Journal articles: 'Cardiac baroreflex sensitivity'

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Kollai, M., G. Jokkel, I. Bonyhay, J. Tomcsanyi, and A. Naszlady. "Relation between baroreflex sensitivity and cardiac vagal tone in humans." American Journal of Physiology-Heart and Circulatory Physiology 266, no. 1 (January 1, 1994): H21—H27. http://dx.doi.org/10.1152/ajpheart.1994.266.1.h21.

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The extent of dependence of cardiac vagal tone on arterial baroreceptor input has been studied in 12 healthy, young adult subjects. Cardiac vagal tone was defined as the chang in R-R interval after complete cholinergic blockade by atropine. Baroreflex sensitivity was determined with the "Oxford-method": R-R interval was regressed against systolic pressure. The interindividual correlation between cardiac vagal tone and baroreflex sensitivity for falling pressures was found to be significant, but not close (R = 0.81, P = 0.002). In each subject, the baroreflex regression line for falling pressures was extrapolated to the post-atropine R-R interval level; 50 mmHg was considered as minimum and 80 mmHg as maximum threshold level for the integrated baroreflex. From the relation between the individual regression lines and the minimum and maximum threshold levels, it was concluded that cardiac vagal tone could be generated by both baroreflex-dependent and -independent mechanisms, the ratio of which varies in different individuals, with the baroreflex-dependent mechanism being the dominant factor.

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Bealer, Steven L. "Peripheral hyperosmolality reduces cardiac baroreflex sensitivity." Autonomic Neuroscience 104, no. 1 (February 2003): 25–31. http://dx.doi.org/10.1016/s1566-0702(02)00265-5.

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Akimoto, Toshinari, Jun Sugawara, Daisuke Ichikawa, Nobuyuki Terada, Paul J. Fadel, and Shigehiko Ogoh. "Enhanced open-loop but not closed-loop cardiac baroreflex sensitivity during orthostatic stress in humans." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 301, no. 5 (November 2011): R1591—R1598. http://dx.doi.org/10.1152/ajpregu.00347.2011.

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The neural interaction between the cardiopulmonary and arterial baroreflex may be critical for the regulation of blood pressure during orthostatic stress. However, studies have reported conflicting results: some indicate increases and others decreases in cardiac baroreflex sensitivity (i.e., gain) with cardiopulmonary unloading. Thus the effect of orthostatic stress-induced central hypovolemia on regulation of heart rate via the arterial baroreflex remains unclear. We sought to comprehensively assess baroreflex function during orthostatic stress by identifying and comparing open- and closed-loop dynamic cardiac baroreflex gains at supine rest and during 60° head-up tilt (HUT) in 10 healthy men. Closed-loop dynamic “spontaneous” cardiac baroreflex sensitivities were calculated by the sequence technique and transfer function and compared with two open-loop carotid-cardiac baroreflex measures using the neck chamber system: 1) a binary white-noise method and 2) a rapid-pulse neck pressure-neck suction technique. The gain from the sequence technique was decreased from −1.19 ± 0.14 beats·min−1·mmHg−1 at rest to −0.78 ± 0.10 beats·min−1·mmHg−1 during HUT ( P = 0.005). Similarly, closed-loop low-frequency baroreflex transfer function gain was reduced during HUT ( P = 0.033). In contrast, open-loop low-frequency transfer function gain between estimated carotid sinus pressure and heart rate during white-noise stimulation was augmented during HUT ( P = 0.01). This result was consistent with the maximal gain of the carotid-cardiac baroreflex stimulus-response curve (from 0.47 ± 0.15 beats·min−1·mmHg−1 at rest to 0.60 ± 0.20 beats·min−1·mmHg−1 at HUT, P = 0.037). These findings suggest that open-loop cardiac baroreflex gain was enhanced during HUT. Moreover, under closed-loop conditions, spontaneous baroreflex analyses without external stimulation may not represent open-loop cardiac baroreflex characteristics during orthostatic stress.

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PICCIRILLO, Gianfranco, Mauro CACCIAFESTA, Emanuela VIOLA, Elvira SANTAGADA, Marialuce NOCCO, Marco LIONETTI, Carmela BUCCA, Antonio MOISÈ, Sabrina TARANTINI, and Vincenzo MARIGLIANO. "Influence of aging on cardiac baroreflex sensitivity determined non-invasively by power spectral analysis." Clinical Science 100, no. 3 (January 26, 2001): 267–74. http://dx.doi.org/10.1042/cs1000267.

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Aging reduces cardiac baroreflex sensitivity. Our primary aim in the present study was to assess the effects of aging on cardiac baroreflex sensitivity, as determined by power spectral analysis (α index), in a large population of healthy subjects. We also compared the α indexes determined by power spectral analysis with cardiac baroreflex sensitivity measured by the phenylephrine method (BSphen). We studied 142 subjects (79 males/63 females; age range 9–94 years), who were subdivided into five groups according to percentiles of age (25, 50, 75 and 95). Power spectral analysis yields three α indexes: an α low-frequency (LF) index of cardiac baroreflex sensitivity that ranges around 0.1 Hz; an α high-frequency (HF) index reflecting cardiac baroreflex sensitivity corresponding to the respiratory rate; and α total frequency (α TF), a new index whose spectral window includes all power in the range 0.03–0.42 Hz. Spectra were recorded during controlled and uncontrolled respiration. Under both conditions, all three α indexes were higher in the youngest age group (⩽ 34 years old) than in the three oldest groups. Notably, α TF was significantly higher in younger subjects than in the three oldest groups [14±1 ms/mmHg compared with 9±1 (P < 0.05), 8.1±1 (P < 0.001) and 8.1±1 (P < 0.05) ms/mmHg respectively]. BSphen showed a similar pattern [12±1 ms/mmHg compared with 8±0.5 (P < 0.001), 6±0.5 (P < 0.05) and 6±1 (P < 0.05) ms/mmHg respectively]. No significant differences were found for cardiac baroreflex sensitivity among the three oldest groups. All α indexes were correlated inversely with age. The index yielding the closest correlation with BSphen was α TF (r = 0.81, P < 0.001). Cardiac baroreflex sensitivity in normotensive individuals declines with age. It falls predominantly in middle age (from approx. 48 years onwards) and remains substantially unchanged thereafter. The elderly subjects we selected for this study probably had greater resistance to cardiovascular disease that is manifested clinically, with preserved cardiac baroreceptor sensitivity.

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Taylor, C. E., T. Witter, K. El Sayed, S. L. Hissen, A. Johnson, and V. G. Macefield. "Spontaneous sympathetic baroreflex sensitivity is correlated with cardiac baroreflex sensitivity in healthy, young individuals." Autonomic Neuroscience 192 (November 2015): 88. http://dx.doi.org/10.1016/j.autneu.2015.07.109.

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Dutoit, Andrea P., Emma C. Hart, Nisha Charkoudian, B. Gunnar Wallin, Timothy B. Curry, and Michael J. Joyner. "Cardiac Baroreflex Sensitivity Is Not Correlated to Sympathetic Baroreflex Sensitivity Within Healthy, Young Humans." Hypertension 56, no. 6 (December 2010): 1118–23. http://dx.doi.org/10.1161/hypertensionaha.110.158329.

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Taylor, Chloe E., Trevor Witter, Khadigeh El Sayed, Sarah L. Hissen, Aaron W. Johnson, and Vaughan G. Macefield. "Relationship between spontaneous sympathetic baroreflex sensitivity and cardiac baroreflex sensitivity in healthy young individuals." Physiological Reports 3, no. 11 (November 2015): e12536. http://dx.doi.org/10.14814/phy2.12536.

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Padley, James R., David H. Overstreet, Paul M. Pilowsky, and Ann K. Goodchild. "Impaired cardiac and sympathetic autonomic control in rats differing in acetylcholine receptor sensitivity." American Journal of Physiology-Heart and Circulatory Physiology 289, no. 5 (November 2005): H1985—H1992. http://dx.doi.org/10.1152/ajpheart.00430.2005.

