Статті в журналах: "Inotropic interventions"

1

Brixius, Klara, Marcus Pietsch, Susanne Hoischen, Jochen Müller-Ehmsen, and Robert H. G. Schwinger. "Effect of inotropic interventions on contraction and Ca2+ transients in the human heart." Journal of Applied Physiology 83, no. 2 (August 1, 1997): 652–60. http://dx.doi.org/10.1152/jappl.1997.83.2.652.

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Brixius, Klara, Marcus Pietsch, Susanne Hoischen, Jochen Müller-Ehmsen, and Robert H. G. Schwinger. Effect of inotropic interventions on contraction and on Ca2+ transients in the human heart. J. Appl. Physiol. 83(2): 652–660, 1997.—The present study investigated the influences of inotropic intervention on the intracellular Ca2+ transient {intracellular Ca2+concentration ([Ca2+]i)} and contractile twitch. Isometric twitch and [Ca2+]i(fura 2 ratio method) were measured simultaneously (1 Hz, 37°C) after stimulation with Ca2+(0.9–3.2 mM), the cardiac glycoside ouabain (Oua; 0.1 μM), the β1- and β2-adrenoceptor-agonist isoprenaline (Iso; 1–10 nM), and the Ca2+ sensitizer EMD-57033 (30 μM) by using isolated human nonfailing right auricular trabeculae ( n = 19). Inotropic interventions increased force of contraction and peak rate of tension rise (+ T) significantly. Only Iso stimulated peak rate of tension decay (− T) higher than + T ( P< 0.05), thereby reducing time of contraction ( T twitch). EMD-57033 increased + T more effectively than − T and prolonged T twitch( P < 0.05). Ca2+, Oua, and Iso, but not EMD-57033, increased systolic Ca2+. Diastolic Ca2+ increased after stimulation with Oua or Ca2+, but not in the presence of EMD-57033. Iso shortened the Ca2+ transient and did not influence diastolic Ca2+. In conclusion, positive inotropic agents differently affect force and [Ca2+]idepending on their mode of action. Inotropic interventions influence diastolic Ca2+ and thus may be less advantageous in a situation with altered intracellular Ca2+ homeostasis (e.g., heart failure due to dilated cardiomyopathy).

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2

Bing, O. H., N. L. Hague, C. L. Perreault, C. H. Conrad, W. W. Brooks, S. Sen, and J. P. Morgan. "Thyroid hormone effects on intracellular calcium and inotropic responses of rat ventricular myocardium." American Journal of Physiology-Heart and Circulatory Physiology 267, no. 3 (September 1, 1994): H1112—H1121. http://dx.doi.org/10.1152/ajpheart.1994.267.3.h1112.

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To examine the mechanisms by which thyroid hormone modulates the inotropic state of rat myocardium, we studied the effects of thyroid state on isolated rat left ventricular papillary muscle function and intracellular calcium transients in the baseline state and in response to calcium and isoproterenol. Marked differences in contractile state of papillary muscles from hypothyroid and thyroid hormone-treated rats seen under baseline conditions (1.0 mM bath calcium, 30 degrees C, stimulation rate 12/min) do not appear to be due to differences in intracellular calcium concentration ([Ca2+]i) or to changes in myofilament calcium sensitivity but correlate with shifts in myosin isozyme distribution. In response to superimposed inotropic interventions (calcium, 0.625-5.0 mM, or isoproterenol, 10(-8)-10(-6) M), myocardial thyroid state modulates peak [Ca2+]i and inotropy, both of which are increased in thyroid hormone-treated relative to hypothyroid myocardium. The change in inotropy appears to be proportional to peak [Ca2+]i, whether mediated directly by calcium or as a result of beta-adrenergic stimulation. Thus, whereas baseline differences between hypothyroid and thyroid hormone-treated myocardium appear to be due to differences in myosin isozymes and presumed changes in adenosinetriphosphatase activity and cross-bridge cycling, superimposed inotropic responses appear to be mediated by changes in [Ca2+]i.

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3

Bahler, R. C., and P. Martin. "Effects of loading conditions and inotropic state on rapid filling phase of left ventricle." American Journal of Physiology-Heart and Circulatory Physiology 248, no. 4 (April 1, 1985): H523—H533. http://dx.doi.org/10.1152/ajpheart.1985.248.4.h523.

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Afterload, activation sequence, inotropism, and extent of shortening affect the time constant (T) of left ventricular (LV) isovolumic pressure decay, yet it is unknown if they modify peak lengthening velocity of the LV minor axis [(dD/dt)/D]. Accordingly, we studied their effects on (dD/dt)/D, measured by sonomicrometry, in nine anesthetized open-chest dogs during atrial pacing at 2 Hz. Afterload was increased 20-40 mmHg by 1) constricting the ascending aorta and 2) occluding the descending aorta for four beats. Activation was altered by right ventricular pacing. These interventions, plus constriction of venae cavae, were studied during four inotropic states. Aortic stenosis increased (dD/dt)/D (P less than 0.05), whereas occlusion of the descending aorta, vena caval constriction, and right ventricular pacing decreased (dD/dt)/D (P less than 0.05). Left atrial pressure was constant except during vena caval constriction. Alterations in inotropic state modified (dD/dt)/D (P less than 0.001). Extent of shortening and (dD/dt)/D were directly related (r = 0.80, P less than 0.001). Changes in (dD/dt)/D and T were inversely related (r = 0.70, P less than 0.001), and alterations in the interval from -dP/dtpeak to the end of rapid filling were directly related to changes in T (r = 0.75, P less than 0.001). We conclude that (dD/dt)/D can be modified by systolic and diastolic load perturbations, activation sequence, and inotropic interventions. These effects relate to changes in extent of shortening, time course of inactivation, or both.

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4

Binkley, P. F., D. B. Van Fossen, G. J. Haas, and C. V. Leier. "Increased ventricular contractility is not sufficient for effective positive inotropic intervention." American Journal of Physiology-Heart and Circulatory Physiology 271, no. 4 (October 1, 1996): H1635—H1642. http://dx.doi.org/10.1152/ajpheart.1996.271.4.h1635.

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Positive inotropic intervention with dobutamine in patients with congestive heart failure is accompanied by complementary vascular changes, as measured by the aortic input impedance spectrum, that promote the efficient transfer of augmented myocardial contractile power. It is unknown whether this is a nonspecific response to increased ventricular contractility or is a function of the properties of the positive inotropic agent employed. Therefore, the influence of two different positive inotropic interventions, dobutamine and dopamine, on ventricular-vascular coupling was examined in 15 patients with congestive heart failure. Significant reductions in characteristic aortic impedance, wave reflection, and low-frequency impedance moduli were noted with dobutamine and were not seen with dopamine. Consequently, a significantly (P = 0.0008) greater increase in pulsatile, rather than steady-state, power output was noted with dopamine that was reflective of a significantly diminished efficiency of power transfer. Therefore, optimal transfer of increased ventricular contractile power in patients with congestive heart failure requires increases in large vessel compliance and complementary changes in ventriculoarterial coupling.

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5

Rose, Horst, Stefanie Pöpping, Stefan Mruck, and Helmut Kammermeier. "Influence of inotropic interventions on efficiency of cardiomyocyte contraction." Journal of Molecular and Cellular Cardiology 24 (August 1992): S110. http://dx.doi.org/10.1016/0022-2828(92)91811-i.

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6

Neumann, J. "A renaissance of positive inotropic interventions to treat heart failure?" Cardiovascular Research 59, no. 3 (September 1, 2003): 534–35. http://dx.doi.org/10.1016/s0008-6363(03)00557-1.

