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Academic literature on the topic 'Lusitropie'
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Journal articles on the topic "Lusitropie"
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Lim, Chee Chew, Ronglih Liao, Niraj Varma, and Carl S. Apstein. "Impaired lusitropy-frequency in the aging mouse: role of Ca2+-handling proteins and effects of isoproterenol." American Journal of Physiology-Heart and Circulatory Physiology 277, no. 5 (1999): H2083—H2090. http://dx.doi.org/10.1152/ajpheart.1999.277.5.h2083.
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We examined the relationship between age-associated lusitropic impairment, heart rate, and Ca2+-handling proteins and assessed the efficacy of increasing left ventricular (LV) relaxation via β-adrenergic stimulation in adult and aging mouse hearts. LV function was measured in isolated, isovolumic blood-perfused hearts from adult (5 mo), old (24 mo), and senescent (34 mo) mice. Hearts were paced from 5 to 10 Hz, returned to 7 Hz, exposed to 10−6 M isoproterenol, and paced again from 7 to 10 Hz. Age-related alterations in Na+/Ca2+exchanger (NCX), sarcoplasmic reticulum (SR) Ca2+-ATPase (SERCA2a), and phospholamban (PLB) levels were assessed by immunoblot. Despite preserved contractile performance, aging caused impaired lusitropy. Increased pacing caused an elevation in end-diastolic pressure that progressively worsened with age. The time constant of isovolumic pressure decay (τ) was significantly prolonged in old and senescent hearts compared with adults. Relative to adult hearts, the SERCA2a-to-PLB ratios were reduced 68 and 69%, and NCX were reduced 37 and 58% in old and senescent hearts, respectively. Isoproterenol completely reversed the age-associated lusitropic impairments. These data suggest that impaired lusitropy in aging mouse hearts is related to a decreased rate of cytosolic Ca2+ removal and that accelerating SR Ca2+ resequestration via β-adrenergic stimulation can reverse this impairment.
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Vila-Petroff, M., G. N. Perez, B. Alvarez, H. E. Cingolani, and A. Mattiazzi. "Mechanism of negative lusitropic effect of alpha 1-adrenoceptor stimulation in cat papillary muscles." American Journal of Physiology-Heart and Circulatory Physiology 270, no. 2 (1996): H701—H709. http://dx.doi.org/10.1152/ajpheart.1996.270.2.h701.
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Experiments were performed in cat papillary muscles to explore the mechanisms by which alpha 1-adrenoceptor stimulation affects myocardial relaxation. Phenylephrine (PE; 10 microM) + atenolol (1 microM; n = 8 experiments) produced a negative lusitropic effect, i.e., a prolongation of half-relaxation time (t1/2; time to 50% relaxation) by 30 +/- 10% (P < 0.05) and a proportionally smaller increase in maximal velocity of relaxation (-T) than in maximal velocity of contraction (+T), which significantly increased the ratio +T/-T. A similar increase in contractility, produced by increasing calcium, failed to significantly change t1/2 and +T/-T. PE-induced negative lusitropic effect was significantly inhibited by two protein kinase C (PKC) inhibitors, staurosporine (0.1 microM) and chelerythrine (10 microM). PE also increased intracellular pH by 0.18 +/- 0.05 pH units (P < 0.05, n = 4), as measured by the fluorescent dye 2'-7'-bis(2-carboxyethyl)-5(6)-carboxyfluorescein. Intracellular alkalosis and the negative lusitropic effect of PE were prevented by the Na+/H+ exchanger inhibitor ethylisopropylamiloride (10 microM). No significant changes in calcium myofilament sensitivity and maximal tension were detected in trabeculae treated with PE either before or after chemical skinning. These results indicate that a Na+/H+ exchanger-induced intracellular alkalosis, possibly mediated by PKC activation, may fully account for the negative lusitropism of alpha 1-adrenoceptor stimulation.