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Acetylcholine receptors (AChR) are important in premotor and efferent control of autonomic function; however, the extent to which cardiovascular function is affected by genetic variations in AChR sensitivity is unknown. We assessed heart rate variability (HRV) and baroreflex sensitivity (BRS) in rats bred for resistance (FRL) or sensitivity (FSL) to cholinergic agents compared with Sprague-Dawley rats (SD), confirmed by using hypothermic responses evoked by the muscarinic agonist oxotremorine (0.2 mg/kg ip) ( n ≥ 9 rats/group). Arterial pressure, ECG, and splanchnic sympathetic (SNA) and phrenic (PNA) nerve activities were acquired under anesthesia (urethane 1.3 g/kg ip). HRV was assessed in time and frequency domains from short-term R-R interval data, and spontaneous heart rate BRS was obtained by using a sequence method at rest and after administration of atropine methylnitrate (mATR, 2 mg/kg iv). Heart rate and SNA baroreflex gains were assessed by using conventional pharmacological methods. FRL and FSL were normotensive but displayed elevated heart rates, reduced HRV and HF power, and spontaneous BRS compared with SD. mATR had no effect on these parameters in FRL or FSL, indicating reduced cardiovagal tone. FSL exhibited reduced PNA frequency, longer baroreflex latency, and reduced baroreflex gain of heart rate and SNA compared with FRL and SD, indicating in FSL dual impairment of cardiac and circulatory baroreflexes. These findings show that AChR resistance results in reduced cardiac muscarinic receptor function leading to cardiovagal insufficiency. In contrast, AChR sensitivity results in autonomic and respiratory abnormalities arising from alterations in central muscarinic and or other neurotransmitter receptors.

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Sarzi Braga, Simona, Maria Teresa La Rovere, and Roberto Franco Enrico Pedretti. "Baroreflex sensitivity normalization after cardiac resynchronization therapy." International Journal of Cardiology 109, no. 1 (April 2006): 118–20. http://dx.doi.org/10.1016/j.ijcard.2005.03.072.

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Engelke, K. A., D. F. Doerr, and V. A. Convertino. "A single bout of exhaustive exercise affects integrated baroreflex function after 16 days of head-down tilt." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 269, no. 3 (September 1, 1995): R614—R620. http://dx.doi.org/10.1152/ajpregu.1995.269.3.r614.

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We tested the hypothesis that one bout of maximal exercise performed 24 h before reambulation from 16 days of 6 degrees head-down tilt (HDT) could increase integrated baroreflex sensitivity. Isolated carotid-cardiac and integrated baroreflex function was assessed in seven subjects before and after two periods of HDT separated by 11 mo. On the last day of one HDT period, subjects performed a single bout of maximal cycle ergometry (exercise). Subjects did not exercise after the other HDT period (control). Carotid-cardiac baroreflex sensitivity was evaluated using a neck collar device. Integrated baroreflex function was assessed by recording heart rate (HR) and blood pressure (MAP) during a 15-s Valsalva maneuver (VM) at a controlled expiratory pressure of 30 mmHg. The ratio of change in HR to change in MAP (delta HR/ delta MAP) during phases II and IV of the VM was used as an index of cardiac baroreflex sensitivity. Baroreflex-mediated vasoconstriction was assessed by measuring the late phase II rise in MAP. Following HDT, carotid-cardiac baroreflex sensitivity was reduced (2.8 to 2.0 ms/mmHg; P = 0.05) as was delta HR/ delta MAP during phase II (-1.5 to -0.8 beats/mmHg; P = 0.002). After exercise, isolated carotid baroreflex activity and phase II delta HR/ delta MAP returned to pre-HDT levels but remained attenuated in the control condition. Phase IV delta HR/ delta MAP was not altered by HDT or exercise. The late phase II increase of MAP was 71% greater after exercise compared with control (7 vs. 2 mmHg; P = 0.041).(ABSTRACT TRUNCATED AT 250 WORDS)

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La Rovere, Maria Teresa, Roberto Maestri, and Gian Domenico Pinna. "Baroreflex Sensitivity Assessment – Latest Advances and Strategies." European Cardiology Review 7, no. 2 (2011): 89. http://dx.doi.org/10.15420/ecr.2011.7.2.89.

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The baroreflex mechanism has been recognised as a key part of cardiovascular regulation. Alterations in the baroreceptor-heart rate reflex (baroreflex sensitivity [BRS]) contribute to sympathetic–parasympathetic imbalance, playing a major role in the development and progression of many cardiovascular disorders. Therefore, the measurement of the baroreflex is a source of valuable information in the clinical management of cardiac disease patients. This article reviews the most relevant advances for the measurement of BRS and their clinical and prognostic implications. Novel therapeutic strategies, exploring the use of electrical stimulation of the carotid sinus, have been evaluated recently in experimental and preliminary clinical studies to lower blood pressure and to reduce the level of baroreflex-mediated sympathoexcitation in heart failure. A recent study has also shown that the implementation of an artificial baroreflex system to regulate sympathetic vasomotor tone automatically is feasible.

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La Rovere, Maria Teresa, Roberto Maestri, and Gian Domenico Pinna. "Baroreflex Sensitivity Assessment—Latest Advances and Strategies." Spring 9, no. 1 (February 21, 2012): 22–25. http://dx.doi.org/10.15420/usc.2012.9.1.22.

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The baroreflex mechanism has been recognised as a key part of cardiovascular regulation. Alterations in the baroreceptor-heart rate reflex (baroreflex sensitivity [BRS]) contribute to sympathetic–parasympathetic imbalance, playing a major role in the development and progression of many cardiovascular disorders. Therefore, the measurement of the baroreflex is a source of valuable information in the clinical management of cardiac disease patients. This article reviews the most relevant advances for the measurement of BRS and their clinical and prognostic implications. Novel therapeutic strategies, exploring the use of electrical stimulation of the carotid sinus, have been evaluated recently in experimental and preliminary clinical studies to lower blood pressure and to reduce the level of baroreflex-mediated sympathoexcitation in heart failure. A recent study has also shown that the implementation of an artificial baroreflex system to regulate sympathetic vasomotor tone automatically is feasible.

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Bär, Karl-Jürgen, Michael Karl Boettger, Sandy Berger, Vico Baier, Heinrich Sauer, Vikram K. Yeragani, and Andreas Voss. "Decreased baroreflex sensitivity in acute schizophrenia." Journal of Applied Physiology 102, no. 3 (March 2007): 1051–56. http://dx.doi.org/10.1152/japplphysiol.00811.2006.

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Decreased vagal activity has been described in acute schizophrenia and might be associated with altered cardiovascular regulation and increased cardiac mortality. The aim of this study was to assess baroreflex sensitivity in the context of psychopathology. Twenty-one acute, psychotic, unmedicated patients with a diagnosis of paranoid schizophrenia were investigated after admission to the hospital. Results were compared with 21 healthy volunteers matched with respect to age and sex. Cardiovascular parameters obtained included measures for heart rate variability, baroreflex sensitivity, as well as cardiac output, left ventricular work index, and total peripheral resistance. All parameters investigated were analyzed using linear and novel nonlinear techniques. Positive and negative symptoms were assessed to estimate the impact of psychopathology on autonomic parameters. Subjects with acute schizophrenia showed reduction of baroreflex sensitivity accompanied by tachycardia and greatly increased left ventricular work index. Nonlinear parameters of baroreflex sensitivity correlated with positive symptoms. For heart rate variability, mainly parameters indicating parasympathetic modulation were decreased. Vascular pathology could be excluded as a confounding factor. These results reflect a dysfunctional cardiovascular regulation in acute schizophrenic patients at rest. The changes are similar to adaptational regulatory processes following stressful mental or physical tasks in healthy subjects. This study suggests that hyperarousal in acute schizophrenia is accompanied by decreased efferent vagal activity, thus increasing the risk for cardiovascular mortality. Future studies are warranted to examine the role of the sympathetic system and possible autonomic differences in hyperarousal induced by anxiety and/or external stressful events.