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7

Furukawa, Yasuyuki, and Paul Martin. "Attenuation of the responses to repeated cholinergic interventions in the isolated dog atrium." Canadian Journal of Physiology and Pharmacology 64, no. 2 (February 1, 1986): 206–12. http://dx.doi.org/10.1139/y86-031.

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In the isolated, blood-perfused canine right atrium, which was pretreated with propranolol, negative chronotropic and inotropic responses were evoked by stimulation of the intramural parasympathetic nerve fibers or by intra-arterial infusion of acetylcholine (ACh). Successive cholinergic interventions were applied; first, a conditioning intervention for 2 min was given, then this was followed by a test intervention for 4 min. The two interventions were separated by a rest period that varied from 15 to 240 s. The cardiac responses to the conditioning parasympathetic nerve stimulation quickly reached maximum levels, and then they "faded" or progressively diminished back toward the control level. The inotropic responses to the conditioning infusion of ACh (1 μg/min) faded slightly but the chronotropic response did not. After the rest period, the test nerve stimulation evoked responses that also gradually faded with time. The maximal amplitude of the responses to the test simuli were less than those to the conditioning stimuli. This reduction in the maximal amplitude of the cardiac responses to the test stimuli was more pronounced with high frequency stimulation (30 Hz) than with low frequency stimulation (5 Hz). The decrement was also more pronounced the shorter the rest period, and it was greater at earlier times after beginning the stimulation. Conversely, the maximal cardiac responses to test infusions of ACh were not appreciably less than the responses to the conditioning infusions. We conclude, therefore, that the diminution of the cardiac responses to the second test stimulation of the parasympathetic nerve fibers was mainly ascribable to a prejunctional rather than to a postjunctional mechanism.

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8

Krstic, Anna, and Marie-Louise Ward. "CA2+ Handling in Non-Failing Hypertrophic Cardiomyocytes Subjected to Inotropic Interventions." Biophysical Journal 120, no. 3 (February 2021): 110a—111a. http://dx.doi.org/10.1016/j.bpj.2020.11.891.

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9

Langione, Marianna, J. Manuel Pioner, Sonette Steczina, Giulia Vitale, Elisabetta Cerbai, Chiara Tesi, Raffaele Coppini, Michael Regnier, Corrado Poggesi, and Cecilia Ferrantini. "Engineered heart tissues for studying twitch tension and inotropic pharmacological interventions." Biophysical Journal 121, no. 3 (February 2022): 396a. http://dx.doi.org/10.1016/j.bpj.2021.11.778.

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10

van der Linden, L. P., E. T. van der Velde, H. C. van Houwelingen, A. V. Bruschke, and J. Baan. "Determinants of end-systolic pressure during different load alterations in the in situ left ventricle." American Journal of Physiology-Heart and Circulatory Physiology 267, no. 5 (November 1, 1994): H1895—H1906. http://dx.doi.org/10.1152/ajpheart.1994.267.5.h1895.

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Because of the strong dependency of the end-systolic pressure-volume relation on the type of transient loading intervention in the in situ left ventricle (LV), experiments in the basal inotropic state in 16 open-chest anesthetized dogs were reanalyzed to find additional variables to model and predict end-systolic pressure (ESP) of both afterloading and preloading interventions by a single equation. Random-coefficients regression analysis was performed on 22 experiments in the basal inotropic state simultaneously, yielding an overall R2 of 0.97. The major part of total variance of ESP was due to linear terms of end-systolic volume (ESV) (74%) and stroke volume (SV) (19%). The SV effect was consistently negative and quantitatively quite important. An average load-independent end-systolic elastance of 6.7 mmHg/ml and an average SV effect of -5.7 mmHg/ml ejected were estimated, separating the “force-length” property from shortening effects in the in situ LV. History-related effects appeared to be only minor.

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11

Gupta, M. P., I. R. Innes, and N. S. Dhalla. "Responses of contractile function to ruthenium red in rat heart." American Journal of Physiology-Heart and Circulatory Physiology 255, no. 6 (December 1, 1988): H1413—H1420. http://dx.doi.org/10.1152/ajpheart.1988.255.6.h1413.

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Isolated rat hearts exhibited a biphasic contractile response to varying concentrations of ruthenium red. A negative inotropic effect was observed with concentrations of 0.025–0.5 microM, whereas a reversal of these initial changes toward control or even exceeding the predrug values was obtained as ruthenium red concentration was increased to 2.5 or 5.0 microM. High concentrations (12.5–25.0 microM) of ruthenium red caused a sustained contracture. In contrast, isolated frog hearts exhibited only a sustained negative inotropic effect at 0.25–12.5 microM ruthenium red. In studies with rat heart, both negative and positive inotropic effects of 2.5 microM ruthenium red were blocked either by increasing the concentration of Ca2+ (from 1.25 to 5.0 mM) or by decreasing the concentration of Na+ (from 140 to 35 mM) in the perfusion medium. The contracture induced by 12.5 microM ruthenium red was markedly inhibited when Ca2+ in the medium was lowered. The positive inotropic effect and contracture due to ruthenium red were also blocked by 1 microM of verapamil and 1.5 mM of amiloride; however, these interventions did not prevent the initial negative inotropic effect of ruthenium red. These experiments suggest the role of extracellular Ca2+ in the dose- and time-dependent effects of ruthenium red on contractile function of the rat heart. Furthermore, the positive inotropic response to ruthenium red may be related to its actions on the Na+-dependent Ca2+ movements in the cardiac cell.

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12

Popping, S., S. Mruck, Y. Fischer, D. Kulsch, I. Ionescu, H. Kammermeier, and H. Rose. "Economy of contraction of cardiomyocytes as influenced by different positive inotropic interventions." American Journal of Physiology-Heart and Circulatory Physiology 271, no. 1 (July 1, 1996): H357—H364. http://dx.doi.org/10.1152/ajpheart.1996.271.1.h357.

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In the present study the effects of the novel cardiotonic agent EMD-57033 on contraction and energetic demand of isolated, electrically stimulated cardiomyocytes were investigated and compared with the effects of enhancement of extracellular calcium and of the beta-mimetic isoproterenol. In a specially designed setup [H. Rose, K.H. Strotmann, S. Popping, Y. Fischer, D. Kulsch, and H. Kammermeier. Am. J. Physiol. 261 (Heart Circ. Physiol. 30): H1329-H1334, 1991] parameters of contractile behavior and metabolic demand (O2 consumption) of isolated cardiac myocytes were measured. For a given enhancement of contractile performance (cell shortening) the increase in energetic demand (VO2) after application of EMD-57033 were markedly lower than on treatment with elevated extracellular Ca2+ concentration or with isoproterenol. This economization of positive inotropic effects was proposed to be due to two factors. First, stimulation-related ion cycling was only slightly enhanced with marked increase in contraction amplitude after application of EMD-57033. Second, calcium sensitization reflected in a leftward shift of the calcium concentration needed for half-maximum force development could be interpreted to be mediated by modulation of the cross-bridge dynamics of the myofilaments, where reduction of the switch-off rate of the cross bridges and prolongation of their force-generating states were presumed to be involved. Lowered pH (7.0) decreased economy of contraction. EMD-57033 restored contraction amplitude and economy of contraction at lowered pH.