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Vivien, Benoit, Jean-Luc Hanouz, Pierre-Yves Gueugniaud, Yves Lecarpentier, Pierre Coriat, and Bruno Riou. "Myocardial Effects of Halothane and Isoflurane in Hamsters with Hypertrophic Cardiomyopathy." Anesthesiology 87, no. 6 (1997): 1406–16. http://dx.doi.org/10.1097/00000542-199712000-00020.
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Background The effects of halothane and isoflurane on myocardial contraction and relaxation in diseased myocardium are not completely understood. Methods The effects of equianesthetic concentrations of halothane and isoflurane on inotropy and lusitropy in left ventricular papillary muscles of healthy hamsters and those with genetically induced cardiomyopathy (strain BIO 14.6) were investigated in vitro (29 degrees C; pH 7.40; Ca2+ 2.5 mM; stimulation frequency, 3/min) in isotonic and isometric conditions. Results Halothane induced a negative inotropic effect that was greater in cardiomyopathic than in healthy hamsters (1.5 vol%, active isometric force (AF): 19 +/- 8% vs. 28 +/- 11% of control values; P &lt; 0.05). Isoflurane induced a negative inotropic effect that was greater in cardiomyopathic than in healthy hamsters (2.0 vol%, AF: 64 +/- 13% vs. 75 +/- 11% of control values; P &lt; 0.01). However, the negative inotropic effects of halothane and isoflurane were not different for cardiomyopathic or healthy hamsters when their concentrations were corrected for minimum alveolar concentration (MAC) values in each strain. Halothane induced a negative lusitropic effect under low load, which was more important in cardiomyopathic hamsters, suggesting a greater impairment in calcium uptake by the sarcoplasmic reticulum. In contrast, isoflurane induced a moderate positive lusitropic effect under low load in healthy but not in cardiomyopathic hamsters. Halothane and isoflurane induced no significant lusitropic effect under high load. Conclusions Halothane and isoflurane had greater negative inotropic effects in cardiomyopathic than in healthy hamsters. Nevertheless, no significant differences in their inotropic effects were noted when concentrations were correlated as a multiple of MAC in each strain.
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Mizuno, Ju, Satoshi Mohri, Takeshi Yokoyama, Mikiya Otsuji, Hideko Arita, and Kazuo Hanaoka. "Temperature-dependent inotropic and lusitropic indices based on half-logistic time constants for four segmental phases in isovolumic left ventricular pressure–time curve in excised, cross-circulated canine heart." Canadian Journal of Physiology and Pharmacology 95, no. 2 (2017): 190–98. http://dx.doi.org/10.1139/cjpp-2015-0196.
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Varying temperature affects cardiac systolic and diastolic function and the left ventricular (LV) pressure–time curve (PTC) waveform that includes information about LV inotropism and lusitropism. Our proposed half-logistic (h-L) time constants obtained by fitting using h-L functions for four segmental phases (Phases I–IV) in the isovolumic LV PTC are more useful indices for estimating LV inotropism and lusitropism during contraction and relaxation periods than the mono-exponential (m-E) time constants at normal temperature. In this study, we investigated whether the superiority of the goodness of h-L fits remained even at hypothermia and hyperthermia. Phases I–IV in the isovolumic LV PTCs in eight excised, cross-circulated canine hearts at 33, 36, and 38 °C were analyzed using h-L and m-E functions and the least-squares method. The h-L and m-E time constants for Phases I–IV significantly shortened with increasing temperature. Curve fitting using h-L functions was significantly better than that using m-E functions for Phases I–IV at all temperatures. Therefore, the superiority of the goodness of h-L fit vs. m-E fit remained at all temperatures. As LV inotropic and lusitropic indices, temperature-dependent h-L time constants could be more useful than m-E time constants for Phases I–IV.
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Taffet, George E., Lloyd A. Michael, and Charlotte A. Tate. "Exercise training improves lusitropy by isoproterenol in papillary muscles from aged rats." Journal of Applied Physiology 81, no. 4 (1996): 1488–94. http://dx.doi.org/10.1152/jappl.1996.81.4.1488.
