31 ml). Transfer function gain in the high-frequency range, used as an index of vagally mediated arterial-cardiac baroreflex function, decreased significantly (13.4 ± 3.1 to 8.1 ± 2.9 ms/mmHg, P < 0.05) after bed rest. However, reduced transfer function gain was normalized to the pre-bed rest level (12.2 ± 3.6 ms/mmHg) after precise plasma volume restoration. This result confirms that reductions in plasma volume, rather than a unique autonomic nervous system adaptation to bed rest, are largely responsible for the observed changes in spontaneous arterial-cardiac baroreflex function after bed rest.
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Larsen, Peter D., Sheng Zhong, Gerard L. Gebber, and Susan M. Barman. "Differential pattern of spinal sympathetic outflow in response to stimulation of the caudal medullary raphe." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 279, no. 1 (July 1, 2000): R210—R221. http://dx.doi.org/10.1152/ajpregu.2000.279.1.r210.
Повний текст джерелаАнотація:
In urethan-anesthetized cats, frequency domain analysis was used to explore the mechanisms of differential responses of inferior cardiac (CN), vertebral (VN), and renal (RN) sympathetic nerves to electrical stimulation of a discrete region of the medullary raphe (0–2 mm caudal to the obex). Raphe stimulation in baroreceptor-denervated cats at frequencies (7–12 Hz) that entrained the 10-Hz rhythm in nerve activity decreased CN and RN activities but increased VN activity. The reductions in CN and RN discharges were associated with decreased low-frequency (≤6 Hz) power and either increased (low stimulus intensity) or decreased (high stimulus intensity) 10-Hz band power. In contrast, VN 10-Hz band power was increased at all stimulus intensities, without changes in low-frequency power. High-frequency (25 Hz) stimulation decreased low-frequency activity of CN and RN discharges in both baroreceptor-denervated and baroreceptor-intact cats, without decreasing VN low-frequency activity. We propose that the differential pattern produced by raphe stimulation involves resonance at the level of the 10-Hz oscillators and differential inhibition of follower circuits that transmit both 10-Hz and low-frequency activity to sympathetic nerves.
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Dura, B., M. Q. Chen, O. T. Inan, G. T. A. Kovacs, and L. Giovangrandi. "High-Frequency Electrical Stimulation of Cardiac Cells and Application to Artifact Reduction." IEEE Transactions on Biomedical Engineering 59, no. 5 (May 2012): 1381–90. http://dx.doi.org/10.1109/tbme.2012.2188136.
Повний текст джерела
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Berg, Oliver, Axel Heimann, Thomas Münzel, Christian-Friedrich Vahl, Oliver Kempski, Harald Darius, Benjamin Bierbach, and Georg Horstick. "Potent low dose platelet inhibitory effects of clopidogrel and aspirin on coronary thrombus formation in an animal model of acute unstable angina." Thrombosis and Haemostasis 95, no. 02 (2006): 354–61. http://dx.doi.org/10.1160/th05-05-0377.
Повний текст джерелаАнотація:
SummaryApplication of clopidogrel before percutaneous coronary intervention in patients with acute coronary syndrome reduces the risk of cardiac events. Clopidogrel administration before surgery increases bleeding complications after CABG. Therefore, the antithrombotic effect of the low-dose combination of clopidogrel and aspirin was investigated in an in vivo pig model of coronary artery thrombus formation with cyclic flow reductions. The platelet inhibitory effect was determined by platelet aggregation and CFR, according to the methodology described by Folts. CFR were initiated by endothelial damage and placement of a constrictor around the LAD. 30 min after CFR were established, clopidogrel (0.1 mg/kg or5 mg/kg), aspirin (1 mg/kg or 7 mg/kg) or LDC (0.1 mg/kg clopidogrel and 1 mg/kg aspirin) were administered orally. CFR-frequency was determined for further 240 min. CFR-frequency (CFR/30 min) was significantly reduced at 60 min in response to aspirin (7 mg/kg, −48%, p<0.05), and at 120 min in response to clopidogrel (5 mg/kg, −65%, p<0.05) but not at low doses of either compound. In contrast, LDC of clopidogrel (0.1 mg/kg) plus aspirin (1 mg/kg) resulted in a complete and rapid abrogation of CFR at 90 min (−70%, p<0.05). Furthermore, LDC led to reduction of platelet aggregation when CFR-frequency was already significantly decreased. In contrast, high dose groups presented a significant reduction of platelet aggregation prior to CFR-frequency decrease. Low dose combination of clopidogrel plus aspirin demonstrates a potent over additive anti-thrombotic effect in vivo with a significant reduction in thrombus formation early after drug application. The effect occurs before inhibition of platelet aggregation is detectable.
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Burma, Joel S., Paige V. Copeland, Alannah Macaulay, Omeet Khatra, and Jonathan D. Smirl. "Effects of high-intensity intervals and moderate-intensity exercise on baroreceptor sensitivity and heart rate variability during recovery." Applied Physiology, Nutrition, and Metabolism 45, no. 10 (October 2020): 1156–64. http://dx.doi.org/10.1139/apnm-2019-0810.
Повний текст джерелаАнотація:
Numerous studies have examined heart rate variability (HRV) and cardiac baroreceptor sensitivity (BRS) variables during recovery both acutely (under 3 h) and long-term (24, 48, and 72 h) postexercise. However, there is little literature examining HRV and BRS measures between these timepoints. Spontaneous short-term HRV and cardiac BRS measures were collected in 9 participants before and at zero, 1, 2, 4, 6, and 8 h after 3 separate conditions: moderate-intensity continuous exercise (MICE; 45 min at 50% heart rate reserve), high-intensity interval exercise (HIIE; 25 min including ten 1-min intervals at 85% heart rate reserve), and control (30 min quiet rest). HRV measures in the time domain were only affected immediately following HIIE and MICE at hour zero (all p < 0.043), whereas frequency-domain metrics were unaltered (all p > 0.102). These measures were highly consistent across the control day (all p > 0.420). Cardiac BRS was assessed via low-frequency (LF) gain, and revealed reductions following HIIE at hour zero (p < 0.012). Cardiac BRS LF gain remained consistent following MICE and control interventions (all p > 0.280). The common practice of waiting 12 to 24 h is overly conservative as the current findings demonstrate measures return to baseline at ∼60 min after exercise. Moreover, these metrics demonstrated high levels of within- and between-day reliability. Novelty Previously a 12-h minimum restriction from exercise was required before participation in HRV/BRS studies. Recovery from moderate-intensity exercise for HRV and BRS metrics was <60 min; whereas, high-intensity intervals led to alterations for approximately 60 min. Spontaneous HRV and cardiac BRS demonstrated high levels of within-day reproducibility.
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Soon, Chun Siong, Ksenia Vinogradova, Ju Lynn Ong, Vince Calhoun, Thomas Liu, Juan Helen Zhou, Kwun Kei Ng, and Michael Chee. "070 Respiratory, cardiac, EEG, BOLD signals and functional connectivity over multiple microsleep episodes." Sleep 44, Supplement_2 (May 1, 2021): A29. http://dx.doi.org/10.1093/sleep/zsab072.069.