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13

Frampton, J. E., C. H. Orchard, and M. R. Boyett. "Diastolic, systolic and sarcoplasmic reticulum [Ca2+] during inotropic interventions in isolated rat myocytes." Journal of Physiology 437, no. 1 (June 1, 1991): 351–75. http://dx.doi.org/10.1113/jphysiol.1991.sp018600.

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14

Schiffmann, Holger, Markus Flesch, Claudia Häuseler, Annette Pfahlberg, Michael Böhm, and Gerhard Hellige. "Effects of different inotropic interventions on myocardial function in the developing rabbit heart." Basic Research in Cardiology 97, no. 1 (January 1, 2002): 76–87. http://dx.doi.org/10.1007/s395-002-8390-1.

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15

Bavendiek, U., K. Brixius, G. Münch, C. Zobel, J. Müller-Ehmsen, and R. H. G. Schwinger. "Effect of inotropic interventions on the force-frequency relation in the human heart." Basic Research in Cardiology 93 (October 28, 1998): s076—s085. http://dx.doi.org/10.1007/s003950050224.

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16

Hellenbrand, W. K., G. A. Klassen, J. A. Armour, O. Sezerman, and B. Paton. "Autonomic nervous system regulation of epicardial coronary vein systolic and diastolic blood velocity as measured by a laser Doppler velocimeter." Canadian Journal of Physiology and Pharmacology 64, no. 12 (December 1, 1986): 1463–72. http://dx.doi.org/10.1139/y86-248.

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The velocity of blood in a major epicardial coronary vein accompanying the left anterior descending coronary artery of dogs was measured by means of a 140-μm fiber optic probe connected to a laser Doppler velocimeter. Right atrial pressure, left ventricular intramyocardial and cavity pressures, aortic pressure, as well as peripheral and central coronary venous pressures were compared with the velocity of blood measured in the epicardial coronary vein midway between the sites of the catheters measuring proximal and distal coronary vein pressures. During control conditions, coronary vein velocity was 14–18 cm/s during systole and 1.0–2.1 cm/s during diastole. Right stellate ganglion stimulation, norepinephrine or isoproterenol increased diastolic coronary vein velocity significantly, whereas left stellate ganglion stimulation did not. Average peak systolic velocity was not affected by these interventions. During these positive inotropic interventions, the peak coronary vein velocity usually occurred later in the cardiac cycle than during control conditions. Positive inotropic interventions appeared to decrease coronary vein velocity during systole and increase it during diastole. Left vagosympathetic trunk stimulation decreased diastolic but not systolic coronary vein velocity and usually caused peak coronary vein velocity to occur earlier in the cardiac cycle than during control states. Changes induced by vagosympathetic trunk stimulation usually occurred within one cardiac cycle. It is concluded that coronary vein blood velocity can be influenced by the autonomic nervous system.

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17

Prajapati, Ramlal, Priyadarshini Manay, Kavin Sugumar, Vinay Rahandale, and Rajeev Satoskar. "Acute pancreatitis: predictors of mortality, pancreatic necrosis and intervention." Turkish Journal of Surgery 37, no. 1 (March 1, 2021): 13–21. http://dx.doi.org/10.47717/turkjsurg.2021.5072.

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Objective: Several predictive scoring systems are used in the prognostication of acute pancreatitis (AP). However, the quantity of evidence of these prognostic systems in the Indian population remains sparse. The aim of our study was to evaluate the usefulness of such prognostic scores to predict mortality, incidence of pancreatic necrosis and intervention in AP. Material and Methods: This was an observational study of patients diagnosed with AP between June 2012 and November 2013 in a tertiary referral center in India. Vital signs, biochemical tests and CT-findings were recorded to identify SIRS, Ranson’s score and CT-severity index at diagnosis. Chi square test was used to compare incidence of mortality, pancreatic necrosis, and intervention between mild versus severe acute pancreatitis groups. Results: A total of 100 patients with AP were treated during out study period. Ranson’s score more than 7 and presence of pancreatic necrosis were significantly associated with increased mortality (p< 0.05). SIRS, CTSI score more than 7, inotropic support, and complications were more frequently associated with patients with necrosis. Prophylactic antibiotics did not decrease mortality, but decreased intervention rate (p< 0.05). Presence of systemic inflammatory response syndrome (SIRS), Ranson’s score > 7, necrosis, inotropic support and presence of complications were associated with a greater rate of interventions including surgery and percutaneous procedures (p< 0.05). Conclusion: We validate SIRS, Ranson’s, and CTSI score as prognostic markers for AP in the Indian population. These predictors, when used in combination, can direct early monitoring and aggressive management in order to decrease mortality associated with severe AP.

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18

Ravens, Ursula, Susanne Link, Jennifer Gath, and Mark I. M. Noble. "Post-Rest Potentiation and its Decay after Inotropic Interventions in Isolated Rat Heart Muscle." Pharmacology & Toxicology 76, no. 1 (January 1995): 9–16. http://dx.doi.org/10.1111/j.1600-0773.1995.tb00095.x.

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19

JEWELL, B. R., and D. A. HANCK. "Effects of inotropic interventions on end systolic length-force curve of cat ventricular muscle." Cardiovascular Research 21, no. 8 (August 1, 1987): 559–64. http://dx.doi.org/10.1093/cvr/21.8.559.

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20

Caremani, Marco, Francesca Pinzauti, Joseph D. Powers, Serena Governali, Theyencheri Narayanan, Ger J. M. Stienen, Massimo Reconditi, Marco Linari, Vincenzo Lombardi, and Gabriella Piazzesi. "Inotropic interventions do not change the resting state of myosin motors during cardiac diastole." Journal of General Physiology 151, no. 1 (December 3, 2018): 53–65. http://dx.doi.org/10.1085/jgp.201812196.

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When striated (skeletal and cardiac) muscle is in its relaxed state, myosin motors are packed in helical tracks on the surface of the thick filament, folded toward the center of the sarcomere, and unable to bind actin or hydrolyze ATP (OFF state). This raises the question of whatthe mechanism is that integrates the Ca2+-dependent thin filament activation, making myosin heads available for interaction with actin. Here we test the interdependency of the thin and thick filament regulatory mechanisms in intact trabeculae from the rat heart. We record the x-ray diffraction signals that mark the state of the thick filament during inotropic interventions (increase in sarcomere length from 1.95 to 2.25 µm and addition of 10−7 M isoprenaline), which potentiate the twitch force developed by an electrically paced trabecula by up to twofold. During diastole, none of the signals related to the OFF state of the thick filament are significantly affected by these interventions, except the intensity of both myosin-binding protein C– and troponin-related meridional reflections, which reduce by 20% in the presence of isoprenaline. These results indicate that recruitment of myosin motors from their OFF state occurs independently and downstream from thin filament activation. This is in agreement with the recently discovered mechanism based on thick filament mechanosensing in which the number of motors available for interaction with actin rapidly adapts to the stress on the thick filament and thus to the loading conditions of the contraction. The gain of this positive feedback may be modulated by both sarcomere length and the degree of phosphorylation of myosin-binding protein C.

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21

Pioner, Josè Manuel, Lorenzo Santini, Chiara Palandri, Daniele Martella, Flavia Lupi, Marianna Langione, Silvia Querceto, et al. "Optical Investigation of Action Potential and Calcium Handling Maturation of hiPSC-Cardiomyocytes on Biomimetic Substrates." International Journal of Molecular Sciences 20, no. 15 (August 3, 2019): 3799. http://dx.doi.org/10.3390/ijms20153799.