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Taffet, George E., Lloyd A. Michael, and Charlotte A. Tate.Exercise training improves lusitropy by isoproterenol in papillary muscles from aged rats. J. Appl. Physiol. 81(4): 1488–1494, 1996.—Aging is associated with a decreased cardiac responsiveness to β-adrenergic stimulation. We examined the effect of endurance exercise training of old Fischer 344 male rats on β-adrenergic stimulation of the function of isolated left ventricular papillary muscle. Three groups were examined: sedentary mature (SM; 12-mo old), sedentary old (SO; 23–24 mo old), and exercised old (EO; 23–24 mo old) that were treadmill trained for 4–8 wk. The isometric contractile properties were studied at 0.2 Hz and 0.75 mM calcium. Without β-adrenergic stimulation, there were no group differences for peak tension, maximum rate of tension development (+dP/d t), or maximum rate of tension dissipation (−dP/d t). The time to peak tension was longer ( P < 0.05) for both EO and SO than for SM rats. Half relaxation time (RT1/2) was prolonged ( P < 0.05) for SO compared with SM and EO (which did not differ). The three groups did not differ in the β-adrenergic stimulation by isoproterenol of peak tension, −dP/d t, time to peak tension, or contraction duration. The inotropic response (+dP/d t) of SM was greater ( P < 0.05) than that in SO or EO rats (which did not differ); however, the lusitropic response (RT1/2) was lesser ( P < 0.05) in SO than in SM or EO rats (which did not differ). Thus exercise training of old rats improved the lusitropic response to isoproterenol without altering the age-associated impairment in inotropic response.
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Tanigawa, Taketo, Masafumi Yano, Michihiro Kohno, et al. "Mechanism of preserved positive lusitropy by cAMP-dependent drugs in heart failure." American Journal of Physiology-Heart and Circulatory Physiology 278, no. 2 (2000): H313—H320. http://dx.doi.org/10.1152/ajpheart.2000.278.2.h313.
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In tachycardia-induced heart failure (HF), positive lusitropic effects of milrinone or dobutamine were assessed by evaluating the time constant of left ventricular (LV) pressure decay (τ) and Ca2+-ATPase activity of the sarcoplasmic reticulum (SR). The peak value of the positive first derivative of LV pressure (+dP/d t) was less increased, either by dobutamine (2–10 μg ⋅ kg−1 ⋅ min−1) or by milrinone (4–20 μg/kg), in HF than in control ( P< 0.05), whereas τ was shortened to an extent similar to that in control with dobutamine [ P = not significant (NS)] and to an even greater extent with milrinone ( P < 0.05). Ca2+-ATPase activity increased similarly in HF and control with dobutamine (1 μM; +11% in HF vs. +12% in control, P = NS), whereas it increased more with milrinone (1 μM; +19% in HF vs. +11% in control, P < 0.05). Ca2+-ATPase activity-cAMP relationships were shifted to the left by milrinone or dobutamine in HF compared with control. Thus, in HF, the sensitivity of Ca2+-ATPase activity to cAMP was increased on addition of cAMP-dependent inotropic agents, contributing to the preservation of positive lusitropy.
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Hanouz, Jean-Luc, Bruno MD Riou, Laurent Massias, Yves Lecarpentier та Pierre Coriat. "Interaction of Halothane with α- and β-Adrenoceptor Stimulations in Rat Myocardium". Anesthesiology 86, № 1 (1997): 147–59. http://dx.doi.org/10.1097/00000542-199701000-00019.