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Yasumasu, Tomiya, Gustavo A. Reyes del Paso, Kazuo Takahara, and Yasuhide Nakashima. "Reduced baroreflex cardiac sensitivity predicts increased cognitive performance." Psychophysiology 43, no. 1 (January 2006): 41–45. http://dx.doi.org/10.1111/j.1469-8986.2006.00377.x.

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Yanagida, Ryo, Yojiro Ogawa, Kaname Ueda, Ken Aoki, and Ken-ichi Iwasaki. "Sustained mild hypergravity reduces spontaneous cardiac baroreflex sensitivity." Autonomic Neuroscience 185 (October 2014): 123–28. http://dx.doi.org/10.1016/j.autneu.2014.07.010.

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Saleh, Tarek M., and Barry J. Connell. "Role of 17β-estradiol in the modulation of baroreflex sensitivity in male rats." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 275, no. 3 (September 1, 1998): R770—R778. http://dx.doi.org/10.1152/ajpregu.1998.275.3.r770.

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Female mammals have an enhanced baroreflex sensitivity compared with their male counterparts, leading researchers to speculate that estrogen modulates autonomic tone. Therefore, this study tests the hypothesis that exogenous estrogen can enhance the baroreflex sensitivity of male rats. Male Sprague-Dawley rats anesthetized with thiobutabarbitol sodium (50 mg/kg) were instrumented to measure blood pressure and heart rate and for the intravenous injection of drugs. The baroreflex was tested using intravenous injections of phenylephrine (0.025, 0.05, and 0.1 mg/kg), and the cardiovascular responses were plotted to obtain a measure of the sensitivity of the cardiac baroreflex. Intravenous injection of estrogen produced dose-related increases in the baroreflex sensitivity due to an increase in the magnitude of the reflex bradycardia. In a separate group of animals, stimulation of the vagus nerve for 2 h resulted in a decrease in baroreflex sensitivity. This effect was blocked when estrogen (1 × 10−2 mg/kg) was administered immediately before the end of stimulation. In conclusion, intravenous injection of estrogen in male rats significantly enhanced baroreflex sensitivity and blocked the attenuation in the baroreflex sensitivity observed after vagal stimulation.

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Gao, Lie, Zhen Zhu, Irving H. Zucker, and Wei Wang. "Cardiac sympathetic afferent stimulation impairs baroreflex control of renal sympathetic nerve activity in rats." American Journal of Physiology-Heart and Circulatory Physiology 286, no. 5 (May 2004): H1706—H1711. http://dx.doi.org/10.1152/ajpheart.01097.2003.

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It is well known that cardiac sympathetic afferent reflexes contribute to increases in sympathetic outflow and that sympathetic activity can antagonize arterial baroreflex function. In this study, we tested the hypothesis that in normal rats, chemical and electrical stimulation of cardiac sympathetic afferents results in a decrease in the arterial baroreflex function by increasing sympathetic nerve activity. Under α-chloralose (40 mg/kg) and urethane (800 mg/kg ip) anesthesia, renal sympathetic nerve activity, mean arterial pressure, and heart rate were recorded. The arterial baroreceptor reflex was evaluated by infusion of nitroglycerin (25 μg iv) and phenylephrine (10 μg iv). Left ventricular epicardial application of capsaicin (0.4 μg in 2 μl) blunted arterial baroreflex function by 46% (maximum slope 3.5 ± 0.3 to 1.9 ± 0.2%/mmHg, P < 0.01). When the central end of the left cardiac sympathetic nerve was electrically stimulated (7 V, 1 ms, 20 Hz), the sensitivity of the arterial baroreflex was similarly decreased by 42% (maximum slope 3.2 ± 0.3 to 1.9 ± 0.4%/mmHg; P < 0.05). Pretreatment with intracerebroventricular injection of losartan (500 nmol in 1 μl of artificial cerebrospinal fluid) completely prevented the impairment of arterial baroreflex function induced by electrical stimulation of the central end of the left cardiac sympathetic nerve (maximum slope 3.6 ± 0.4 to 3.1 ± 0.5%/mmHg). These results suggest that the both chemical and electrical stimulation of the cardiac sympathetic afferents reduces arterial baroreflex sensitivity and the impairment of arterial baroreflex function induced by cardiac sympathetic afferent stimulation is mediated by central angiotensin type 1 receptors.

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Peotta, Veronica A., Agata L. Gava, Elisardo C. Vasquez, and Silvana S. Meyrelles. "Evaluation of baroreflex control of heart rate in renovascular hypertensive mice." Canadian Journal of Physiology and Pharmacology 85, no. 8 (August 2007): 761–66. http://dx.doi.org/10.1139/y07-067.

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The objective of the present study was to evaluate the baroreflex and the autonomic control of heart rate (HR) in renovascular hypertensive mice. Experiments were carried out in conscious C57BL/6 (n = 16) mice 28 days after a 2-kidney 1-clip procedure (2K1C mice) or a sham operation (sham mice). Baroreflex sensitivity was evaluated by measuring changes in heart rate (HR) in response to increases or decreases in mean arterial pressure (MAP) induced by phenylephrine or sodium nitroprusside. Cardiac autonomic tone was determined by use of atropine and atenolol. Basal HR and MAP were significantly higher in 2K1C mice than in sham mice. The reflex tachycardia induced by decreases in MAP was greatly attenuated in 2K1C mice compared with sham mice. Consequently, the baroreflex sensitivity was greatly decreased (2.2 ± 0.4 vs. 4.4 ± 0.3 beats·min–1·mmHg–1) in hypertensive mice compared with sham mice. The reflex bradycardia induced by increases in MAP and the baroreflex sensitivity were similar in both groups. Evaluation of autonomic control of HR showed an increased sympathetic tone and a tendency to a decreased vagal tone in 2K1C mice compared with that in sham mice. 2K1C hypertension in mice is accompanied by resting tachycardia, increased predominance of the cardiac sympathetic tone over the cardiac vagal tone, and impairment of baroreflex sensitivity.

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Monahan, Kevin D. "Effect of aging on baroreflex function in humans." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 293, no. 1 (July 2007): R3—R12. http://dx.doi.org/10.1152/ajpregu.00031.2007.

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Arterial blood pressure (BP) is regulated via the interaction of various local, humoral, and neural factors. In humans, the major neural pathway for acute BP regulation involves the baroreflexes. In response to baroreceptor activation/deactivation, as occurs during transient changes in BP, key determinants of BP, such as cardiac period/heart rate (via the sympathetic and parasympathetic nervous system) and vascular resistance (via the sympathetic nervous system), are modified to maintain BP homeostasis. In this review, the effects of aging on both the parasympathetic and sympathetic arms of the baroreflex are discussed. Aging is associated with decreased cardiovagal baroreflex sensitivity (i.e., blunted reflex changes in R-R interval in response to a change in BP). Mechanisms underlying this decrease may involve factors such as increased levels of oxidative stress, vascular stiffening, and decreased cardiac cholinergic responsiveness with age. Consequences of cardiovagal baroreflex impairment may include increased levels of BP variability, an impaired ability to respond to acute challenges to the maintenance of BP, and increased risk of sudden cardiac death. In contrast, baroreflex control of sympathetic outflow is not impaired with age. Collectively, changes in baroreflex function with age are associated with an impaired ability of the organism to buffer changes in BP. This is evidenced by the reduced potentiation of the pressor response to bolus infusion of a pressor drug after compared to before systemic ganglionic blockade in older compared with young adults.