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Cardiomyocytes from human induced pluripotent stem cells (hiPSC-CMs) are the most promising human source with preserved genetic background of healthy individuals or patients. This study aimed to establish a systematic procedure for exploring development of hiPSC-CM functional output to predict genetic cardiomyopathy outcomes and identify molecular targets for therapy. Biomimetic substrates with microtopography and physiological stiffness can overcome the immaturity of hiPSC-CM function. We have developed a custom-made apparatus for simultaneous optical measurements of hiPSC-CM action potential and calcium transients to correlate these parameters at specific time points (day 60, 75 and 90 post differentiation) and under inotropic interventions. In later-stages, single hiPSC-CMs revealed prolonged action potential duration, increased calcium transient amplitude and shorter duration that closely resembled those of human adult cardiomyocytes from fresh ventricular tissue of patients. Thus, the major contribution of sarcoplasmic reticulum and positive inotropic response to β-adrenergic stimulation are time-dependent events underlying excitation contraction coupling (ECC) maturation of hiPSC-CM; biomimetic substrates can promote calcium-handling regulation towards adult-like kinetics. Simultaneous optical recordings of long-term cultured hiPSC-CMs on biomimetic substrates favor high-throughput electrophysiological analysis aimed at testing (mechanistic hypothesis on) disease progression and pharmacological interventions in patient-derived hiPSC-CMs.

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22

Caremani, Marco, Serena Governali, Massimo Reconditi, Francesca Pinzauti, Theyencheri Narayanan, Ger J. Stienen, Marco Linari, Vincenzo Lombardi, and Gabriella Piazzesi. "Modumodulation by Inotropic Interventions of the Regulatory State of the Cardiac Thick Filament in Diastole." Biophysical Journal 118, no. 3 (February 2020): 593a. http://dx.doi.org/10.1016/j.bpj.2019.11.3212.

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23

Butler, C. K., A. Y. K. Wong, and J. A. Armour. "Systolic pressure gradients between the wall of the left ventricle, the left ventricular chamber, and the aorta during positive inotropic states: implications for left ventricular efficiency." Canadian Journal of Physiology and Pharmacology 66, no. 7 (July 1, 1988): 873–79. http://dx.doi.org/10.1139/y88-142.

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To study systolic pressure gradients developed between the left ventricular wall, its chamber, and the aortic root, in one group of dogs left ventricle ventral wall intramyocardial pressure, left ventricular outflow tract pressure, and aorta pressure were compared with aortic flow as well as left ventricular dimension changes during control conditions as well as during positive intropic states induced by isoproterenol, stellate ganglion stimulation, and noradrenaline. In another group of dogs systolic pressures in the ventral wall of the left ventricle, the main portion of the left ventricular chamber, and the aorta were compared with aortic flow during similar interventions, before and after the administration of phentolamine. Pressure gradients between the wall of the left ventricle and the outflow tract of the left ventricle were minimal during control states, but during the three positive inotropic states were increased significantly. In contrast, pressure gradients between the outflow tract of the left ventricle and the aortic root were insignificant during positive inotropic states; those between the wall and main portion of the chamber were only significantly different during left stellate ganglion stimulation. The data derived from these experiments indicate that useful peak power output of the left ventricle (systolic aortic pressure × flow) is unchanged following isoproterenol infusion, but is increased by stellate ganglion stimulation and noradrenaline. The useful peak power output index (an index of left ventricular efficiency derived by dividing useful peak power output by peak intramyocardial pressure) was reduced more by isoproterenol than the other two interventions. It is concluded that the product of aortic flow and pressure does not accurately indicate the efficiency of the heart during hyperdynamic states. Second, a derived momentum equation indicates that the relatively large pressure gradients which develop between the main chamber of the left ventricle and the aortic root during positive inotropic states are due primarily to fluid dynamic changes and internal dimension changes within the chamber.

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24

De Marco, Teresa, and Kanu Chatterjee. "Refractory Heart Failure: A Therapeutic Approach." Journal of Intensive Care Medicine 11, no. 3 (May 1996): 121–48. http://dx.doi.org/10.1177/088506669601100301.

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Optimal “triple therapy” for patients with chronic congestive heart failure (CHF) includes diuretics, digoxin, and either angiotensin-converting enzyme inhibitors or hydralazine plus nitrates. Refractory CHF is defined as symptoms of CHF at rest or repeated exacerbations of CHF despite “optimal” triple-drug therapy. Most patients with refractory CHF require hemodynamic monitoring and treatment in the intensive care unit. If easily reversible causes of refractory CHF cannot be identified, then more aggressive medical and surgical interventions are necessary. The primary goal of intervention is to improve hemodynamics to palliate CHF symptoms and signs (i.e., dyspnea, fatigue, edema). Secondary goals include improved vital organ and tissue perfusion, discharge from the intensive care unit, and, in appropriate patients, bridge to cardiac transplantation. Medical interventions include inotropic resuscitation (e.g., adrenergic agents, phosphodiesterase inhibitors, allied nonglycoside inodilators), load resuscitation (e.g., afterload and preload reduction with nitroprusside or nitroglycerin; preload reduction with diuretics and diuretic facilitators, such as dopaminergic agents or ultrafiltration), and electrical resuscitation (e.g., prevention of sudden death, correction of new or rapid atrial fibrillation, or dual chamber pacing in the setting of relative prolongation of the PR interval and diastolic mitral/tricuspid regurgitation). Surgical interventions are temporizing (e.g., intra-aortic balloon pump and other mechanical assist devices) or definitive (e.g., coronary artery revascularization, valvular surgery, and cardiac transplantation). Although these interventions may improve immediate survival in the short term, only coronary artery revascularization and cardiac transplantation have been shown to improve long-term survival.

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25

Affolter, Jeremy T., and Nancy S. Ghanayem. "Preoperative management of the neonate with critical aortic valvar stenosis." Cardiology in the Young 24, no. 6 (December 2014): 1111–16. http://dx.doi.org/10.1017/s1047951114002029.

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AbstractNeonatal critical aortic stenosis is a rare form of CHD that often presents with cardiogenic shock. Although surgical and cardiac catheterisation-based interventions have been successful in alleviating left ventricular outflow tract obstruction, it remains associated with high morbidity and mortality. Critical aortic stenosis results in elevated left ventricular wall stress, which ultimately increases myocardial oxygen consumption and disrupts coronary artery perfusion during diastole, leading to ventricular dysfunction and cardiogenic shock. Critical care management before definitive intervention should be tailored to optimising oxygen delivery and reducing metabolic consumption of the myocardium and peripheral organ systems. This can be accomplished with prostaglandin infusion to maintain system perfusion through patency of the arterial duct, inotropic support, mechanical ventilation, and central nervous system abrogation. Management should also include a multi-specialty medical team including paediatric cardiothoracic surgeons and paediatric cardiologists with expertise in cardiac catheterisation, imaging, and transplantation.

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Chiu, Y. C., K. R. Walley, and L. E. Ford. "Comparison of the effects of different inotropic interventions on force, velocity, and power in rabbit myocardium." Circulation Research 65, no. 5 (November 1989): 1161–71. http://dx.doi.org/10.1161/01.res.65.5.1161.

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Stemmer, Paul, Tai Akera, Theodore M. Brody, and Eikichi Hosoya. "13-propylberberine reduces response of guinea-pig myocardium to inotropic interventions including changes in extracellular Ca2+." Life Sciences 39, no. 16 (October 1986): 1411–16. http://dx.doi.org/10.1016/0024-3205(86)90544-8.