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Background Halothane induces negative inotropic and lusitropic effects in myocardium. It has been suggested that halothane potentiates beta-adrenoceptor stimulation. However, its effects on the inotropic response to alpha-adrenoceptor stimulation and its effects on the lusitropic effects of alpha- and beta-adrenoceptor stimulation are unknown. Methods The effects of halothane (0.5 and 1 minimum alveolar concentration [MAC]) on the inotropic responses induced by phenylephrine (10(-8) to 10(-4) M) and isoproterenol (10(-8) to 10(-4) M) were studied in rat left ventricular papillary muscles in vitro (in Krebs-Henseleit solution at 29 degrees C, pH 7.40, with 0.5 mM calcium and stimulation frequency at 12 pulses/min). The lusitropic effects were studied in isotonic (R1) and isometric (R2) conditions. Results One MAC halothane induced a negative inotropic effect (54 +/- 3%, P &lt; 0.05), increased R1 (109 +/- 3%, P &lt; 0.05), and decreased R2 (88 +/- 2%, P &lt; 0.05). In control groups, phenylephrine (137 +/- 7%, P &gt; 0.05) and isoproterenol (162 +/- 6%, P &lt; 0.05) induced a positive inotropic effect. Halothane did not significantly modify the positive inotropic effect of calcium, suggesting that it did not modify the inotropic reserve of papillary muscles. In contrast, 1 MAC halothane enhanced the positive inotropic effects of phenylephrine (237 +/- 19%, P &lt; 0.05) and isoproterenol (205 +/- 11%, P &lt; 0.05). Halothane did not modify the lusitropic effect of phenylephrine under high or low load. In contrast, 1 MAC halothane impaired the positive lusitropic effect of isoproterenol under low load (P &lt; 0.05), whereas it did not modify the positive lusitropic effect of isoproterenol under high load. Conclusions At clinically relevant concentrations, halothane potentiated the positive inotropic effects of both alpha- and beta-adrenoceptor stimulation. Furthermore, halothane alters the positive lusitropic-effect of beta-adrenoceptor stimulation under low load.
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David, Jean-Stéphane, Benoît Vivien, Yves Lecarpentier, Pierre Coriat та Bruno Riou. "Interaction of Protamine with α- and β-Adrenoceptor Stimulations in Rat Myocardium". Anesthesiology 95, № 5 (2001): 1226–33. http://dx.doi.org/10.1097/00000542-200111000-00029.
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Background Protamine alters the inotropic responses to beta-adrenoceptor stimulation, but its mechanism of action is not well-understood. Moreover, its interaction with alpha-adrenoceptor stimulation and the lusitropic (relaxation) response to beta-adrenoceptor stimulation remain unknown. Methods The effects of protamine (10 or 100 microg/ml) on the responses induced by phenylephrine and isoproterenol were studied in rat left ventricular papillary muscles. Inotropic and lusitropic effects were studied under low and high loads. The authors also studied the interaction of protamine with forskolin (50 microm) and dibutyryl 3',5'-cAMP (0.5 mm). Data are mean percentage of baseline active force +/- SD. Results In control groups, phenylephrine (135 +/- 17%, P &lt; 0.05) and isoproterenol (185 +/- 44%, P &lt; 0.05) induced a positive inotropic effect. Isoproterenol induced positive lusitropic effects under low and high loads. Protamine abolished the inotropic responses to alpha- (102 +/- 23%, not significant) and beta-adrenoceptor stimulations (99 +/- 17%, not significant) but did not modify the lusitropic responses to isoproterenol. Protamine abolished the inotropic responses to forskolin (89 +/- 6 vs. 154 +/- 20%, P &lt; 0.05) and markedly decreased that of dibutyryl 3',5'-cAMP (132 +/- 31 vs. 167 +/- 30%, P &lt; 0.05) but did not modify their lusitropic responses. Conclusions Protamine abolished the inotropic responses to alpha- and beta-adrenoceptor stimulations but preserved the lusitropic responses to beta-adrenoceptor stimulation. Although protamine may act at several sites on the adrenoceptor stimulation cascade, one of its main sites of action is situated downstream from cAMP-mediated phosphorylation.
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Aprigliano, O., V. O. Rybin, E. Pak, R. B. Robinson, and S. F. Steinberg. "beta 1-and beta 2-adrenergic receptors exhibit differing susceptibility to muscarinic accentuated antagonism." American Journal of Physiology-Heart and Circulatory Physiology 272, no. 6 (1997): H2726—H2735. http://dx.doi.org/10.1152/ajpheart.1997.272.6.h2726.