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Shite, Junya, Erdon Dong, Hiroya Kawai, Suzanne Y. Stevens, and Chang-Seng Liang. "Selegiline improves cardiac sympathetic terminal function and β-adrenergic responsiveness in heart failure." American Journal of Physiology-Heart and Circulatory Physiology 279, no. 3 (September 1, 2000): H1283—H1290. http://dx.doi.org/10.1152/ajpheart.2000.279.3.h1283.

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Selegiline is a centrally acting sympatholytic agent with neuroprotective properties. It also has been shown to promote sympathetic reinnervation after sympathectomy. These actions of selegiline may be beneficial in heart failure that is characterized by increased sympathetic nervous activity and functional sympathetic denervation. Twenty-seven rabbits with rapid cardiac pacing (360 beats/min, 8 wk) and twenty-three rabbits without pacing were randomly assigned to receive selegiline (1 mg/day, 8 wk) or placebo. Rapid pacing increased plasma norepinephrine (NE) and decreased left ventricular fractional shortening, baroreflex sensitivity, cardiac sympathetic nerve terminal profiles, cardiac NE uptake activity, and myocardial β-adrenoceptor density. Selegiline administration to animals with rapid ventricular pacing attenuated the increase in plasma NE and decreases in fractional shortening, baroreflex sensitivity, sympathetic nerve profiles, NE uptake activity and β-adrenoceptor density. Thus selegiline appears to exert a sympatholytic and cardiac neuroprotective effect in pacing-induced cardiomyopathy. The effects are potentially beneficial because selegiline not only improves cardiac function but also increases baroreflex sensitivity in heart failure.

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Gratadour, P., J. P. Viale, J. Parlow, P. Sagnard, H. Counioux, G. Bagou, G. Annat, R. Hughson, and L. Quintin. "Sympathovagal Effects of Spinal Anesthesia Assessed by the Spontaneous Cardiac Baroreflex." Anesthesiology 87, no. 6 (December 1, 1997): 1359–67. http://dx.doi.org/10.1097/00000542-199712000-00015.

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Background The changes in sympathovagal balance induced by spinal anesthesia remain controversial. The spontaneous baroreflex method allows the continuous assessment of the spontaneous engagement of the cardiac baroreflex, giving an index of sympathovagal balance. The purpose of this study was to follow the effects of spinal anesthesia on spontaneous baroreflex sensitivity. Methods Continuous electrocardiogram and noninvasive blood pressure were recorded in 24 patients scheduled for elective inguinal hernia repair and randomly assigned to three groups: (1) no volume loading, (2) volume loading of 15 ml/kg lactated Ringer's solution, and (3) continuous infusion of etilefrine (an ephedrine-like drug). Each patient was studied before, during, and after bupivacaine-induced spinal anesthesia (mean sensory block: T4). Spontaneous baroreflex sensitivity and parameters of time-domain analysis of heart rate variability were calculated from 30 min of recording of each period. Results No significant change in spontaneous baroreflex slope or parameters of time-domain analysis were observed after regional anesthesia in any group. However, three patients experienced episodes of bradycardia and hypotension in the absence of a high block; these three patients showed an increase in spontaneous baroreflex sensitivity and time-domain parameters. Conclusions Using a noninvasive, continuous technique to estimate cardiac sympathovagal balance, no significant variation in autonomic balance induced by spinal anesthesia was observed. However, untoward episodes of bradycardia and hypotension occurred in three patients, who could not be prospectively identified by the parameters studied.

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COOKE, William H., David A. LUDWIG, Paul S. HOGG, Dwain L. ECKBERG, and Victor A. CONVERTINO. "Does the menstrual cycle influence the sensitivity of vagally mediated baroreflexes?" Clinical Science 102, no. 6 (May 17, 2002): 639–44. http://dx.doi.org/10.1042/cs1020639.

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The menstrual cycle provokes several physiological changes that could influence autonomic regulatory mechanisms. We studied the carotid-cardiac baroreflex in ten healthy young women on four occasions over the course of their menstrual cycles (days 0-8, 9-14, 15-20 and 21-25). We drew blood during each session for analysis of oestrogen, progesterone and noradrenaline (norepinephrine) levels, and assessed carotid-cardiac baroreflex function by analysing R-R interval responses to graded neck pressure sequences. Oestrogen levels followed a classical two-peak (cubic) response, with elevated levels on days 9-14 and 21-25 compared with days 0-8 and 15-20 (P =0.0032), while progesterone levels increased exponentially from days 9-14 to days 21-25 (P = 0.0063). Noradrenaline levels increased from an average of 137pg/ml during the first three measurement periods to 199pg/ml during days 21-25 (P = 0.0456). Carotid-cardiac baroreflex gain and operational point were not statistically different at any of the time points during the menstrual cycle (P⩾0.18). These findings are consistent with the notion that beat-to-beat vagal-cardiac regulation does not change over the course of the normal menstrual cycle.

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Saleh, Tarek M., and Barry J. Connell. "Role of the insular cortex in the modulation of baroreflex sensitivity." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 274, no. 5 (May 1, 1998): R1417—R1424. http://dx.doi.org/10.1152/ajpregu.1998.274.5.r1417.

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Cervical vagal stimulation for 2 h results in a depressed baroreflex sensitivity produced by an enhanced sympathetic output, as indicated by increased plasma norepinephrine levels. The current study examined the role of the insular cortex in modulating the vagal stimulation-induced changes in baroreflex sensitivity. Male Sprague-Dawley rats were anesthetized with thiobutabarbitol sodium and instrumented for recording blood pressure, heart rate, intravenous drug administration, and vagal afferent nerve stimulation. Stereotaxic microinjections (300 nl) of either 5% lidocaine or 0.9% saline were made bilaterally into the insula. Thirty minutes after 2 h of vagal stimulation, the baroreflex was significantly depressed and plasma norepinephrine levels were significantly elevated in both groups. The baroreflex was also significantly depressed after bilateral lidocaine injections into the insula, independent of vagal stimulation. However, no significant change in plasma norepinephrine was observed, suggesting that an attenuated parasympathetic output contributed to the altered baroreflex. Taken together, the results suggest that the insular cortex modulates the cardiac baroreflex through a modulation of parasympathetic output.

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Matsukawa, Kanji, Kei Ishii, Ryota Asahara, and Mitsuhiro Idesako. "Central command does not suppress baroreflex control of cardiac sympathetic nerve activity at the onset of spontaneous motor activity in the decerebrate cat." Journal of Applied Physiology 121, no. 4 (October 1, 2016): 932–43. http://dx.doi.org/10.1152/japplphysiol.00299.2016.

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Our laboratory has reported that central command blunts the sensitivity of the aortic baroreceptor-heart rate (HR) reflex at the onset of voluntary static exercise in animals. We have examined whether baroreflex control of cardiac sympathetic nerve activity (CSNA) and/or cardiovagal baroreflex sensitivity are altered at the onset of spontaneously occurring motor behavior, which was monitored with tibial nerve activity in paralyzed, decerebrate cats. CSNA exhibited a peak increase (126 ± 17%) immediately after exercise onset, followed by increases in HR and mean arterial pressure (MAP). With development of the pressor response, CSNA and HR decreased near baseline, although spontaneous motor activity was not terminated. Atropine methyl nitrate (0.1-0.2 mg/kg iv) with little central influence delayed the initial increase in HR but did not alter the response magnitudes of HR and CSNA, while atropine augmented the pressor response. The baroreflex-induced decreases in CSNA and HR elicited by brief occlusion of the abdominal aorta were challenged at the onset of spontaneous motor activity. Spontaneous motor activity blunted the baroreflex reduction in HR by aortic occlusion but did not alter the baroreflex inhibition of CSNA. Similarly, atropine abolished the baroreflex reduction in HR but did not influence the baroreflex inhibition of CSNA. Thus it is likely that central command increases CSNA and decreases cardiac vagal outflow at the onset of spontaneous motor activity while preserving baroreflex control of CSNA. Accordingly, central command must attenuate cardiovagal baroreflex sensitivity against an excess rise in MAP as estimated from the effect of muscarinic blockade.