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Teitel, David F., R. Klautz, P. Steenduk, E. T. van der Velde, F. van Bel, and J. Baan. "The End-Systolic Pressure-Volume Relationship in the Newborn Lamb: Effects of Loading and Inotropic Interventions." Pediatric Research 29, no. 5 (May 1991): 473–82. http://dx.doi.org/10.1203/00006450-199105010-00012.

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29

PIESKE, B. "Influence of positive inotropic interventions on the force-frequency-relation in nonfailing and failing human myocardium." Journal of Molecular and Cellular Cardiology 23 (July 1991): S86. http://dx.doi.org/10.1016/0022-2828(91)90771-d.

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BUSSELEN, P. "Inotropic interventions and sarcoplasmic reticulum calcium content estimated by caffeine rapid cooling contractures in heart muscle." Journal of Molecular and Cellular Cardiology 24 (July 1992): 44. http://dx.doi.org/10.1016/0022-2828(92)93452-p.

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Hexeberg, E., K. Matre, S. Birkeland, and J. Lekven. "Nonuniform shortening of the anterior wall of feline left ventricles." American Journal of Physiology-Heart and Circulatory Physiology 257, no. 4 (October 1, 1989): H1165—H1173. http://dx.doi.org/10.1152/ajpheart.1989.257.4.h1165.

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Recorded performance of segments between implanted ultrasonic crystals placed at midwall position of the left ventricle reportedly depends almost exclusively on midwall function and alignment with fibers. Accordingly, one would expect the ratio between performance of a segment perpendicular to midwall fiber direction (transverse) and a parallel segment (longitudinal) to be constant and independent of changes in preload, afterload, and the inotropic state. We tested this hypothesis by implanting cross-oriented crystal pairs in nine open-chest cats and studied their performance during preload and afterload changes with and without isoproterenol infusion. Fiber orientation across the ventricular wall was determined by serial histological sectioning. The ratio between performance of transverse and longitudinal segments (trans/long) changed with interventions. Increased end-diastolic pressure leads to increased segment performances as well as trans/long. Inotropic stimulation produced increased sensitivity to preload changes both for individual segment performances and for trans/long. These results suggest that longitudinal segments represent the function of midwall fibers, whereas transverse segments may well represent the function of sub-endocardial fibers, which run closer to this orientation. Thus trans/long provides a way to quantify nonuniformity of local myocardial contraction.

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Schmidt, Ulrich, Robert H. G. Schwinger, and Michael Bohm. "Halothane Restores the Altered Force-Frequency Relationship in Failing Human Myocardium." Anesthesiology 82, no. 6 (June 1, 1995): 1456–62. http://dx.doi.org/10.1097/00000542-199506000-00017.

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Background The terminally failing human myocardium exerts a negative force-frequency relationship (FFR), whereas a positive FFR occurs in nonfailing myocardium. To study the possibility of pharmacologically influencing this defect of the failing human heart, the effect of halothane on the basal FFR and the FFR in the presence of isoproterenol and ouabain was investigated. Methods Experiments were performed on isolated, electrically driven (0.5-2 Hz, 37 degrees C, Ca2+ 1.8 mmol/l) ventricular preparations. Myocardium from human failing and nonfailing hearts was obtained at cardiac surgery. To further characterize the studied myocardium, the positive inotropic effect of isoproterenol and the density of beta-adrenoceptors were measured using the radioligand 125I-CYP. Results Halothane produced a negative inotropic effect. The anesthetic (0.38 mmol/l) reversed the negative FFR in failing myocardium, antagonized the effect of isoproterenol (0.1 mumol/l) on FFR, and restored the FFR in the presence of ouabain. Conclusions Halothane restores the FFR in human failing myocardium possibly by influencing the intracellular Ca2+ homeostasis. These findings provide evidence that pharmacologic interventions, e.g., during anesthesia, may influence contractility also as a result of a depressed or enhanced FFR.

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Scheffer, Ashley. "Methylene blue treatment of pediatric patients in the cardiovascular intensive care unit." Southwest Journal of Pulmonary and Critical Care 23, no. 1 (July 3, 2021): 8–17. http://dx.doi.org/10.13175/swjpcc022-21.

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Background: In both adults and children, hypotension related to a vasoplegic state has multiple etiologies, including septic shock, burn injury or cardiopulmonary bypass-induced vasoplegic syndrome likely due to an increase in nitric oxide (NO) within the vasculature. Methylene blue is used at times to treat this condition, but its use in pediatric cardiac patients has not been described previously in the literature. Objective: 1) Analyze the mean arterial blood pressures and vasoactive-inotropic scores of pediatric patients whose hypotension was treated with methylene blue compared to hypotensive controls; 2) Describe the dose administered and the pathologies of hypotension cited for methylene blue use; 3) Compare the morbidity and mortality of pediatric patients treated with methylene blue versus controls. Design: A retrospective chart review. Setting: Cardiac ICU in a quaternary care free-standing children’s hospital. Patients: Thirty-two patients with congenital heart disease who received methylene blue as treatment for hypotension, fifty patients with congenital heart disease identified as controls. Interventions: None. Measurements and Main Results: Demographic and vital sign data was collected for all pediatric patients treated with methylene blue during a three-year study period. Mixed effects linear regression models analyzed mean arterial blood pressure trends for twelve hours post methylene blue treatment and vasoactive-inotropic scores for twenty-four hours post treatment. Methylene blue use correlated with an increase in mean arterial blood pressure of 10.8mm Hg over a twelve-hour period (p< 0.001). Mean arterial blood pressure trends of patients older than one year did not differ significantly from controls (p=1.00), but patients less than or equal to one year of age had increasing mean arterial blood pressures that were significantly different from controls (p=0.02). Mixed effects linear regression modeling found a statistically significant decrease in vasoactive-inotropic scores over a twenty-four-hour period in the group treated with methylene blue (p< 0.001). This difference remained significant comparted to controls (p=0.003). Survival estimates did not detect a difference between the two groups (p=0.39). Conclusion: Methylene blue may be associated with a decreased need for vasoactive-inotropic support and may correlate with an increase in mean arterial blood pressure in patients who are less than or equal to one year of age.

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LEE, J. A., and D. G. ALLEN. "Comparison of the effects of inotropic interventions on isometric tension and shortening in isolated ferret ventricular muscle." Cardiovascular Research 23, no. 9 (September 1, 1989): 748–55. http://dx.doi.org/10.1093/cvr/23.9.748.

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Greyson, Clifford, Ya Xu, Li Lu, and Gregory G. Schwartz. "Right ventricular pressure and dilation during pressure overload determine dysfunction after pressure overload." American Journal of Physiology-Heart and Circulatory Physiology 278, no. 5 (May 1, 2000): H1414—H1420. http://dx.doi.org/10.1152/ajpheart.2000.278.5.h1414.

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Volume expansion and inotropic stimulation are used clinically to augment cardiac output during acute right ventricular (RV) pressure overload. We previously showed that a brief period of RV pressure overload causes RV free wall dysfunction that persists after normal loading conditions have been restored. However, the impact of volume expansion and inotropic stimulation on the severity of RV dysfunction after acute pressure overload is unknown. We hypothesized that the severity of RV dysfunction after RV pressure overload would be related to the level of RV free wall systolic stress during RV pressure overload, rather than to the specific interventions used to augment RV function. Chloralose-anesthetized, open-chest pigs were subjected to 1 h of RV pressure overload caused by pulmonary artery constriction, followed by 1 h of recovery after release of pulmonary artery constriction. A wide range of RV free wall systolic stress during RV pressure overload was achieved by either closing or opening the pericardium (to simulate volume expansion) and by administering or not administering dobutamine. The severity of RV free wall dysfunction 1 h after RV pressure overload was strongly and directly correlated with the values of two hemodynamic variables during RV pressure overload: RV free wall area at peak RV systolic pressure (determined by sonomicrometry) and peak RV systolic pressure, two of the major determinants of peak RV free wall systolic stress. Opening or closing the pericardium, and using or not using dobutamine during RV pressure overload, had no independent effects on the severity of RV dysfunction. The findings suggest that the goal of therapeutic intervention during RV pressure overload should be to achieve the required augmentation of cardiac output with the smallest possible increase in RV free wall systolic stress.