Повний текст джерелаАнотація:
Abstract Introduction Brief intrusions of unintended sleep can occur in various contexts, for example during resting-state fMRI scans. In addition to changes in neural activity, such microsleep episodes are also associated with shifts in respiration and heartrate. Here we investigated how these concurrent changes alter the dynamics of the BOLD signal in the brain and estimates of functional connectivity. Methods Ten participants underwent 6 runs of 20 minute resting-state fMRI scans with concurrent respiration, PPG and EEG recording. Realtime eye-closure monitoring combined with post eye-opening self-reports were used to identify microsleep episodes of different durations. Results During microsleep, sustained reductions were observed in arousal as assessed by EEG (ratio of alpha to delta and theta bands), as expected. In comparison, cortical BOLD signal exhibited more complex, temporally multiphasic changes which were consistent across different microsleep durations from 4 to 44s: (i) an initial sleep-onset dip reaching a nadir after ~6s, followed by (ii) an increase above wake baseline that plateaued till awakening. On awakening, (iii) a transient positive bump occurred up to 6s, followed by (iv) an undershoot below baseline lasting ~30s. While seen across the whole brain, these changes showed regional variations, e.g., the signal plateau in the thalamus remained below wake baseline. Sleep onset and awakening were also associated with respective reductions and increases in respiration and heart rate, which affect blood oxygen levels. Brain functional connectivity estimates were altered by the frequency of falling asleep, and this was not resolved by global signal regression. Conclusion Falling asleep and awakening are shown here to be associated with large, widespread BOLD signal changes consistent across varied durations of microsleep. These signal changes are intimately intertwined with shifts in respiration and heart rate, which are influenced by common brainstem nuclei controlling sleep. These autonomic contributions to ‘brain signal’ changes at microsleep onset and awakening are integral to sleep, and urge the integration of autonomic and central nervous system contributions to BOLD signal into frameworks for understanding brain function using fMRI. In addition, the correlation between frequency of microsleep and extent of altered functional connectivity highlight the need to minimize sleep during resting state scans. Support (if any) NMRC/STaR/015/2013
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WIJEYSUNDERA, Duminda N., Gary C. BUTLER, Shin-ichi ANDO, Michael J. POLLARD, Peter PICTON, and John S. FLORAS. "Attenuated cardiac baroreflex in men with presyncope evoked by lower body negative pressure." Clinical Science 100, no. 3 (January 31, 2001): 303–9. http://dx.doi.org/10.1042/cs1000303.
Повний текст джерелаАнотація:
Mechanisms responsible for presyncope during lower body negative pressure (LBNP) in otherwise healthy subjects are poorly understood. Muscle sympathetic nerve activity (MSNA), blood pressure, heart rate (HR), HR power spectra, central venous pressure (CVP) and stroke volume were determined in 14 healthy men subjected to incremental LBNP. Of these, seven experienced presyncope at LBNP >-15 mmHg. Subjects who tolerated LBNP >-15 mmHg had significantly lower CVP (2.6±1.0 versus 7.2±1.2 mmHg; means±S.E.M., P < 0.02), HR (59±2 versus 66±3 beats/min, P < 0.05) and MSNA burst frequency (29.0±2.4 versus 39.0±3.5 bursts/min, P < 0.05) during supine rest. LBNP at -15 mmHg had no effect on blood pressure, but caused similar and significant reductions in stroke volume and cardiac output in both groups. Subjects who tolerated LBNP had significant reflex increases in HR, MSNA burst frequency and burst amplitude with LBNP of -15 mmHg. These responses were absent in those who experienced presyncope. The gain of the cardiac baroreflex regulation of MSNA was markedly attenuated in pre-syncopal subjects (1.2±0.6 versus 8.8±1.4 bursts/100 heart beats per mmHg; P < 0.001). Healthy subjects who experience presyncope in response to LBNP appear more dependent, when supine, upon MSNA to maintain preload, and less able to increase sympathetic vasoconstrictor discharge to skeletal muscle reflexively in response to orthostatic stimuli.
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Hodson, W. Alan. "High-Frequency Oscillatory Ventilation." International Journal of Technology Assessment in Health Care 7, S1 (January 1991): 41–46. http://dx.doi.org/10.1017/s0266462300012484.
Повний текст джерелаАнотація:
The improved survival rate of premature infants with respiratory failure is attributable to advances in mechanical ventilation, although an adverse consequence has been an increased incidence of bronchopulmonary dysplasia (BPD) (1;32). Positive pressure ventilation with its attendant “barotrauma” is suspected in the causation of BPD. While many attempts to alter respirator variables, such as pressure and time components, have produced optimal patterns for gas exchange, evidence is lacking to support any one pattern that minimizes the incidence of chronic lung injury. The high incidence of BPD has promoted a search for alternative methods of ventilation that might reduce lung injury through a reduction in peak pressure applied to the lung. Additional motivation has come from the need for oxygenation when mechanical ventilation has failed or pulmonary interstitial emphysema has developed. Less compelling reasons have come from the desire to avoid high swings in thoracic pressure that might adversely affect cardiac output, venous return, and cerebral blood flow.
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Крачак, Д. И. "Analysis of the Frequency of Acute Kidney Injury after Cardiac Interventions at the Cardiac Surgery Department." Кардиология в Беларуси, no. 5 (January 5, 2021): 656–67. http://dx.doi.org/10.34883/pi.2020.12.5.004.
Повний текст джерелаАнотація:
Цель. Определить частоту развития острого повреждения почек в раннем послеоперационном периоде после выполнения кардиохирургической операции в условиях искусственного кровообращения, а также возможные предикторы.Материалы и методы. Согласно выбранному дизайну проводилось исследование 50 пациентов, прооперированных в период с 1 января по 29 февраля 2020 г. Пациенты были разделены на две группы: группа с развитием ОПП и контрольная группа. Для определения состояния функции почек проводился мониторинг значений сывороточного креатинина, а также выполнялся расчет скорости клубочковой фильтрации по креатинину с использованием формулы CKD-EPI. Определение стадии ОПП было выполнено с применением критериев шкалы AKIN. Результаты. Острое повреждение почек развилось у 28% пациентов. С использованием ROC-анализа определены прогностические способности дооперационных и интраоперационных факторов риска развития острого повреждения почек, а также их пороговые уровни. Установлено, что основными дооперационными предикторами развития острого повреждения почек являются: исходное состояние функции почек (скорость клубочковой фильтрации менее 60 мл/мин/1,73, сывороточный креатинин более 96 мкмоль/л), а также сывороточный общий белок менее 70 г/л.Заключение. Интраоперационной стратегией снижения вероятности развития острого повреждения почек может являться уменьшение длительности искусственного кровообращения и использование аппаратов для аутогемотрансфузии. Purpose. To determine the frequency of acute kidney injury in the early postoperative period after cardiac interventions with bypass application and potential predictors of acute kidney injury.Materials and methods. During this research, 50 patients, who underwent cardiac interventions in the period from January 1 to February 29, 2020, were examined. The patients were divided in 2 groups: the group with acute kidney injury and the control group. The level of serum creatinine and glomerular filtration rate (CKD-EPI equation) were monitored to determine the kidney function. The stage of acute kidney injury was defined using the AKIN scale.Results. It was revealed that 28% of patients had acute kidney injury. The predictive capability of preoperative and intraoperative risk factors of acute kidney injury and their threshold values were determined using the ROC analysis. The main preoperative predictors of acute kidney injury were revealed: preoperative condition of kidney function (glomerular filtration rate less than 60 ml/min/1,73; serum creatinine higher than 96 micromole/l), serum total protein less than 70 g/l. Conclusion. Reduction of the time of bypass usage and application of cell salvage devices can be suggested as intraoperative strategy for kidney protection.