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Neonatal rat ventricular myocytes express both beta 1-and beta 2-adrenergic receptors linked to enhanced intracellular adenosine 3',5'-cyclic monophosphate (cAMP) accumulation and the modulation of contractile function. This study tests the hypothesis that muscarinic agonists act via distinct mechanisms to interfere with beta 1-and beta 2-adrenergic receptor actions. The beta 2-selective agonist zinterol (10(-7) M) elicits approximately a fourfold increase in cAMP accumulation, which is mimicked, both in magnitude and kinetics, by 10(-9) M of the mixed beta 1-receptor agonist/beta 2-receptor agonist isoproterenol. At these concentrations, isoproterenol and zinterol elicit equivalent inotropic and lusitropic (i.e., enhanced relaxation) responses. Carbachol inhibits all three responses (cAMP, inotropic, and lusitropic) elicited by isoproterenol. In contrast, carbachol does not interfere with the effect of zinterol to augment cAMP accumulation or to induce a positive inotropic response. However, carbachol inhibits the lusitropic response to zinterol via an action at an M2-muscarinic receptor linked to a pertussis toxin-sensitive pathway. Additional studies indicate that beta 2-receptor-dependent phosphorylation of troponin I and phospholamban is substantially attenuated by carbachol. We conclude that carbachol interferes with beta 1-receptor actions by reducing cAMP accumulation. In contrast, the anti-beta 2-receptor actions of carbachol are mediated by a mechanism that is distinct from inhibition of cAMP accumulation, involving an M2-muscarinic receptor coupled to a pertussis toxin-sensitive G protein, which leads to inhibition of troponin I and phospholamban phosphorylation and inhibition of the beta 2-receptor-dependent lusitropic response.
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Hanouz, Jean-Luc, Pierre-Yves Gueugniaud, Yves Lecarpentier, Pierre Coriat та Bruno Riou. "Interaction of Isoflurane and Sevoflurane with α- and β-adrenoceptor Stimulations in Rat Myocardium". Anesthesiology 88, № 5 (1998): 1249–58. http://dx.doi.org/10.1097/00000542-199805000-00016.
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Background Halothane potentiates the positive inotropic effects of alpha- and beta-adrenoceptor stimulations but impairs the positive lusitropic effect of beta-adrenoceptor stimulations. However, the interactions of isoflurane and sevoflurane with alpha- and beta-adrenoceptor stimulation have not been entirely defined. Methods The effects of 1 minimum alveolar concentration isoflurane and sevoflurane on the inotropic responses induced by phenylephrine (10(-8) to 10(-4) M) or isoproterenol (10(-8 to 10(-4) M) were studied in rat left ventricular papillary muscles in vitro (Krebs-Henseleit solution, 29 degrees C; pH, 7.4; 0.5 mM calcium; stimulation frequency, 12 pulses/min). The positive lusitropic effects of alpha- and beta-adrenoceptor stimulations were studied under isotonic and isometric conditions. Data are mean percentages of baseline +/- SEM. Results In control groups, phenylephrine (134 +/- 8%; P &lt; 0.05) and isoproterenol (171 +/- 7%; P &lt; 0.05) induced a positive inotropic effect. Isoflurane enhanced the positive inotropic effects of phenylephrine (185 +/- 10%; P &lt; 0.05) and of isoproterenol (203 +/- 11%; P &lt; 0.05). Sevoflurane enhanced the positive inotropic effects of phenylephrine (187 +/- 10%; P &lt; 0.05) and of isoproterenol (228 +/- 11%; P &lt; 0.05). These potentiations were similar to those previously reported with halothane. Isoflurane and sevoflurane did not modify the positive lusitropic effects under low and high loads of isoproterenol. Conclusion Although isoflurane and sevoflurane have moderate negative inotropic effects, they potentiated the positive inotropic effects of alpha- and beta-adrenoceptor stimulations but did not modify the positive lusitropic effects of beta-adrenoceptor stimulation.