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Buuse, Maarten, David P. Wilks, and Jennifer L. Cornish. "INHIBITION OF CARDIAC BAROREFLEX SENSITIVITY AFTER CENTRAL DOPAMINERGIC STIMULATION." Clinical and Experimental Pharmacology and Physiology 25, no. 7-8 (August 1998): 624–26. http://dx.doi.org/10.1111/j.1440-1681.1998.tb02264.x.

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Ikegami, Haruhiko, Naoki Matsuda, Tsuyosi Shiga, Mitsuru Momose, Katsuya Kajimoto, Masatoshi Kawana, Akihiko Kawai, Mitsuhiro Hachida, Hitoshi Koyanagi, and Hiroshi Kasanuki. "Vagal reinnervation after cardiac transplantation-evaluation by baroreflex sensitivity." Journal of Cardiac Failure 5, no. 3 (September 1999): 91. http://dx.doi.org/10.1016/s1071-9164(99)91326-x.

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Wesseling, Karel H., John M. Karemaker, Paolo Castiglioni, Emil Toader, Andrei Cividjian, Jos J. Settels, Luc Quintin, and Berend E. Westerhof. "Validity and variability of xBRS: instantaneous cardiac baroreflex sensitivity." Physiological Reports 5, no. 22 (November 2017): e13509. http://dx.doi.org/10.14814/phy2.13509.

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Lhuillier, F., E. D. Dalmas, P. M. Gratadour, A. A. Cividjian, O. C. Boillot, L. Quintin, and J. P. Viale. "Spontaneous baroreflex cardiac sensitivity in end-stage liver disease." European Journal of Anaesthesiology 23, no. 5 (May 2006): 426–32. http://dx.doi.org/10.1017/s0265021506000184.

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Swenne, Cees A., Marianne Bootsma, Barry W. Hyndman, Janine Voogd, and Albert V. G. Bruschke. "Heart Rate Variability, Baroreflex Sensitivity, and Cardiac Vagal Tone." Clinical Science 91, s1 (December 1, 1996): 113–15. http://dx.doi.org/10.1042/cs0910113supp.

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Bealer, Steven L. "Preoptic recess noradrenergic receptors control modification of baroreflex sensitivity by hypertonicity." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 276, no. 1 (January 1, 1999): R44—R51. http://dx.doi.org/10.1152/ajpregu.1999.276.1.r44.

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These studies examined the effects of α1- and α2-adrenoreceptor blockade in the anteroventral portion of the third cerebral ventricle (AV3V) on modification of baroreflex-induced changes in heart rate and renal sympathetic nerve activity (RSNA) induced by hyperosmolality. Local administration of hypertonic artificial cerebrospinal fluid (aCSF) in the AV3V significantly increased baroreflex-induced bradycardia during intravenous phenylephrine but did not alter changes in RSNA during the pressor response or alter tachycardia and neural responses evoked by decreased blood pressure. The enhanced cardiac response was not observed during simultaneous administration of phentolamine (α1- and α2-antagonist) or yohimbine (selective α2-antagonist) in the AV3V region. However, treatment with prazosin (α1-antagonist) did not alter the exaggerated cardiac response evoked by hypertonic aCSF to increased blood pressure. These data demonstrate that acute, local hypertonic stimulation in the AV3V region selectively enhances baroreflex-induced bradycardia by stimulation of α2-adrenergic receptors during acute pressor responses.

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Iliescu, Radu, Ionut Tudorancea, Eric D. Irwin, and Thomas E. Lohmeier. "Chronic baroreflex activation restores spontaneous baroreflex control and variability of heart rate in obesity-induced hypertension." American Journal of Physiology-Heart and Circulatory Physiology 305, no. 7 (October 1, 2013): H1080—H1088. http://dx.doi.org/10.1152/ajpheart.00464.2013.

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The sensitivity of baroreflex control of heart rate is depressed in subjects with obesity hypertension, which increases the risk for cardiac arrhythmias. The mechanisms are not fully known, and there are no therapies to improve this dysfunction. To determine the cardiovascular dynamic effects of progressive increases in body weight leading to obesity and hypertension in dogs fed a high-fat diet, 24-h continuous recordings of spontaneous fluctuations in blood pressure and heart rate were analyzed in the time and frequency domains. Furthermore, we investigated whether autonomic mechanisms stimulated by chronic baroreflex activation and renal denervation—current therapies in patients with resistant hypertension, who are commonly obese—restore cardiovascular dynamic control. Increases in body weight to ∼150% of control led to a gradual increase in mean arterial pressure to 17 ± 3 mmHg above control (100 ± 2 mmHg) after 4 wk on the high-fat diet. In contrast to the gradual increase in arterial pressure, tachycardia, attenuated chronotropic baroreflex responses, and reduced heart rate variability were manifest within 1–4 days on high-fat intake, reaching 130 ± 4 beats per minute (bpm) (control = 86 ± 3 bpm) and ∼45% and <20%, respectively, of control levels. Subsequently, both baroreflex activation and renal denervation abolished the hypertension. However, only baroreflex activation effectively attenuated the tachycardia and restored cardiac baroreflex sensitivity and heart rate variability. These findings suggest that baroreflex activation therapy may reduce the risk factors for cardiac arrhythmias as well as lower arterial pressure.

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Shi, X., J. T. Potts, B. H. Foresman, and P. B. Raven. "Carotid baroreflex responsiveness to lower body positive pressure-induced increases in central venous pressure." American Journal of Physiology-Heart and Circulatory Physiology 265, no. 3 (September 1, 1993): H918—H922. http://dx.doi.org/10.1152/ajpheart.1993.265.3.h918.

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Lower body positive pressure (LBPP) was applied at 4 and 30 Torr to increase central venous pressure (CVP). CVP increased with LBPP (r = 0.55, P < 0.01), and the increases were significant at 4 and 30 Torr (7.4 and 7.8 mmHg) from the control (6.0 mmHg). During LBPP cardiac output increased, which was significantly related to the increase in CVP (r = 0.63, P < 0.01). The carotid baroreflex was elicited by trains of neck pressure and suction from 40 to -65 Torr. The carotid-cardiac and carotid-vasomotor baroreflex responses were assessed by determining the maximal gains of heart rate (HR) interval and intraradial mean arterial pressure (MAP) to changes in carotid sinus pressure using a logistic model. The carotid-cardiac and carotid-vasomotor baroreflex gains were negatively related to LBPP, and at 30 Torr, both gains (5.6 ms/mmHg and -0.14 mmHg/mmHg) were significantly smaller than the control (12.4 ms/mmHg and -0.24 mmHg/mmHg). The decreases in carotid-cardiac and carotid-vasomotor baroreflex sensitivity during LBPP were primarily associated with the increases in CVP (r = -0.52, P < 0.01, and r = -0.74, P < 0.01, respectively). These data suggest that the increases in CVP and/or central blood volume diminish the sensitivity of the carotid baroreflex control of HR and MAP by enhancing the tonic inhibitory influence from the cardiopulmonary baroreceptors.

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Saleh, Tarek M., Barry J. Connell, and Gary V. Allen. "Visceral afferent activation-induced changes in sympathetic nerve activity and baroreflex sensitivity." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 276, no. 6 (June 1, 1999): R1780—R1791. http://dx.doi.org/10.1152/ajpregu.1999.276.6.r1780.