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Huang, Z. S., K. J. Varner, S. M. Barman, and G. L. Gebber. "Diencephalic regions contributing to sympathetic nerve discharge in anesthetized cats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 254, no. 2 (February 1, 1988): R249—R256. http://dx.doi.org/10.1152/ajpregu.1988.254.2.r249.
Повний текст джерелаАнотація:
We reported that the forebrain is responsible for a significant component (38%) of inferior cardiac postganglionic sympathetic nerve discharge (SND) in baroreceptor-denervated cats anesthetized with alpha-chloralose [Huang et al., Am. J. Physiol. 252 (Regulatory Integrative Comp. Physiol. 21): R645-R652, 1987]. The current study was initiated to assess the contribution of various diencephalic regions to the forebrain-dependent component of SND in this preparation. For this purpose, the reductions in inferior cardiac SND and blood pressure produced acutely by midbrain transection at stereotaxic plane A3 in nonlesioned control cats were compared with those in cats in which diencephalic lesions were made with radio-frequency current. Lesions of the anterior medial hypothalamus including the paraventricular nucleus failed to attenuate the decreases in SND and blood pressure produced by midbrain transection. In contrast, the effects of midbrain transection were significantly attenuated by lesions of the lateral hypothalamus (including medial forebrain bundle), posterior medial hypothalamus, or the medial thalamus. We conclude that both the hypothalamus and medial thalamus contribute to SND in anesthetized cats.
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Claassen, Dale E., Richard J. Fels, and Michael J. Kenney. "Altered frequency characteristics of sympathetic nerve activity after sustained elevation in arterial pressure." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 274, no. 3 (March 1, 1998): R694—R703. http://dx.doi.org/10.1152/ajpregu.1998.274.3.r694.
Повний текст джерелаАнотація:
We tested the hypothesis that sustained elevation in mean arterial pressure (MAP) alters the frequency-domain characteristics of efferent sympathetic nerve discharge (SND) after the return of MAP to control levels. Renal, lumbar, and splanchnic SND were recorded before, during, and after a 30-min increase in MAP produced by phenylephrine (PE) infusion in α-chloralose-anesthetized, spontaneously hypertensive (SH) rats. The following observations were made. 1) The basic cardiac-locked pattern of renal, lumbar, and splanchnic SND bursts was altered after sustained elevation in MAP, demonstrating prolonged effects on the neural circuits involved in entraining efferent SND to the cardiac cycle. Importantly, discharge bursts in afferent baroreceptor nerve activity remained pulse-synchronous after sustained increases in arterial pressure. 2) The frequency-domain relationships between the activity in sympathetic nerve pairs were altered after sustained elevation in MAP, suggesting a transformation from a system of tightly coupled neural circuits to one of multiple generators exerting selective control over SND. 3) The most prominent reduction in SND power after sustained elevation in MAP occurred in the frequency band containing the cardiac cycle, indicating that the prolonged suppression of SND after sustained increases in arterial pressure is due primarily to the selective inhibition of cardiac-related SND bursts. We conclude that sustained elevation in MAP profoundly affects the neural circuits responsible for the frequency components of basal SND in SH rats.
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Zhu, Chi, Jung-Hee Seo, and Rajat Mittal. "Computational modelling and analysis of haemodynamics in a simple model of aortic stenosis." Journal of Fluid Mechanics 851 (July 19, 2018): 23–49. http://dx.doi.org/10.1017/jfm.2018.463.
Повний текст джерелаАнотація:
In a study motivated by considerations associated with heart murmurs and cardiac auscultation, numerical simulations are used to analyse the haemodynamics in a simple model of an aorta with an aortic stenosis. The aorta is modelled as a curved pipe with a$180^{\circ }$turn, and three different stenoses with area reductions of 50 %, 62.5 % and 75 % are examined. A uniform steady inlet velocity with a Reynolds number of 2000 is used for all of the cases and direct numerical simulation is employed to resolve the dynamics of the flow. The poststenotic flow is dominated by the jet that originates from the stenosis as well as the secondary flow induced by the curvature, and both contribute significantly to the flow turbulence. On the anterior surface of the modelled aorta, the location with maximum pressure fluctuation, which may be considered as the source location for the murmurs, is found to be located around$60^{\circ }$along the aortic arch, and this location is relatively insensitive to the severity of the stenosis. For all three cases, this high-intensity wall pressure fluctuation includes contributions from both the jet and the secondary flow. Spectral analysis shows that for all three stenoses, the Strouhal number of the vortex shedding of the jet shear layer is close to 0.93, which is higher than the shedding frequency of a corresponding free jet or a jet confined in a straight pipe. This frequency also appears in the pressure spectra at the location postulated as the source of the murmurs, in the form of a ‘break frequency.’ The implications of these findings for cardiac auscultation-based diagnosis of aortic stenosis are also discussed.
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Farrell, A. P., S. Small, and M. S. Graham. "Effect of heart rate and hypoxia on the performance of a perfused trout heart." Canadian Journal of Zoology 67, no. 2 (February 1, 1989): 274–80. http://dx.doi.org/10.1139/z89-040.
Повний текст джерелаАнотація:
While adrenergic stimulation and increased filling pressure of the heart are recognized to increase cardiac stroke volume in the trout heart, the effects of factors such as heart rate and oxygen supply have not been examined. The present study used isolated, saline-perfused trout hearts to determine the maximum cardiac performance during hypoxic perfusion and during changes in pacing frequency similar to the range of heart rate observed in intact trout. The threshold oxygen tension of the perfusate was between 25 and 46 Torr (3.33–6.13 kPa) for maintaining resting and maximum cardiac ouput, but was between 46 and 67 Torr (6.13 – 8.93 kPa) for maintaining maximum power output. Increasing the pacing frequency from 30 to 58 beats/min did not produce a proportionate increase in the maximum cardiac output because maximum stroke volume was reduced significantly. It is suggested that the reduction in maximum stroke volume occurs because atrial filling time is compromised at higher pacing frequencies in the isolated perfused heart.
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Billman, George E., Kristen L. Cagnoli, Thomas Csepe, Ning Li, Patrick Wright, Peter J. Mohler, and Vadim V. Fedorov. "Exercise training-induced bradycardia: evidence for enhanced parasympathetic regulation without changes in intrinsic sinoatrial node function." Journal of Applied Physiology 118, no. 11 (June 1, 2015): 1344–55. http://dx.doi.org/10.1152/japplphysiol.01111.2014.