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Lee, En-Pei, Jainn-Jim Lin, Shao-Hsuan Hsia, Oi-Wa Chan, Sheng-Ling Jan, and Han-Ping Wu. "Cutoff Values of Hemodynamic Parameters in Pediatric Refractory Septic Shock." Children 9, no. 3 (February 22, 2022): 303. http://dx.doi.org/10.3390/children9030303.

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Background: Refractory septic shock can cause severe morbidities and mortalities in children. Resuscitation based on hemodynamics is important in children with critical illness. Thus, this study aimed to identify the hemodynamics of refractory septic shock associated with poor prognosis at an early stage to allow for timely interventions. Methods: We evaluated children with refractory septic shock admitted to a pediatric intensive care unit (PICU) and monitored their hemodynamics using a pulse index continuous cardiac output (PiCCO) system. The serial cardiac index (CI), systemic vascular resistance index (SVRI), and vasoactive–inotropic score (VIS) were recorded during the first 72 h after PICU admission. Results: Thirty-three children with refractory septic shock were enrolled. The SVRI and VIS were both associated with fatality from septic shock. The non-survivors had lower serial SVRI and higher VIS (both p < 0.05). Based on the area under the ROC curve, the SVRI was the predictor during the early resuscitative stage (first 36 h) in pediatric refractory septic shock. Conclusions: Both SVRI and VIS are predictors of mortality in children with refractory septic shock, and the SVRI is the powerful predictor of mortality in the early resuscitative stage. A low serial SVRI may allow for the early awareness of disease severity and strategies for adjusting vasoactive–inotropic agents to increase the SVRI.

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Parker, J. L., and H. R. Adams. "Development of myocardial dysfunction in endotoxin shock." American Journal of Physiology-Heart and Circulatory Physiology 248, no. 6 (June 1, 1985): H818—H826. http://dx.doi.org/10.1152/ajpheart.1985.248.6.h818.

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Isolated heart muscle preparations were used to investigate the onset and development of myocardial inotropic dysfunction during endotoxin shock in guinea pigs. Left atrial muscles were removed from separate groups of animals at increasing time intervals after administration of either 4 mg/kg purified Escherichia coli endotoxin (shock groups) or an equivalent volume of isotonic saline (control groups). Peak developed contractile tension (CT) and maximal rate of tension development (+dT/dtmax) were significantly depressed in shock tissues as early as 2 h postendotoxin (P less than 0.01), with the magnitude of the contractile deficit progressively increasing during 4, 6, and 12 h postendotoxin. Contractility remained significantly depressed (P less than 0.001) at 16 and 24 h postendotoxin but progressively recovered toward control levels during 16, 24, 48, and 72 h postendotoxin. Shock-induced myocardial dysfunction was characterized by altered contractile responsiveness to low-Ca2+ medium (0.5 mM), gentamicin (4 mM), and hypoxia; altered inotropic reactivity to these interventions followed similar temporal development as the postendotoxin changes in basal contractile parameters. Left ventricular papillary muscles obtained at 16 h postendotoxin corroborated the shock-induced contractile depression observed in atria. These studies provide evidence for early and progressive intrinsic myocardial dysfunction in endotoxin shock and demonstrate that this dysfunction can be unmasked through the study of in vitro atrial and ventricular heart muscle preparations isolated from in vivo shocked animals.

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Scognamiglio, R., G. Fasoli, L. Visintin, and S. Dalla-Volta. "Effects of unloading and positive inotropic interventions on left ventricular function in asymptomatic patients with chronic severe aortic insufficiency." Clinical Cardiology 10, no. 12 (December 1987): 804–10. http://dx.doi.org/10.1002/clc.4960101206.

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Van Hessen, M. W., P. Schiereck, A. A. Stokhof, E. L. De Beer, J. B. Hak, H. Wesenhagen, M. G. Bruens, W. te Kloeze, and A. Crowe. "Effect of timing of transient diastolic changes in ventricular filling on LV performance in dogs." American Journal of Physiology-Heart and Circulatory Physiology 257, no. 1 (July 1, 1989): H305—H313. http://dx.doi.org/10.1152/ajpheart.1989.257.1.h305.

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The influence of acute volume changes during diastole on the contractile state of the left ventricle has been studied in the closed-chest dog. Volume changes were introduced by means of a servo-controlled pump system connected to the left ventricular cavity by an apical cannula. Pressure measurements were made in the left ventricle and aorta. Flow sensors in the mitral valve and around the ascending aorta monitored ventricular inflow and outflow patterns. The ventricular performance was evaluated in terms of the ratio between end-systolic pressure and end-systolic volume (P/Ves). By changing the time of occurrence of the volume interventions from the rapid filling phase of diastole to the atrial contraction phase, the relative contributions of rapid filling and atrial contraction to the mitral flow were changed. When the rapid filling was changed by the volume intervention, the effect on the contractile status of the heart, expressed as the P/Ves value, was small. In contrast, when the volume intervention took place during the atrial contraction phase, the effect on the P/Ves value was much larger. Comparison with muscle fiber experiments suggests that length-dependent calcium sensitivity of troponin and length-dependent conductivity of the sarcolemma are the underlying fundamental mechanisms. Therefore, we conclude that the influence of an intervention in ventricular filling on the inotropic state of the left ventricle is dependent on the timing of the intervention.

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Reconditi, Massimo, Marco Caremani, Marco Linari, Ilaria Morotti, Matteo Marcello, Theyencheri Narayanan, Vincenzo Lombardi, and Gabriella Piazzesi. "The effect of physiological and pharmacological inotropic interventions on the regulatory state of the thick filament in intact cardiac trabeculae." Biophysical Journal 122, no. 3 (February 2023): 403a. http://dx.doi.org/10.1016/j.bpj.2022.11.2196.

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Sutko, J. L., D. M. Bers, and J. P. Reeves. "Postrest inotropy in rabbit ventricle: Na+-Ca2+ exchange determines sarcoplasmic reticulum Ca2+ content." American Journal of Physiology-Heart and Circulatory Physiology 250, no. 4 (April 1, 1986): H654—H661. http://dx.doi.org/10.1152/ajpheart.1986.250.4.h654.

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To determine whether Na+-Ca2+ exchange is a physiologically significant Ca2+ efflux mechanism in rabbit ventricle, we investigated the effects exerted on postrest contractions by interventions that alter the transmembrane distribution of Na+ or Ca2+ so as to retard Ca2+ efflux via this system. Contractions elicited after rest periods of 0.25-10 min in duration were studied. The following interventions increased postrest contractions much more than those elicited by rhythmic stimulation: 1) Na+ pump inhibition by cardiac glycosides or by a reduction in extracellular K+, 2) reduction of extracellular Na+ (maintaining a constant [Ca2+]-to-[Na+]2 ratio), and 3) elevation of extracellular Ca2+. In contrast, isoproterenol, norepinephrine, and histamine produced comparable increases in both rhythmically stimulated and postrest contractions, suggesting that the postrest contractile potentiation was not just the result of a general increase in inotropic state. Ryanodine, which appears to antagonize sarcoplasmic reticulum (SR) Ca2+ release in cardiac muscle, markedly reduced the amplitude of the postrest contractions, but only modestly decreased rhythmically stimulated responses. Results suggest 1) that Ca2+ released from SR is involved in postrest response, 2) that Na+-Ca2+ exchange serves as a Ca2+ efflux pathway in normally polarized resting rabbit ventricle, and 3) that this activity in part determines the amount of Ca2+ available for release from SR.