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The following experiments were done to determine whether changes in baroreflex sensitivity evoked by cervical vagus nerve stimulation are due to sympathoexcitation mediated by the parabrachial nucleus. The relative contribution of cardiopulmonary and general gastric afferents within the cervical vagus nerve to the depression in baroreflex sensitivity are also investigated. Male Sprague-Dawley rats anesthetized with thiobutabarbital sodium (50 mg/kg) were instrumented to measure blood pressure and heart rate or for the continuous monitoring of renal sympathetic nerve activity. Baroreflex sensitivity was measured using bolus injections of phenylephrine. Electrical stimulation of the cervical vagus (with or without the aortic depressor nerve) or the abdominal vagus nerve produced a significant increase in renal nerve activity and a decrease in baroreflex sensitivity. Both of these effects were blocked after the microinjection of lidocaine into the parabrachial nucleus before nerve stimulation. Therefore, we conclude that an increase in the activity of cardiac, pulmonary, or general gastric afferents mediated the increased sympathetic output and decreased baroreflex sensitivity via a pathway involving the parabrachial nucleus.

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Arnold, Amy C., and Debra I. Diz. "Endogenous leptin contributes to baroreflex suppression within the solitary tract nucleus of aged rats." American Journal of Physiology-Heart and Circulatory Physiology 307, no. 11 (December 1, 2014): H1539—H1546. http://dx.doi.org/10.1152/ajpheart.00282.2014.

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The decline in cardiovagal baroreflex function that occurs with aging is accompanied by an increase in circulating leptin levels. Our previous studies showed that exogenous leptin impairs the baroreflex sensitivity for control of heart rate in younger rats, but the contribution of this hormone to baroreflex dysfunction during aging is unknown. Thus we assessed the effect of bilateral leptin microinjection (500 fmol/60 nl) within the solitary tract nucleus (NTS) on the baroreflex sensitivity in older (66 ± 2 wk of age) urethane/chloralose anesthetized Sprague-Dawley rats with elevated circulating leptin levels. In contrast to the 63% reduction observed in younger rats, leptin did not alter the baroreflex sensitivity for bradycardia evoked by phenylephrine in older rats (0.76 ± 0.19 baseline vs. 0.71 ± 0.15 ms/mmHg after leptin; P = 0.806). We hypothesized that this loss of sensitivity reflected endogenous suppression of the baroreflex by elevated leptin, rather than cardiovascular resistance to the peptide. Indeed, NTS administration of a leptin receptor antagonist (75 pmol/120 nl) improved the baroreflex sensitivity for bradycardia in older rats (0.73 ± 0.13 baseline vs. 1.19 ± 0.26 at 10 min vs. 1.87 ± 0.32 at 60 min vs. 1.22 ± 0.54 ms/mmHg at 120 min; P = 0.002), with no effect in younger rats. There was no effect of the leptin antagonist on the baroreflex sensitivity for tachycardia, responses to cardiac vagal chemosensitive fiber activation, or resting hemodynamics in older rats. These findings suggest that the actions of endogenous leptin within the NTS, either produced locally or derived from the circulation, contribute to baroreflex suppression during aging.

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Duschek, Stefan, Alexandra Hoffmann, Casandra I. Montoro, and Gustavo A. Reyes del Paso. "Autonomic Cardiovascular Dysregulation at Rest and During Stress in Chronically Low Blood Pressure." Journal of Psychophysiology 33, no. 1 (January 1, 2019): 39–53. http://dx.doi.org/10.1027/0269-8803/a000204.

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Abstract. Chronic low blood pressure (hypotension) is accompanied by symptoms such as fatigue, reduced drive, faintness, dizziness, cold limbs, and concentration difficulties. The study explored the involvement of aberrances in autonomic cardiovascular control in the origin of this condition. In 40 hypotensive and 40 normotensive subjects, impedance cardiography, electrocardiography, and continuous blood pressure recordings were performed at rest and during stress induced by mental calculation. Parameters of cardiac sympathetic control (i.e., stroke volume, cardiac output, pre-ejection period, total peripheral resistance), parasympathetic control (i.e., heart rate variability), and baroreflex function (i.e., baroreflex sensitivity) were obtained. The hypotensive group exhibited markedly lower stroke volume, heart rate, and cardiac output, as well as higher pre-ejection period and baroreflex sensitivity than the control group. Hypotension was furthermore associated with a smaller blood pressure response during stress. No group differences arose in total peripheral resistance and heart rate variability. While reduced beta-adrenergic myocardial drive seems to constitute the principal feature of the autonomic impairment that characterizes chronic hypotension, baroreflex-related mechanisms may also contribute to this state. Insufficient organ perfusion due to reduced cardiac output and deficient cardiovascular adjustment to situational requirements may be involved in the manifestation of bodily and mental symptoms.

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James, Martin A., Ronney B. Panerai, and John F. Potter. "Applicability of New Techniques in the Assessment of Arterial Baroreflex Sensitivity in the Elderly: A Comparison with Established Pharmacological Methods." Clinical Science 94, no. 3 (March 1, 1998): 245–53. http://dx.doi.org/10.1042/cs0940245.

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1. There has been considerable interest in techniques recently developed for the study of arterial baroreceptor—cardiac reflex sensitivity based on analysis of spontaneous baroreflex sequences and on spectral analysis. This study examined how these newer techniques agreed with the established pharmacological methods in elderly subjects. 2. In 20 elderly subjects [10 hypertensive (clinic blood pressure 180 ± 4/88 ± 2 mmHg) and 10 normotensive (clinic blood pressure 136 ± 3/73 ± 2 mmHg)], we assessed baroreflex sensitivity from spontaneous sequences of increasing and decreasing blood pressure and pulse interval and their mean, and from spectral analysis to derive α, the index of overall baroreflex gain. Pharmacological baroreflex sensitivity was derived from the blood pressure and pulse interval responses to depressor (sodium nitroprusside) and pressor (phenylephrine) stimuli, and their mean. 3. Baroreflex sensitivity was significantly lower in the hypertensive group by the pharmacological, sequence and spectral methods (all P < 0.05). 4. There was acceptable agreement between pharmacological baroreflex sensitivity and sequences of the same direction, but with some systematic bias. There was also reasonable agreement between pharmacological and spectral baroreflex sensitivity and close agreement without bias between sequence and spectral methods. 5. The newer and established techniques demonstrate acceptable agreement in the elderly, albeit with some systematic bias. Pharmacological methods have enjoyed historical precedence but newer techniques give equivalent results, and are preferable in some circumstances. The newer techniques may be more descriptive of the spontaneous behaviour of the arterial baroreflex at rest rather than under artificially stimulated conditions.

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Liu, Jun-Li, Hiroshi Murakami, Max Sanderford, Vernon S. Bishop, and Irving H. Zucker. "ANG II and baroreflex function in rabbits with CHF and lesions of the area postrema." American Journal of Physiology-Heart and Circulatory Physiology 277, no. 1 (July 1, 1999): H342—H350. http://dx.doi.org/10.1152/ajpheart.1999.277.1.h342.

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Blockade of the angiotensin II (ANG II) type 1 receptor (AT1) has been shown to restore baroreflex sensitivity in rats and rabbits with experimental chronic heart failure (CHF). Because the modulation of baroreflex function in response to ANG II is mediated in part by AT1 receptors located in the area postrema, we hypothesized that lesions of the area postrema would prevent the enhancement in baroreflex function in response to AT1-receptor blockade in rabbits with pacing-induced CHF. Experiments were carried out on 24 male New Zealand White rabbits that were divided into sham ( n = 12) and lesioned ( n = 12) groups further divided into normal and CHF subgroups ( n = 6 each). All rabbits were identically instrumented to measure cardiac external dimensions, central venous pressure, arterial pressure, heart rate (HR), and renal sympathetic nerve activity (RSNA). After 3–4 wk of pacing, baroreflex sensitivity (infusions of phenylephrine and nitroprusside) was evaluated before and after intravenous administration of the AT1-receptor antagonist L-158,809. Maximum baroreflex sensitivity in nonpaced rabbits was 5.4 ± 0.7 beats ⋅ min−1 ⋅ mmHg−1and 5.2 ± 0.5% of maximum/mmHg for HR and RSNA curves, respectively, and was not altered by L-158,809 in either intact or lesioned rabbits. In contrast, L-158,809 enhanced baroreflex sensitivity in intact rabbits with CHF (HR from 1.6 ± 0.3 to 4.1 ± 0.7 beats ⋅ min−1 ⋅ mmHg−1, P < 0.001; RSNA from 2.3 ± 0.2 to 4.9 ± 0.4% of maximum/mmHg, P < 0.001). However, in CHF rabbits with area postrema lesions, L-158,809 failed to enhance baroreflex sensitivity. Interestingly, area postrema lesions did not normalize the baroreflex in CHF rabbits. From these data we conclude that the area postrema mediates the normalization of baroreflex sensitivity after AT1 blockade in rabbits with CHF but does not modify resting baroreflex function.