Повний текст джерелаАнотація:
The mechanisms responsible for exercise-induced reductions in baseline heart rate (HR), known as training bradycardia, remain controversial. Therefore, changes in cardiac autonomic regulation and intrinsic sinoatrial nodal (SAN) rate were evaluated using dogs randomly assigned to either a 10- to 12-wk exercise training ( Ex, n = 15) or an equivalent sedentary period ( Sed, n = 10). Intrinsic HR was revealed by combined autonomic nervous system (ANS) blockade (propranolol + atropine, iv) before and after completion of the study. At the end of the study, SAN function was further evaluated by examining the SAN recovery time (SNRT) following rapid atrial pacing and the response to adenosine in anesthetized animals. As expected, both the response to submaximal exercise and baseline HR significantly ( P < 0.01) decreased, and heart rate variability (HRV; e.g., high-frequency R-R interval variability) significantly ( P < 0.01) increased in the Ex group but did not change in the Sed group. Atropine also induced significantly ( P < 0.01) greater reductions in HRV in the Ex group compared with the Sed group; propranolol elicited similar HR and HRV changes in both groups. In contrast, neither intrinsic HR ( Ex before, 141.2 ± 6.7; Ex after, 146.0 ± 8.0 vs. Sed before, 143.3 ± 11.1; Sed after, 141.0 ± 11.3 beats per minute), the response to adenosine, corrected SNRT, nor atrial fibrosis and atrial fibrillation inducibility differed in the Ex group vs. the Sed group. These data suggest that in a large-animal model, training bradycardia results from an enhanced cardiac parasympathetic regulation and not from changes in intrinsic properties of the SAN.
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Murrell, Carissa, Luke Wilson, James D. Cotter, Samuel Lucas, Shigehiko Ogoh, Keith George, and Philip N. Ainslie. "Alterations in autonomic function and cerebral hemodynamics to orthostatic challenge following a mountain marathon." Journal of Applied Physiology 103, no. 1 (July 2007): 88–96. http://dx.doi.org/10.1152/japplphysiol.01396.2006.
Повний текст джерелаАнотація:
We examined potential mechanisms (autonomic function, hypotension, and cerebral hypoperfusion) responsible for orthostatic intolerance following prolonged exercise. Autonomic function and cerebral hemodynamics were monitored in seven athletes pre-, post- (<4 h), and 48 h following a mountain marathon [42.2 km; cumulative gain ∼1,000 m; ∼15°C; completion time, 261 ± 27 (SD) min]. In each condition, middle cerebral artery blood velocity (MCAv), blood pressure (BP), heart rate (HR), and cardiac output (Modelflow) were measured continuously before and during a 6-min stand. Measurements of HR and BP variability and time-domain analysis were used as an index of sympathovagal balance and baroreflex sensitivity (BRS). Cerebral autoregulation was assessed using transfer-function gain and phase shift in BP and MCAv. Hypotension was evident following the marathon during supine rest and on standing despite increased sympathetic and reduced parasympathetic control, and elevations in HR and cardiac output. On standing, following the marathon, there was less elevation in normalized low-frequency HR variability ( P < 0.05), indicating attenuated sympathetic activation. MCAv was maintained while supine but reduced during orthostasis postmarathon [−10.4 ± 9.8% pre- vs. −15.4 ± 9.9% postmarathon (%change from supine); P < 0.05]; such reductions were related to an attenuation in BRS ( r = 0.81; P < 0.05). Cerebral autoregulation was unchanged following the marathon. These findings indicate that following prolonged exercise, hypotension and postural reductions in autonomic function or baroreflex control, or both, rather than a compromise in cerebral autoregulation, may place the brain at risk of hypoperfusion. Such changes may be critical factors in collapse following prolonged exercise.
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Kimura, Tomomasa, Toru Komatsu, Jun Takezawa, and Yasuhiro Shimada. "Alterations in Spectral Characteristics of Heart Rate Variability as a Correlate of Cardiac Autonomic Dysfunction after Esophagectomy or Pulmonary Resection." Anesthesiology 84, no. 5 (May 1, 1996): 1068–76. http://dx.doi.org/10.1097/00000542-199605000-00008.
Повний текст джерелаАнотація:
Background Both esophagectomy and pulmonary resection are associated with postoperative cardiac complications, partly because of autonomic perturbations involving the heart. This study was undertaken to determine whether heart rate variability (HRV), employed as an index of cardiac autonomic function, changes in patients undergoing esophagectomy or pulmonary resection. Methods Electrocardiographic RR intervals were measured in 20 esophagectomized patients, 10 undergoing right and 10 undergoing left pulmonary resection on the preoperative day as baseline data and on postoperative days 1, 3, 5, 7, 14, and 30. Instantaneous heart rate was calculated every 250 ms from 416-s data of RR intervals. Power spectra of HRV for 128 s were computed using a fast Fourier transform and normalized by squared mean heart rate. The average ten sets of normalized HRV power were obtained by integrating the following power spectral bands: the low-, (0.06-0.10 Hz), high- (0.15-0.40 Hz), and total-frequency regions (0.01-0.40 Hz). Results In the esophagectomy group, mean low-, high-, and total-frequency HRV power decreased after surgery to 17%, 6%, and 15% of their preoperative values, respectively, and these indexes remained suppressed for up to 30 days. After right pulmonary resection, low- and total-frequency HRV power decreased through 30 and 7 postoperative days, respectively. In the left pulmonary resection group, HRV remained unchanged. In the esophagectomy group, mean (+/- SEM) heart rate increased from 78 (+/- 3) bpm to more than 90 bpm throughout the study, and body temperature from 36.5 (+/- 0.1) degrees C to more than 37.0 degrees C through 14 postoperative days. Heart rate and body temperature remained increased for 3 days after pulmonary surgery. Mean arterial pressure remained unchanged in the three surgical groups. Conclusions Reductions indicate HRV after esophagectomy or right pulmonary resection indicate a substantial and prolonged surgical injury to the autonomic nervous control of pulse rate.
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Kozlov, I. A., A. M. Ovezov, and A. A. Pivovarova. "Reduction of risk of perioperative complications in case of cardiac comorbidity." Messenger of ANESTHESIOLOGY AND RESUSCITATION 17, no. 2 (May 15, 2020): 38–48. http://dx.doi.org/10.21292/2078-5658-2020-17-2-38-48.
Повний текст джерелаАнотація:
The objective: based on the published data to describe the conceptual issues of the problem of perioperative cardiac complications in non-cardiac surgery.Results: changes made to international guidelines over the past 3–4 years based on evidence-based studies and meta-analyzes have been analyzed. The article presents data on the etiopathogenesis of various postoperative cardiac complications, assessment of their risk based on the evaluation of functional activities of patients, cardiac risk indices, and modern biomarkers (B-type natriuretic peptides, cardiospecific troponins). The contemporary recommendations on adjuvant pharmacological cardioprotection and rational pharmacotherapy in the perioperative period are analyzed. The article describes specific parameters of diagnostic, treatment and prevention tactics in patients with coronary heart disease, hypertension, chronic heart failure, heart defects, and implanted electronic devices. It concludes that the implementation of the comprehensive strategy aimed at the reduction of risk of pulmonary complications should ensure the decrease in their frequency and mortality due to them.