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Babu, Swapna Mandala, Deepak Ivan Tauro, Indira Menon, Deepa Das, Shivkumar Shivanna, and Philip Karkare. "Study on clinical profile, scoring systems and outcomes of obstetric patients in our intensive care unit." International Journal of Reproduction, Contraception, Obstetrics and Gynecology 11, no. 11 (October 28, 2022): 3135. http://dx.doi.org/10.18203/2320-1770.ijrcog20222809.

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Background: Obstetric patients in ICU, pose a clinical challenge to intensivists and obstetricians. The objective of our study was to evaluate the incidence, indications and interventions in these patients. Secondly to assess whether clinical scores can help to estimate severity of the condition, predict mortality and morbidity in these patients.Methods: It was a retrospective observational study including all antepartum and postpartum patients admitted to ICU between January 2018 to June 2020.Results: Majority of patients needing ICU care were in the antepartum period (82.8%). Multigravida (55.2%) and unbooked cases (60.4%) constituted a major proportion of patients. Hypertensive disorders of pregnancy followed by sepsis amounted for common etiologies. Transfusions (43.2%), ventilatory support (26%) followed by inotropic support (14.9%) were the interventions required in the majority number of patients. Maternal mortality rate was 2.23%. Out of the clinical scores, OEWS (Obstetric early warning score) was a better modality to assess the severity of the disease and the need for ICU care.Conclusions: A multidisciplinary approach and close coordinated care of obstetric patients can reduce the maternal mortality rate. Early identification of critically ill obstetric patients using clinical scores can help us in triaging patients to high dependency units/ICU. OEWS is a very simple score which helps us in identifying patients needing intensive care.

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Varelmann, Dirk J., and Jochen Daniel Muehlschlegel. "Noteworthy Literature published in 2017 for Cardiothoracic Anesthesiologists." Seminars in Cardiothoracic and Vascular Anesthesia 22, no. 1 (February 5, 2018): 9–17. http://dx.doi.org/10.1177/1089253217753396.

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The year 2017 was a year dominated by large-scale clinical studies reporting the outcome of various interventions in cardiac surgery and heart failure (HF) patients, relevant to all cardiothoracic anesthesiologists. Among them were studies investigating the addition of levosimendan, an alternative inotropic agent, to standard management of patients with HF undergoing cardiac surgery. Also, corticosteroids have been used for various purposes in cardiac patients. Here, a new study reports the effect of high-dose methylprednisolone on recovery and delirium. Furthermore, with increasing evidence that transfusions increase morbidity and mortality, a publication reports the use of rotational thromboelastometry to reduce transfusion requirements. In addition, several randomized controlled multicenter studies report the outcomes of patients undergoing cardiac procedures: surgical versus transcatheter aortic valve replacement in intermediate-risk patients and the use of centrifugal-flow versus axial-flow left-ventricular devices in patients with HF. These studies demonstrate the dynamic and ever-evolving state of perioperative cardiovascular medicine and show us the direction of future developments.

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Bottari, Gabriella, Isabella Guzzo, Marco Marano, Francesca Stoppa, Lucilla Ravà, Matteo Di Nardo, and Corrado Cecchetti. "Hemoperfusion with Cytosorb in pediatric patients with septic shock: A retrospective observational study." International Journal of Artificial Organs 43, no. 9 (January 31, 2020): 587–93. http://dx.doi.org/10.1177/0391398820902469.

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Objective: To determine the clinical effect of continuous hemoperfusion with Cytosorb associated with standard Continuous Renal Replacement Therapy on hemodynamics and on clinically relevant outcome parameters in children with septic shock. Design: Retrospective analysis. Setting: Pediatric intensive care unit. Patients: Eight consecutive children with septic shock who received hemoperfusion with Cytosorb while on Continuous Renal Replacement Therapy. Interventions: Continuous hemoperfusion with Cytosorb (adsorber was changed every 24 h). Measurements and main results: Vasoactive-Inotropic Score was measured before and after the extracorporeal blood purification treatment. Bedside refractory septic shock score was calculated before the onset of the extracorporeal blood purification treatment. Time course of cytokines interleukin-6, interleukin-10, and tumor necrosis factor–alpha was measured at Time 0, then every 12 h until the end of blood purification treatment (72 or 96 h). Pediatric intensive care unit survival in our cohort was 90%. Median bedside refractory septic shock score was 2.1. Patients showed improved Vasoactive-Inotropic Score following blood purification (pre: 40.00 post: 8.89 p = 0.0076). Measurement of cytokines level showed a significant reduction of interleukin-6 plasma levels (7977.27–210.18 pg/mL, p = 0.0077) and interleukin-10 plasma levels (from 687.19 to 36.95 pg/mL, p = 0.0180). In those patients with detectable tumor necrosis factor–alpha plasma level, its reduction was not significant ( p = 0.138). The median removal ratio was 80% for interleukin-6, 90% for interleukin-10, and 29% for tumor necrosis factor–alpha. Conclusion: The use of Cytosorb in combination with Continuous Renal Replacement Therapy as blood purification strategy in pediatric septic shock is associated with a rapid hemodynamic stabilization in the first 48 h of treatment and a significant reduction of interleukin-6 and interleukin-10.

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ENDOH, Masao. "Changes in Intracellular Ca2+ Mobilization and Ca2+ Sensitization as Mechanisms of Action of Physiological Interventions and Inotropic Agents in Intact Myocardial Cells." Japanese Heart Journal 39, no. 1 (1998): 1–44. http://dx.doi.org/10.1536/ihj.39.1.

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Rabbany, S. Y., J. Y. Kresh, and A. Noordergraaf. "Intramyocardial pressure: interaction of myocardial fluid pressure and fiber stress." American Journal of Physiology-Heart and Circulatory Physiology 257, no. 2 (August 1, 1989): H357—H364. http://dx.doi.org/10.1152/ajpheart.1989.257.2.h357.

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Previous measurements of intramyocardial pressure (IMP) have yielded systolic pressures that range from values lower than to far exceeding systolic left ventricular pressure (LVP). This study identifies a possible mechanism underlying these divergent observations by building on established morphology of the ventricular wall. It is hypothesized here that the generation of fiber stress as a manifestation of myocardial contraction increases fluid pressure in the myocytes and the interstitial spaces. This increase in fluid pressure in turn generates the pressure in the ventricular cavity. Thus there are two quantities of interest: intramyocardial fluid pressure (IFP) and intramyocardial fiber stress (IFS). To test the hypothesis, we conducted experiments on conditioned dogs, utilizing a side-mounted catheter-tip strain gauge transducer to sense IMP as the sum of IFP and some component of IFS. In addition, a recessed end-tip fiber-optic transducer with its sensing element shielded from local myocardial fibers was employed to sense IFP. Both IFP and IMP were measured at various depths in the left ventricular free wall. The effects of inotropic interventions by administration of epinephrine and propranolol, mechanical interventions via clamping of the aorta and ligation of the left anterior descending coronary artery, and neural interventions by stimulation of the ansa subclavian of the stellate ganglion and right vagus were recorded. A transmural gradient in the wall for both IMP and IFP was observed. Systolic values of IFP recorded in the endocardium match those of LVP, with peak IMP exceeding both. The results support the hypothesis and offer an interpretation of the long-standing controversy regarding the magnitude of IMP with respect to LVP.