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Sykora, Marek, and Jennifer Diedler. "Modulation of Baroreceptor Reflex Sensitivity May Represent a New Therapeutic Target in Acute Stroke." European Neurological Review 4, no. 2 (2009): 46. http://dx.doi.org/10.17925/enr.2009.04.02.46.

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Acute stroke has been associated with several manifestations of autonomic dysfunction including cardiovascular, sudomotor, thermoregulatory, gastrointestinal and urogenital symptoms. In particular, cardiovascular autonomic impairment including blunted baroreflex has been repeatedly shown to be of prognostic importance in acute stroke. Pathophysiological mechanisms of baroreflex changes in acute stroke include lesions of the central autonomic processing with consequent sympathetic system overactivation and impairment of baroreflex functioning. Previous studies have shown that patients with shifted autonomic balance are more prone to develop cardiac complications and have increased cardiovascular morbidity and mortality. Moreover, autonomic dysregulation may play an important role in secondary brain injury after stroke. Therefore, modifying autonomic functions may have important therapeutic implications in acute stroke. In this article, the role of baroreflex impairment in acute stroke and its possible therapeutic relevance is discussed.

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Muzi, Michael, and Thomas J. Ebert. "A Comparison of Baroreflex Sensitivity during Isoflurane and Desflurane Anesthesia in Humans." Anesthesiology 82, no. 4 (April 1, 1995): 919–25. http://dx.doi.org/10.1097/00000542-199504000-00015.

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Background Desflurane anesthesia has been associated with heart rate (HR) and sympathetic nerve activity (SNA) responses that differ from those during isoflurane anesthesia. Whether these differences might be due to better preservation by desflurane of the baroreceptor reflex control of HR or SNA in humans was examined. Methods Baroreflex sensitivity was assessed in 18 volunteers anesthetized with either desflurane or isoflurane. Measurements of HR, blood pressure (BP), and efferent SNA (percutaneous recordings from the peroneal nerve) were made, and baroreflex sensitivity was evaluated at conscious baseline and during 0.5, 1.0, and 1.5 MAC anesthesia. Baroreflex responses were triggered by bolus intravenous injections of nitroprusside (100 micrograms) and phenylephrine (150 micrograms). The linear portions of the baroreflex curves relating HR to mean arterial pressure and relating SNA to diastolic pressure were determined to obtain cardiac and sympathetic baroslopes, respectively. Results Cardiac (HR) baroslopes were equally diminished at increasing MAC of both anesthetics. Sympathetic baroslopes were preserved at 0.5 MAC isoflurane but diminished at 0.5 MAC desflurane. Higher MAC produced equal depression of sympathetic baroslopes with both anesthetics. Conclusions Increasing MAC of desflurane and isoflurane anesthesia results in similar and progressive decreases in BP but dissimilar SNA and HR responses. These differences are not explained by disparate effects of these anesthetics on the baroreceptor reflex control of SNA or HR.

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Abdel-Rahman, Abdel A. "Gender difference in baroreflex-mediated bradycardia in young rats: role of cardiac sympathetic and parasympathetic components." Canadian Journal of Physiology and Pharmacology 77, no. 5 (June 15, 1999): 358–66. http://dx.doi.org/10.1139/y99-028.

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In a previous clinical study we have demonstrated a significantly lower baroreflex-mediated bradycardic response in young women compared with men. The present study determined whether sexual dimorphism in baroreflex sensitivity in young rats also covers the reflex tachycardic response. The study was then extended to test the hypothesis that an attenuated cardiac cholinergic component of the baroreflex heart rate response in females may account for the gender difference. Baroreflex sensitivity (BRS) was expressed as the regression coefficient of the reciprocal relationship between evoked changes in blood pressure and heart rate. BRS measured in conscious rats with phenylephrine (BRSPE) and nitroprusside (BRSNP) represented the reflex bradycardic and tachycardic responses, respectively. Female rats exhibited significantly lower BRSPE compared with male rats (-1.53 ± 0.1 vs. -2.36 ± 0.13 beats·min-1·mmHg-1; p < 0.05) but similar BRSNP (-2.60 ± 0.20 vs. -2.29 ± 0.17 beats·min-1·mmHg-1). Blockade of cardiac muscarinic receptors with atropine methyl bromide elicited greater attenuation of BRSPE in male than in female rats (72 ± 4.6 vs. 53 ± 6.7% inhibition; p < 0.01) and abolished the gender difference. In male rats cardiac muscarinic blockade attenuated BRSPE significantly more than did cardiac beta-adrenergic receptor blockade with propranolol (72 ± 4.6 vs. 43 ± 2.7; p < 0.01), which suggests greater dependence of BRSPE on the parasympathetic component. In females, muscarinic and beta-adrenergic blockade elicited similar attenuation of BRSPE. The findings suggest that (i) BRS is differentially influenced by gender; female rats exhibit substantially lower BRSPE but similar BRSNP compared with age-matched male rats and (ii) the sexual dimorphism in BRSPE results, at least partly, from a smaller increase in vagal outflow to the heart in response to baroreceptor activation.Key words: gender difference, baroreflex sensitivity, vagal outflow, conscious rats.

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Brown, C. Ann, Larry A. Wolfe, Sylvia Hains, Glorianne Ropchan, and Joel Parlow. "Spontaneous baroreflex sensitivity after coronary artery bypass graft surgery as a function of gender and age." Canadian Journal of Physiology and Pharmacology 81, no. 9 (September 1, 2003): 894–902. http://dx.doi.org/10.1139/y03-087.

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The effects of coronary artery bypass graft (CABG) surgery on spontaneous baroreflex (SBR) sensitivity and heart rate variability were examined in 11 women and 23 men preoperatively and 5 days postoperatively. Electrocardiograph RR interval and beat-by-beat arterial blood pressure data were collected continuously for 20 min in the supine and standing postures. Coarse graining spectral analysis was performed on the heart rate variability data. Spontaneous baroreflex sensitivity declined after surgery with a differential influence of gender. Men showed a decrease in SBR slope following surgery, with a greater decrease in the standing posture; the parasympathetic (PNS) indicator was lower postoperatively and in the standing posture; the reduction in low-frequency (LF) power was greater for the younger men. In women, the PNS indicator was lower in the standing posture. Both men and women showed a decrease in high-frequency power following CABG surgery, which decreased the sensitivity of the short-term cardiac control mechanisms that modulate heart rate, with the greater effects occurring in men. The reduction in SBR sensitivity indicates that the ability of the cardiovascular system to respond rapidly to changing stimuli was compromised. The decline in the PNS indicator implies that patients were vulnerable to the risks of myocardial ischemia, sympathetically mediated cardiac dysrhythmias, and sudden cardiac death.Key words: spectral analysis, spontaneous baroreflex sensitivity, CABG surgery, gender, age, posture.

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Dworkin, Barry R., and Susan Dworkin. "Baroreflexes of the rat. III. Open-loop gain and electroencephalographic arousal." American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 286, no. 3 (March 2004): R597—R605. http://dx.doi.org/10.1152/ajpregu.00469.2003.