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Henry, Rebecca A., I.-Li Lu, Larry A. Beightol, and Dwain L. Eckberg. "Interactions between CO2chemoreflexes and arterial baroreflexes." American Journal of Physiology-Heart and Circulatory Physiology 274, no. 6 (June 1, 1998): H2177—H2187. http://dx.doi.org/10.1152/ajpheart.1998.274.6.h2177.
Повний текст джерелаАнотація:
We studied interactions between CO2 chemoreflexes and arterial baroreflexes in 10 supine healthy young men and women. We measured vagal carotid baroreceptor-cardiac reflexes and steady-state fast Fourier transform R-R interval and photoplethysmographic arterial pressure power spectra at three arterial pressure levels (nitroprusside, saline, and phenylephrine infusions) and three end-tidal CO2 levels (3, 4, and 5%, fixed-frequency, large-tidal-volume breathing, CO2 plus O2). Our study supports three principal conclusions. First, although low levels of CO2 chemoreceptor stimulation reduce R-R intervals and R-R interval variability, statistical modeling suggests that this effect is indirect rather than direct and is mediated by reductions of arterial pressure. Second, reductions of R-R intervals during hypocapnia reflect simple shifting of vagally mediated carotid baroreflex responses on the R-R interval axis rather than changes of baroreflex gain, range, or operational point. Third, the influence of CO2 chemoreceptor stimulation on arterial pressure (and, derivatively, on R-R intervals and R-R interval variability) depends critically on baseline arterial pressure levels: chemoreceptor effects are smaller when pressure is low and larger when arterial pressure is high.
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Kokkinos, Peter. "Physical Activity, Health Benefits, and Mortality Risk." ISRN Cardiology 2012 (October 30, 2012): 1–14. http://dx.doi.org/10.5402/2012/718789.
Повний текст джерелаАнотація:
A plethora of epidemiologic evidence from large studies supports unequivocally an inverse, independent, and graded association between volume of physical activity, health, and cardiovascular and overall mortality. This association is evident in apparently healthy individuals, patients with hypertension, type 2 diabetes mellitus, and cardiovascular disease, regardless of body weight. Moreover, the degree of risk associated with physical inactivity is similar to, and in some cases even stronger than, the more traditional cardiovascular risk factors. The exercise-induced health benefits are in part related to favorable modulations of cardiovascular risk factors observed by increased physical activity or structured exercise programs. Although the independent contribution of the exercise components, intensity, duration, and frequency to the reduction of mortality risk is not clear, it is well accepted that an exercise volume threshold defined at caloric expenditure of approximately 1,000 Kcal per week appears to be necessary for significant reduction in mortality risk. Further reductions in risk are observed with higher volumes of energy expenditure. Physical exertion is also associated with a relatively low and transient increase in risk for cardiac events. This risk is significantly higher for older and sedentary individuals. Therefore, such individuals should consult their physician prior to engaging in exercise.
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Heffernan, Kevin S., Sae Young Jae, Victoria J. Vieira, Gary A. Iwamoto, Kenneth R. Wilund, Jeffrey A. Woods, and Bo Fernhall. "C-reactive protein and cardiac vagal activity following resistance exercise training in young African-American and white men." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 296, no. 4 (April 2009): R1098—R1105. http://dx.doi.org/10.1152/ajpregu.90936.2008.
Повний текст джерелаАнотація:
African Americans have a greater prevalence of hypertension and diabetes compared with white Americans, and both autonomic dysregulation and inflammation have been implicated in the etiology of these disease states. The purpose of this study was to examine the cardiac autonomic and systemic inflammatory response to resistance training in young African-American and white men. Linear (time and frequency domain) and nonlinear (sample entropy) heart rate variability, baroreflex sensitivity, tonic and reflex vagal activity, and postexercise heart rate recovery were used to assess cardiac vagal modulation. C-reactive protein (CRP) and white blood cell count were used as inflammatory markers. Twenty two white and 19 African-American men completed 6 wk of resistance training followed by 4 wk of exercise detraining (Post 2). Sample entropy, tonic and reflex vagal activity, and heart rate recovery were increased in white and African-American men following resistance training ( P < 0.05). Following detraining (Post 2), sample entropy, tonic and reflex vagal activity, and heart rate recovery returned to baseline values in white men but remained above baseline in African-American men. While there were no changes in white blood cell count or CRP in white men, these inflammatory markers decreased in African-American men following resistance training, with reductions being maintained following detraining ( P < 0.05). In conclusion, resistance training improves cardiac autonomic function and reduces inflammation in African-American men, and these adaptations remained after the cessation of training. Resistance training may be an important lifestyle modification for improving cardiac autonomic health and reducing inflammation in young African-American men.
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Abad-Alegrìa, Francisco, Carlos Pomaròn, Cristina Aznar, Cristina Muñoz, and Sonia Adelantado. "Objective Assessment of the Sympatholytic Action of Nei-Kuan Acupoint." American Journal of Chinese Medicine 29, no. 02 (January 2001): 201–10. http://dx.doi.org/10.1142/s0192415x0100023x.
Повний текст джерелаАнотація:
From animal experiments and clinical trials, we can think that acupuncture of Nei-Kuan (EH-6) is effective in the control of some vegetative functions. We have tried to determine the real reach of these assumptions by means of simple quantitative measurement methods, such as detection of cardiac frequency and systolic and diastolic blood pressure, and the sympathetic electrical response. The experiments were performed on 29 healthy volunteers. Basal values of these parameters were recorded, and also after orthodox Nei-Kuan acupuncture, non-acupunctural point puncture, supine lying by 15 min, Chü-Tze (EH-3) acupuncture and bipolar electrical stimulus of the median nerve at the Nei-Kuan level in the wrist. Such conditions were designed to evaluate non-specific puncture, repose and direct median nerve stimulation influences in the effects of Nei-Kuan acupuncture. We conclude that Nei-Kuan acupuncture strongly inhibits sympathetic tone, with reduction of cardiac frequency, systolic blood pressure and an important reduction of the amplitude of the sympathetic electrical response; the latency of the electrical response was also prolonged. Some weak effects on blood pressure and cardiac frequency were observed also, as non-specific effects of puncture and median nerve stimulation. From previous anatomical data, we hypothesize that the level of such actions is suprametameric, with strong implication of the diencephalon and cerebral cortex.
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Shi, Ping, Ying Chen, Ming-Ming Guo, and Hong-Liu Yu. "ACUTE EFFECTS OF ALCOHOL ON HEART RATE VARIABILITY: TIME-RELATED CHANGES AND GENDER DIFFERENCE." Biomedical Engineering: Applications, Basis and Communications 26, no. 03 (March 17, 2014): 1450048. http://dx.doi.org/10.4015/s1016237214500483.