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Layland, J., I. S. Young, and J. D. Altringham. "The effects of adrenaline on the work- and power-generating capacity of rat papillary muscle in vitro." Journal of Experimental Biology 200, no. 3 (February 1, 1997): 503–9. http://dx.doi.org/10.1242/jeb.200.3.503.

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The work loop technique was used to examine the effects of adrenaline on the mechanics of cardiac muscle contraction in vitro. The length for maximum active force (Lmax) and net work production (Lopt) for rat papillary muscles was determined under control conditions (without adrenaline). The concentration of adrenaline producing the maximum inotropic effect was determined. This concentration was used in the remainder of the experiments. Sinusoidal strain cycles about Lopt were performed over a physiologically relevant range of cycle frequencies (4-11 Hz). Maximum work and the frequency for maximum work increased from 1.91 J kg-1 at 3 Hz in controls to 2.97 J kg-1 at 6 Hz with adrenaline. Similarly, maximum power output and the frequency for maximum power output (fopt) increased from 8.62 W kg-1 at 6 Hz in controls to 19.95 W kg-1 at 8 Hz with adrenaline. We suggest that the power-frequency relationship, derived using the work loop technique, represents a useful index with which to assess the effects of pharmacological interventions on cardiac muscle contractility.

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MacGowan, Guy A., Congwu Du, David F. Wieczorek та Alan P. Koretsky. "Compensatory changes in Ca2+ and myocardial O2 consumption in β-tropomyosin transgenic hearts". American Journal of Physiology-Heart and Circulatory Physiology 281, № 6 (1 грудня 2001): H2539—H2548. http://dx.doi.org/10.1152/ajpheart.2001.281.6.h2539.

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Transgenic mice overexpressing β-tropomyosin have increased myofilament Ca2+ sensitivity that we hypothesized would result in altered relationships among pressure and heart rates, intracellular Ca2+, and myocardial O2 consumption. In perfused hearts from transgenic mice there was a marked negative force-frequency response between 6 and 10 Hz with a 30 ± 3% reduction in peak-positive first derivative of pressure development over time (dP/d t) compared with 14 ± 2% in wild-type mice ( P < 0.001). At 8 Hz systolic pressures were normal, though peak systolic intracellular Ca2+ was significantly reduced in transgenic mice versus wild type (726 ± 61 vs. 936 ± 67 nM, P < 0.05) indicating an alteration in the pressure-Ca2+ relationship. Over a wide range of positive and negative inotropic interventions there were normal developed pressures, though marked elevations in myocardial O2 consumption (15–54%). Because pressures are normal and intracellular Ca2+ decreased and myocardial O2 consumption increased, this suggests that these abnormalities are at least in part compensatory mechanisms to the altered myofilament function.

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Vittone, L., C. Mundina, G. Chiappe de Cingolani, and A. Mattiazzi. "cAMP and calcium-dependent mechanisms of phospholamban phosphorylation in intact hearts." American Journal of Physiology-Heart and Circulatory Physiology 258, no. 2 (February 1, 1990): H318—H325. http://dx.doi.org/10.1152/ajpheart.1990.258.2.h318.

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The present work was undertaken with two main goals: 1) to further elucidate the physiological role of the adenosine 3',5'-cyclic monophosphate (cAMP) and Ca2(+)-calmodulin (Ca2(+)-Cm)-dependent mechanisms of phospholamban phosphorylation (32PiPHL), and 2) to study the possible interaction between these two systems in the intact heart. Interventions that increased twitch or tetanic tension without modifying cAMP levels [high extracellular Ca2+ concentration [( Ca2+]o) or BAY K 8644 in catecholamine-depleted hearts] failed to alter 32PiPHL. Moderate and high beta-adrenergic stimulation (3 x 10(-9) and 3 x 10(-8) M isoproterenol, respectively) increased cAMP from 0.345 +/- 0.032 to 0.636 +/- 0.069 and 0.772 +/- 0.060 pmol/mg wet wt, and 32PiPHL from 26.8 +/- 4.1 to 58.6 +/- 13.1 and 174.7 +/- 13.8 pmol 32Pi/mg sarcoplasmic reticular [SR] protein, respectively. Both doses of isoproterenol produced an enhanced myocardial relaxation. Reversal of the positive inotropic effect of isoproterenol by interventions that decrease intracellular Ca2+ supply failed to reduce the enhancement in 32PiPHL and myocardial relaxation elicited by 3 x 10(-9) M isoproterenol but diminished the increase in 32PiPHL induced by 3 x 10(-8) M isoproterenol to 116.3 +/- 10.9 without significant changes in cAMP. Changes in myocardial relaxation closely paralleled the changes in 32PiPHL. These results suggest that 1) 32PiPHL may be enhanced by the cAMP-dependent mechanism independently of the Ca2(+)-Cm system, and 2) 32PiPHL and myocardial relaxation may be modified by intracellular Ca2+ changes only at high-intracellular cAMP levels.

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Leite, C. M., D. V. Vassallo, and J. G. Mill. "Characteristics of tetanic contractions in caffeine-treated rat myocardium." Canadian Journal of Physiology and Pharmacology 73, no. 5 (May 1, 1995): 638–43. http://dx.doi.org/10.1139/y95-081.

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Skinned fiber preparations are used to obtain the maximal contractile activation of isolated myocardial preparations. Tetanic contractions elicited in the presence of sarcoplasmic reticulum inhibitors have also been used as an alternative method to produce maximal active tension in the intact myocardium. In this work our purpose was to define the best conditions to obtain tetanic contractions in the rat myocardium and to compare the influence of muscle length and inotropic interventions (Ca2+ and Bay K8644) in the tension produced in twitches and tetanic contractures. Papillary muscles were mounted in a perfusion chamber to record isometric force. Tetanic contractions were elicited by using suprathreshold stimulation with rectangular pulses (10 ms duration) at 5 Hz in the presence of 2.5 mM caffeine. Caffeine depressed the twitch tension but the tetanic tension was similar to that produced under steady-state stimulation (0.5 Hz) in control conditions. Tetanic and twitch tensions were similar along the whole extension of the length–tension curve and under the positive inotropic effects produced by Ca2+ (0.25 to 3.75 mM) or by the Ca2+-channel agonist Bay K8644 (1 μM). During long tetanic stimuli (60 s) a time-dependent tension decay was observed. This decay was prolonged by reducing the extracellular K+ from 5.4 to 1.0 mM, suggesting that Ca2+ extrusion through the Na–Ca exchanger seems to occur during tetanic stimulation. Since tetanic tension was never higher than the tension obtained in twitches elicited at the same Ca2+ concentration (0.5 Hz), we conclude that tetanic contractures represent a useful tool to investigate the contractile response of intact myocardial preparations with a nonfunctional sarcoplasmic reticulum. However, our results indicate that the maximal activation of the contractile machinery in the rat myocardium seems to be only achieved in twitches elicited in high extracellular Ca2+ concentrations and with a functional sarcoplasmic reticulum.Key words: cardiac muscle, excitation–contraction coupling, sarcoplasmic reticulum, tetanic contracture, Na–Ca exchange.

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