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In early studies of humans, baroreflex sensitivity was found to be higher during sleep; however, subsequent observations in several species, including humans, have been at variance with the original reports. Sleep and arousal are behavioral states, and it is difficult to accurately and repeatedly measure baroreflex sensitivity in behaving animals. However, pharmacologically immobilized (neuromuscularly blocked) rats have apparently normal sleep-wakefulness cycles, and baroreflex gain can be measured directly in this preparation. Using the delta band of the EEG (EEGδ) as an index of sleep and arousal and open-loop aortic depressor nerve (ADN) stimulation as a baroreflex input, we found that blood pressure (BP) level depended on arousal ( r = -0.416; P < 0.0001), and BP baroreflex gain depended on BP level ( r = 0.496; P < 0.0001), but that BP baroreflex gain was independent of arousal ( r = 0.001; NS). Heart period (HP) was different; although HP level depended on arousal ( r = 0.352; P < 0.0001), HP baroreflex gain did not depend on HP level ( r = 0.029; NS), and HP baroreflex gain increased with arousal ( r = 0.315; P < 0.0001). A partial-correlations analysis showed that the presence of the relationship between BP level and BP baroreflex gain probably attenuated the relationship between arousal and BP gain. The results are consistent 1) with physiological findings showing that arousal attenuates afferent transmission through the nucleus of the solitary tract and enhances sympathoinhibition at the rostral ventrolateral medulla; and 2) with observations in humans and animals showing increased cardiac baroreflex sensitivity during sleep, but little if any effect of sleep on BP baroreflex sensitivity. The findings are relevant to all methods of baroreflex gain estimation that use HP as the index of baroreflex activation.

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Crandall, C. G., K. A. Engelke, V. A. Convertino, and P. B. Raven. "Aortic baroreflex control of heart rate after 15 days of simulated microgravity exposure." Journal of Applied Physiology 77, no. 5 (November 1, 1994): 2134–39. http://dx.doi.org/10.1152/jappl.1994.77.5.2134.

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To determine the effects of simulated microgravity on aortic baroreflex control of heart rate, we exposed seven male subjects (mean age 38 +/- 3 yr) to 15 days of bed rest in the 6 degrees head-down position. The sensitivity of the aortic-cardiac baroreflex was determined during a steady-state phenylephrine-induced increase in mean arterial pressure combined with lower body negative pressure to counteract central venous pressure increases and neck pressure to offset the increased carotid sinus transmural pressure. The aortic-cardiac baroreflex gain was assessed by determining the ratio of the change in heart rate to the change in mean arterial pressure between baseline conditions and aortic baroreceptor-isolated conditions (i.e., phenylephrine + lower body negative pressure + neck pressure stage). Fifteen days of head-down tilt increased the gain of the aortic-cardiac baroreflex (from 0.45 +/- 0.07 to 0.84 +/- 0.18 beats.min-1.mmHg-1; P = 0.03). Reductions in blood volume and/or maximal aerobic capacity may represent the underlying mechanism(s) responsible for increased aortic baroreflex responsiveness after exposure to a ground-based analogue of microgravity.

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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.

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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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Cowie, M. R., and J. M. Rawles. "A Modified Method of Quantifying the Carotid Baroreceptor-Heart Rate Reflex in Man: The Effect of Age and Blood Pressure." Clinical Science 77, no. 2 (August 1, 1989): 223–28. http://dx.doi.org/10.1042/cs0770223.

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1. Carotid baroreceptor-heart rate sensitivity has been measured non-invasively by a modified neck-chamber method that utilizes all cardiac intervals recorded in 6 min during 84 respiratory cycles. 2. In a replication study in 10 subjects the mean baroreflex sensitivity was 5.52 ms/mmHg and the mean (sd) difference between determinations was 0.70 (0.74) ms/mmHg. 3. Baroreflex sensitivity was measured in 48 untreated subjects of mean age 43 (range 20–71) years with blood pressures ranging from 104 to 202 mmHg (13.9 to 26.9 kPa) systolic and 52 to 120 mmHg (6.9 to 16.0 kPa) diastolic [average 142/87 mmHg (18.9/11.6 kPa)]. Both systolic and diastolic pressures correlated with age (r = 0.53, P < 0.001 and r = 0.44, P < 0.01). 4. Baroreflex sensitivity determined throughout respiration was log-normally distributed with a median value of 2.24 ms/mmHg, which declined with age (r = −0.63, P < 0.001). 5. After allowing for the effects of age, baroreflex sensitivity throughout respiration was not independently related to either systolic or diastolic blood pressure.

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Sullebarger, J. T., C. S. Liang, P. D. Woolf, A. E. Willick, and J. F. Richeson. "Comparison of phenylephrine bolus and infusion methods in baroreflex measurements." Journal of Applied Physiology 69, no. 3 (September 1, 1990): 962–67. http://dx.doi.org/10.1152/jappl.1990.69.3.962.

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Phenylephrine (PE) bolus and infusion methods have both been used to measure baroreflex sensitivity in humans. To determine whether the two methods produce the same values of baroreceptor sensitivity, we administered intravenous PE by both bolus injection and graded infusion methods to 17 normal subjects. Baroreflex sensitivity was determined from the slope of the linear relationship between the cardiac cycle length (R-R interval) and systolic arterial pressure. Both methods produced similar peak increases in arterial pressure and reproducible results of baroreflex sensitivity in the same subjects, but baroreflex slopes measured by the infusion method (9.9 +/- 0.7 ms/mmHg) were significantly lower than those measured by the bolus method (22.5 +/- 1.8 ms/mmHg, P less than 0.0001). Pretreatment with atropine abolished the heart rate response to PE given by both methods, whereas plasma catecholamines were affected by neither method of PE administration. Naloxone pretreatment exaggerated the pressor response to PE and increased plasma beta-endorphin response to PE infusion but had no effect on baroreflex sensitivity. Thus our results indicate that 1) activation of the baroreflex by the PE bolus and infusion methods, although reproducible, is not equivalent, 2) baroreflex-induced heart rate response to a gradual increase in pressure is less than that seen with a rapid rise, 3) in both methods, heart rate response is mediated by the vagus nerves, and 4) neither the sympathetic nervous system nor the endogenous opiate system has a significant role in mediating the baroreflex control of heart rate to a hypertensive stimulus in normal subjects.

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Sich??, Jean P., Roland G. Asmar, Jean M. Mallion, Daniel Herpin, Pascal Poncelet, Bernard Chamontin, Vincent Comparat, Virginie Gressin, and Sophie Boutelant. "Non-invasive ambulatory blood pressure variability and cardiac baroreflex sensitivity." Journal of Hypertension 13, no. 12 (December 1995): 1654???1659. http://dx.doi.org/10.1097/00004872-199512010-00026.

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Petraki, M., E. Kouidi, D. Grekas, and A. Deligiannis. "Effects of exercise training during hemodialysis on cardiac baroreflex sensitivity." Clinical Nephrology 70, no. 09 (September 1, 2008): 210–19. http://dx.doi.org/10.5414/cnp70210.

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Fisher, James P., Abrar Ahmed, Jasmine Nelson, Shigehiko Ogoh, and Paul J. Fadel. "Influence Of Age On Cardiac Baroreflex Sensitivity During Dynamic Exercise." Medicine & Science in Sports & Exercise 38, Suppl 1 (November 2006): S18. http://dx.doi.org/10.1249/00005768-200611001-00069.

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ROVERE, MARIA TERESA, and PETER J. SCHWARTZ. "Baroreflex Sensitivity as a Cardiac and Arrhythmia Mortality Risk Stratifier." Pacing and Clinical Electrophysiology 20, no. 10 (October 1997): 2602–13. http://dx.doi.org/10.1111/j.1540-8159.1997.tb06110.x.

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Journal articles on the topic 'Cardiac baroreflex sensitivity'

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