Повний текст джерелаАнотація:
Objectives: Alcohol consumption is associated with a broad array of physiologic and behavioral effects including changes in cardiac autonomic activity. In the present study, time-related acute effects of alcohol have been characterized and compared between genders. Methods: A total of 30 healthy subjects (15 males and 15 females) were enrolled in this study. The red wine was given to each subject at a dosage of 0.27 g of pure ethanol per kilogram of body weight. 5-min electrocardiograms (ECGs) were collected before (BR) and at 15 min (P15), 30 min (P30), 45 min (P45) and 60 min (P60) after alcohol intake. Time- and frequency-domain analysis of heart rate variability (HRV) was performed. The time-domain HRV indices include mean RR interval, pNN50, SDNN and RMSSD. The low- (LF: 0.04 to 0.15 Hz) and high-frequency (HF: 0.15 to 0.4 Hz) components along with LF/HF ratio were calculated for frequency-domain analysis of HRV. HRV was also analyzed by mathematical models, e.g. Poincaré plot, which uses a nonlinear geometric representation of change in interbeat heart rate. Poincaré plots indices, SD1, SD2, SD1/SD2 ratio and r RR , were applied in this study for HRV assessment. Results: Alcohol intake was associated with decreased HRV in both time and frequency domains. The lowest HRV was observed 30–40 min after the intake of alcohol. The alcohol intake also caused the decrease of Poincaré plots indices (SD1 and SD1/SD2 in P30, P40 and P60, and r RR in P45), accompanied with a narrower plot area. The changes of HRV indices differed by gender. The male subjects demonstrated a greater decrease of parameters measured in this study compared to the female subjects. Conclusion: Acute effects of alcohol ingestion resulted in reductions in HRV, indicating impaired cardiac autonomic nervous activity. Autonomic nervous activity in the females was less dampened by the alcohol compared to the males.
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Muijtjens, A. M., J. M. Roos, T. T. Prinzen, A. Hasman, R. S. Reneman, and T. Arts. "Noise reduction in estimating cardiac deformation from marker tracks." American Journal of Physiology-Heart and Circulatory Physiology 258, no. 2 (February 1, 1990): H599—H605. http://dx.doi.org/10.1152/ajpheart.1990.258.2.h599.
Повний текст джерелаАнотація:
Deformation of the cardiac wall is measured by using optical or radiopaque markers attached to the wall. When digitized images are used, the accuracy of the measurement of a marker position is limited by pixel resolution and the size of the marker. The spatial accuracy is improved by singular value decomposition (SVD) filtering. This filtering procedure is based on the assumption that displacements of markers are mutually related because they are embedded in a common continuum. In a computer stimulation with 48 markers in 51 video frames, the accuracy of the measurement of a marker position improved from 0.14 to 0.045 (SD) pixel. In an open-chest animal experiment, with markers on the surface of the heart, the deformation patterns were extracted more clearly using SVD filtering, while mutually related high-frequency components were not suppressed. In a 50-frame sequence of 256 X 256 video images of a 45 mm X 35 mm deforming surface with 50 markers of 8 pixels in diameter, the marker position resolution improves from 0.1 to 0.03 (SD) pixel (6 microns). Strain is determined with an accuracy of 0.002 over a distance of 30 pixels (6 mm).
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Houle, Melanie S., and George E. Billman. "Low-frequency component of the heart rate variability spectrum: a poor marker of sympathetic activity." American Journal of Physiology-Heart and Circulatory Physiology 276, no. 1 (January 1, 1999): H215—H223. http://dx.doi.org/10.1152/ajpheart.1999.276.1.h215.
Повний текст джерелаАнотація:
The low-frequency component of the heart rate variability spectrum (0.06–0.10 Hz) is often used as an accurate reflection of sympathetic activity. Therefore, interventions that enhance cardiac sympathetic drive, e.g., exercise and myocardial ischemia, should elicit increases in the low-frequency power. Furthermore, because an enhanced sympathetic activation has been linked to an increased propensity for malignant arrhythmias, one might also predict a greater low-frequency power in animals that are susceptible to ventricular fibrillation than in resistant animals. To test these hypotheses, a 2-min coronary occlusion was made during the last minute of exercise in 71 dogs with healed myocardial infarctions: 43 had ventricular fibrillation (susceptible) and 28 did not experience arrhythmias (resistant). Exercise or ischemia alone provoked significant heart rate increases in both groups of animals, with the largest increase in the susceptible animals. These heart rate increases were attenuated by β-adrenergic receptor blockade. Despite the sympathetically mediated increases in heart rate, the low-frequency power decreased, rather than increased, in both groups, with the largest decrease again in the susceptible animals: 4.0 ± 0.2 (susceptible) vs. 4.1 ± 0.2 ln ms2 (resistant) in preexercise control and 2.2 ± 0.2 (susceptible) vs. 2.9 ± 0.2 ln ms2 (resistant) at highest exercise level. In a similar manner the parasympathetic antagonist atropine sulfate elicited significant reductions in the low-frequency power. Although sympathetic nerve activity was not directly recorded, these data suggest that the low-frequency component of the heart rate power spectrum probably results from an interaction of the sympathetic and parasympathetic nervous systems and, as such, does not accurately reflect changes in the sympathetic activity.
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Schwäbe, Frederic V., Emanuel K. Peter, Manuel H. Taft та Dietmar J. Manstein. "Assessment of the Contribution of a Thermodynamic and Mechanical Destabilization of Myosin-Binding Protein C Domain C2 to the Pathomechanism of Hypertrophic Cardiomyopathy-Causing Double Mutation MYBPC3Δ25bp/D389V". International Journal of Molecular Sciences 22, № 21 (4 листопада 2021): 11949. http://dx.doi.org/10.3390/ijms222111949.
Повний текст джерелаАнотація:
Mutations in the gene encoding cardiac myosin-binding protein-C (MyBPC), a thick filament assembly protein that stabilizes sarcomeric structure and regulates cardiac function, are a common cause for the development of hypertrophic cardiomyopathy. About 10% of carriers of the Δ25bp variant of MYBPC3, which is common in individuals from South Asia, are also carriers of the D389V variant on the same allele. Compared with noncarriers and those with MYBPC3Δ25bp alone, indicators for the development of hypertrophic cardiomyopathy occur with increased frequency in MYBPC3Δ25bp/D389V carriers. Residue D389 lies in the IgI-like C2 domain that is part of the N-terminal region of MyBPC. To probe the effects of mutation D389V on structure, thermostability, and protein–protein interactions, we produced and characterized wild-type and mutant constructs corresponding to the isolated 10 kDa C2 domain and a 52 kDa N-terminal fragment that includes subdomains C0 to C2. Our results show marked reductions in the melting temperatures of D389V mutant constructs. Interactions of construct C0–C2 D389V with the cardiac isoforms of myosin-2 and actin remain unchanged. Molecular dynamics simulations reveal changes in the stiffness and conformer dynamics of domain C2 caused by mutation D389V. Our results suggest a pathomechanism for the development of HCM based on the toxic buildup of misfolded protein in young MYBPC3Δ25bp/D389V carriers that is supplanted and enhanced by C-zone haploinsufficiency at older ages.
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Minasyan, Siranush M., Emma S. Gevorkyan, Tsovinar I. Adamyan, Susanna H. Sargsyan, and Lilit E. Ghukasyan. "FEATURES OF CHANGES IN CARDIAC ACTIVITY UNDER VIBRATION EXPOSURE." Proceedings of the YSU B: Chemical and Biological Sciences 55, no. 2 (255) (August 30, 2021): 189–95. http://dx.doi.org/10.46991/pysu:b/2021.55.2.189.
Повний текст джерелаАнотація:
The results of the study have shown that when exposed to vibration, changes in cardiac activity occur in rabbits, the nature and direction of which depend on the parameters of the dynamic factor. Vibration with a frequency of 20 Hz causes moderate tachycardia, and 40 and 80 Hz – severe tachycardia. Three months of vibration in the first month of exposure causes tachycardia, and after three months of exposure, bradycardia. There is also a reduction in respiratory movements and a decrease in the activity of the enzyme succinate dehydrogenase.
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Weston, Philip J., Martin A. James, Ronnie Panerai, Paul G. McNally, John F. Potter, Herbert Thurston, and John D. Swales. "Abnormal Baroreceptor—Cardiac Reflex Sensitivity is Not Detected by Conventional Tests of Autonomic Function in Patients with Insulin-Dependent Diabetes Mellitus." Clinical Science 91, no. 1 (July 1, 1996): 59–64. http://dx.doi.org/10.1042/cs0910059.
Повний текст джерелаАнотація:
1. Autonomic neuropathy is a common complication of diabetes mellitus and is a major risk factor for sudden death. 2. A group of 30 patients with insulin-dependent diabetes mellitus and 30 age-, sex- and blood pressure-matched control subjects underwent traditional tests of autonomic function. Resting supine R—R interval and systolic blood pressure variability were assessed using spectral analysis methods. In addition, we assessed the baroreceptor—cardiac reflex from the linear relation of the change in R—R interval to the increasing systolic blood pressure measured noninvasively with the Finapres monitor during phase 4 of the Valsalva manoeuvre and from resting heart rate and systolic blood pressure power spectra. 3. Whereas standard tests of autonomic function revealed no differences between patients with insulin-dependent diabetes mellitus and control subjects, there was a significant reduction in power spectral density of heart rate variability around the high-frequency region (125.2 ± 112.9 versus 459.3 ± 189.8 ms2, mean ± SD). Furthermore, reductions in baroreflex sensitivity calculated from the Valsalva manoeuvre were detected in diabetics compared with controls (3.3 ± 1.6 versus 9.5 ± 2.5 ms/mmHg, mean ± SD, P > 0.00001). There were significant relations between impairment of the baroreflex and duration of diabetes (P > 0.001) and poor diabetic control (P > 0.05). 4. In summary, autonomic dysfunction occurs much more frequently in diabetic patients than conventional tests would suggest. Abnormal baroreceptor—cardiac reflex sensitivity in patients with insulin-dependent diabetes mellitus may in part be explained by abnormal parasympathetic function. This unrecognized abnormality may have a role in the increased incidence of sudden death seen in young diabetic subjects.
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Penttilä, Jani, Antti Helminen, Markku Anttila, Susanna Hinkka, and Harry Scheinin. "Cardiovascular and parasympathetic effects of dexmedetomidine in healthy subjects." Canadian Journal of Physiology and Pharmacology 82, no. 5 (May 1, 2004): 359–62. http://dx.doi.org/10.1139/y04-028.
Повний текст джерелаАнотація:
We evaluated the cardiovascular effects of intravenously (i.v.) and buccally administered dexmedetomidine, a selective α2-adrenoceptor agonist. Six healthy male subjects were studied unmedicated and after 2 µg/kg i.v. or buccal doses of dexmedetomidine, using repeated recordings of ECG and blood pressure. Cardiac parasympathetic activity was estimated by measurements of high-frequency (HF) heart rate variability. Intravenous, but not buccal, dexmedetomidine raised systolic blood pressure by 11 ± 5 mmHg (mean ± SEM) and diastolic by 16 ± 3 mmHg (maxima at 10 min). Later on, both i.v., and buccal dexmedetomidine produced a very similar hypotensive effect: on average, [Formula: see text]10 mmHg reductions in systolic and diastolic pressure at 3 h. Intravenous dosing was followed by a decline in heart rate (–11 ± 2 beats/min) accompanied by a trend toward enhanced HF variability (maximal effect at 10 min), which probably reflected baroreflex-mediated parasympathetic efferent neuronal activation. Buccal dexmedetomidine increased significantly the HF variability (maximum at 45 min) without influencing heart rate. We conclude that dexmedetomidine, when administered by a method that avoids concentration peaks, e.g., buccal dosing, can be used to produce a prolonged augmentation of cardiac parasympathetic efferent neuronal activity.Key words: dexmedetomidine, parasympathetic nervous system, heart rate, blood pressure.
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Liu, L., V. I. Krinsky, A. O. Grant, and C. F. Starmer. "Cardiac transient outward potassium current: a pulse chemistry model of frequency-dependent properties." American Journal of Physiology-Heart and Circulatory Physiology 270, no. 1 (January 1, 1996): H386—H397. http://dx.doi.org/10.1152/ajpheart.1996.270.1.h386.
Повний текст джерелаАнотація:
Recent voltage-clamp studies of isolated myocytes have demonstrated widespread occurrence of a transient outward current (I(to)) carried by potassium ions. In the canine ventricle, this current is well developed in epicardial cells but not in endocardial cells. The resultant spatial dispersion of refractoriness is potentially proarrhythmic and may be amplified by channel blockade. The inactivation and recovery time constants of this channel are in excess of several hundred milliseconds, and consequently channel availability is frequency dependent at physiological stimulation rates. When the time constants associated with transitions between different channel conformations are rapid relative to drug binding kinetics, the interactions between drugs and an ion channel can be approximated by a sequence of first-order reactions, in which binding occurs in pulses in response to pulse train stimulation (pulse chemistry). When channel conformation transition time constants do not meet this constraint, analytical characterizations of the drug-channel interaction must then be modified to reflect the channel time-dependent properties. Here we report that the rate and steady-state amount of frequency-dependent inactivation of I(to) are consistent with a generalization of the channel blockade model: channel availability is reduced in a pulsatile exponential pattern as the stimulation frequency is increased, and the rate of reduction is a linear function of the pulse train depolarizing and recovery intervals. I(to) was reduced in the presence of quinidine. After accounting for the use-dependent availability of I(to) channels, we found little evidence of an additional use-dependent component of block after exposure to quinidine, suggesting that quinidine reacts with both open and closed I(to) channels as though the binding site is continuously accessible. The model provides a useful tool for assessing drug-channel interactions when the reaction cannot be continuously monitored.
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Tozzi, P., D. Hayoz, C. Oedman, I. Mallabiabarrena, and L. K. Von Segesser. "Systolic axial artery length reduction: an overlooked phenomenon in vivo." American Journal of Physiology-Heart and Circulatory Physiology 280, no. 5 (May 1, 2001): H2300—H2305. http://dx.doi.org/10.1152/ajpheart.2001.280.5.h2300.
Повний текст джерелаАнотація:
To demonstrate axial artery motion during the cardiac cycle, the common carotid arteries (CCA) of 10 pigs were exposed and equipped with piezoelectric crystals sutured onto the artery as axial position detectors. An echo-tracking system was used to simultaneously measure the CCA diameter. For each animal, data for pressure, length, and diameter were collected at a frequency of 457 Hz. At a mean pulse pressure of 33 ± 8 mmHg, the mean systolodiastolic length difference was 0.3 ± 0.01 mm for a mean arterial segment of 11.35 ± 1.25 mm. Systolic and diastolic diameters were 4.1 ± 0.3 and 3.9 ± 0.2 mm, respectively. The examined CCA segment displayed a mean axial systolic shortening of 2.7%. This study clearly demonstrates, for the first time, that the length of a segment of the CCA changes during the cardiac cycle and that this movement is inversely correlated with pulse pressure. It is also apparent that the segmental axial strain is significantly smaller than the diameter variation during the cardiac cycle and that the impact of the axial strain for compliance computation should be further evaluated.
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Nava, S., and F. Bellemare. "Cardiovascular failure and apnea in shock." Journal of Applied Physiology 66, no. 1 (January 1, 1989): 184–89. http://dx.doi.org/10.1152/jappl.1989.66.1.184.
Повний текст джерелаАнотація:
A model of shock was developed in anesthetized dogs by limiting venous return with a balloon inflated in the right atrium. The change in ventilation (VE) in response to a sustained decrease in arterial pressure (Pa) to 50–60 Torr was studied by recording transdiaphragmatic pressure (Pdi) and diaphragm (Edi) and parasternal intercostal (Eic) electrical activity. Four dogs died of cardiac arrest after 20–60 min. In 11 dogs, VE, after an initial increase, decreased progressively until apnea occurred after 103 +/- 24 min, after 60% reductions in breathing frequency, Pdi, and Eic and a 30% fall in Edi. No decrease in diaphragm contractility was found in response to artificial phrenic nerve stimulation. The cardiocirculatory function deteriorated during shock until it became irreversible at apneic time. No recovery from apnea occurred without a recovery of Pa. We conclude that the fall in VE and ensuing apnea in this model resulted from a decrease in central respiratory neural output associated with a progressive deterioration of the cardiocirculatory function.
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Owain, Williams, Hu Mo, Changaradil Deepthi, Fry Andrew, and Powell Robert. "THUR 054 The heart holds answers the brain cannot to see." Journal of Neurology, Neurosurgery & Psychiatry 89, no. 10 (September 13, 2018): A6.3—A6. http://dx.doi.org/10.1136/jnnp-2018-abn.23.
Повний текст джерелаАнотація:
Neuronal ceroid lipofuscinosis (NCL) is a range of inherited lysosomal storage disorders. This case highlights the cardiac pathology associated with NCL and reports improved seizure control following correction of cardiac arrhythmias.A 26-year-old woman presented with episodes of altered awareness with head and eye deviation on a background of a progressive neurodegenerative disorder. She initially presented at 7 years of age with progressive retinal dystrophy. As a teenager she developed seizures with prominent myoclonus, psychosis, cognitive impairment and immobility. Her epilepsy was refractory to treatment and seizures had increased in frequency prior to admission.ECG demonstrated sinus bradycardia of 30bpm and episodes of 20 s sinus arrest. This was managed by the insertion of a pacemaker, resulting in a dramatic reduction in the frequency of her seizures. Investigation into the underlying disorder was revisited identifying vacuolated lymphocytes and homozygous CLN3 gene deletions. These findings are consistent with a diagnosis of juvenile NCL (Batten disease).This case demonstrates the importance of cardiac monitoring in investigating a change in seizure pattern. We hypothesise that the patient presented with reflex hypoxic seizures secondary to asystolic episodes. It also highlights the value of securing a diagnosis to enable appropriate cardiac screening in NCL patients.
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Le Manach, Yannick, Gary S. Collins, Cristina Ibanez, Jean Pierre Goarin, Pierre Coriat, Julien Gaudric, Bruno Riou та Paul Landais. "Impact of Perioperative Bleeding on the Protective Effect of β-Blockers during Infrarenal Aortic Reconstruction". Anesthesiology 117, № 6 (1 грудня 2012): 1203–11. http://dx.doi.org/10.1097/aln.0b013e31825adaea.
Повний текст джерелаАнотація:
Background The use of β-blockers during the perioperative period remains controversial. Although some studies have demonstrated their protective effects regarding postoperative cardiac complications, others have demonstrated increased mortality when β-blockers were introduced before surgery. Methods In this observational study involving 1,801 patients undergoing aortic reconstruction, we prospectively assessed β-blocker therapy compared with no β-blocker therapy, with regard to cardiac and noncardiac postoperative outcomes using a propensity score approach. The impact of β-blockers was analyzed according to the intraoperative bleeding estimated by transfusion requirements. Results In-hospital mortality was 2.5% (n=45), β-blocker use was associated with a reduced frequency of postoperative myocardial infarction (OR=0.46, 95% CI [0.26; 0.80]) and myocardial necrosis (OR=0.62, 95% CI [0.43; 0.88]) in all patients, but also with an increased frequency of multiple organ dysfunction syndromes (OR=2.78, 95% CI [1.71; 4.61]). In patients with severe bleeding (n=163; 9.1%), the frequency of in-hospital death (OR=6.65, 95% CI [1.09; 129]) and/or multiple organ dysfunction syndromes (OR=4.18, 95% CI [1.81; 10.38]) were markedly increased. Furthermore, no more than 28% of the patients who died presented with postoperative myocardial infarction, whereas 69% of the patient with a postoperative myocardial infarction also presented an excessive bleeding. Conclusions Perioperative β-blocker therapy was associated with an overall reduction in postoperative cardiac events. In the vast majority of patients with low perioperative bleeding, the global effect of β-blockers was protective; in contrast, patients given β-blockers who experienced severe bleeding had higher mortality and an increased frequency of multiorgan dysfunction syndrome.
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Schwarz, Jürgen R., and Christiane K. Bauer. "The ether-à-go-go-Related Gene K+ Current: Functions of a Strange Inward Rectifier." Physiology 14, no. 4 (August 1999): 135–42. http://dx.doi.org/10.1152/physiologyonline.1999.14.4.135.
Повний текст джерелаАнотація:
The erg channels mediate an inward-rectifying K+ current because of their peculiar gating kinetics. They are involved in repolarization of the cardiac action potential, frequency adaptation, and maintenance of the resting potential. Reduction of erg currents via an intracellular signal cascade underlies the thyrotropin-releasing hormone-induced increase in prolactin secretion.