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Journal articles on the topic 'Lusitropie'

Author: Grafiati

Published: 4 June 2021

Last updated: 1 February 2022

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1

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 (November 1, 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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2

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 (February 1, 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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3

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 (December 1, 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 < 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 < 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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4

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 (February 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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5

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 (October 1, 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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6

Tanigawa, Taketo, Masafumi Yano, Michihiro Kohno, Takeshi Yamamoto, Takayuki Hisaoka, Kaoru Ono, Takeshi Ueyama, 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 (February 1, 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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7

Hanouz, Jean-Luc, Bruno MD Riou, Laurent Massias, Yves Lecarpentier, and Pierre Coriat. "Interaction of Halothane with α- and β-Adrenoceptor Stimulations in Rat Myocardium." Anesthesiology 86, no. 1 (January 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 < 0.05), increased R1 (109 +/- 3%, P < 0.05), and decreased R2 (88 +/- 2%, P < 0.05). In control groups, phenylephrine (137 +/- 7%, P > 0.05) and isoproterenol (162 +/- 6%, P < 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 < 0.05) and isoproterenol (205 +/- 11%, P < 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 < 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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8

David, Jean-Stéphane, Benoît Vivien, Yves Lecarpentier, Pierre Coriat, and Bruno Riou. "Interaction of Protamine with α- and β-Adrenoceptor Stimulations in Rat Myocardium." Anesthesiology 95, no. 5 (November 1, 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 < 0.05) and isoproterenol (185 +/- 44%, P < 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 < 0.05) and markedly decreased that of dibutyryl 3',5'-cAMP (132 +/- 31 vs. 167 +/- 30%, P < 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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9

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 (June 1, 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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10

Hanouz, Jean-Luc, Pierre-Yves Gueugniaud, Yves Lecarpentier, Pierre Coriat, and Bruno Riou. "Interaction of Isoflurane and Sevoflurane with α- and β-adrenoceptor Stimulations in Rat Myocardium." Anesthesiology 88, no. 5 (May 1, 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 < 0.05) and isoproterenol (171 +/- 7%; P < 0.05) induced a positive inotropic effect. Isoflurane enhanced the positive inotropic effects of phenylephrine (185 +/- 10%; P < 0.05) and of isoproterenol (203 +/- 11%; P < 0.05). Sevoflurane enhanced the positive inotropic effects of phenylephrine (187 +/- 10%; P < 0.05) and of isoproterenol (228 +/- 11%; P < 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.

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11

Biais, Matthieu, Romain Jouffroy, Aude Carillion, Sarah Feldman, Aude Jobart-Malfait, Bruno Riou, and Julien Amour. "Interaction of Metabolic and Respiratory Acidosis with α and β-adrenoceptor Stimulation in Rat Myocardium." Anesthesiology 117, no. 6 (December 1, 2012): 1212–22. http://dx.doi.org/10.1097/aln.0b013e3182753264.

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Background The effects of acute respiratory versus metabolic acidosis on the myocardium and their consequences on adrenoceptor stimulation remain poorly described. We compared the effects of metabolic and respiratory acidosis on inotropy and lusitropy in rat myocardium and their effects on the responses to α- and β-adrenoceptor stimulations. Methods The effects of acute respiratory and metabolic acidosis (pH 7.10) and their interactions with α and β-adrenoceptor stimulations were studied in isolated rat left ventricular papillary muscle (n=8 per group). Intracellular pH was measured using confocal microscopy and a pH-sensitive fluorophore in isolated rat cardiomyocytes. Data are mean percentages of baseline±SD. Results Respiratory acidosis induced more pronounced negative inotropic effects than metabolic acidosis did both in isotonic (45±3 versus 63±6%, P<0.001) and isometric (44±5 versus 64±3%, P<0.001) conditions concomitant with a greater decrease in intracellular pH (6.85±0.07 versus 7.12±0.07, P<0.001). The response to α-adrenergic stimulation was not modified by respiratory or metabolic acidosis. The inotropic response to β-adrenergic stimulation was impaired only in metabolic acidosis (137±12 versus 200±33%, P<0.001), but this effect was not observed with administration of forskolin or dibutiryl-cyclic adenosine monophosphate. This effect might be explained by a change in transmembrane pH gradient only observed with metabolic acidosis. The lusitropic response to β-adrenergic stimulation was not modified by respiratory or metabolic acidosis. Conclusion Acute metabolic and respiratory acidosis induce different myocardial effects related to different decreases in intracellular pH. Only metabolic acidosis impairs the positive inotropic effect of β-adrenergic stimulation.

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12

Katz, A. M. "Inotropic and lusitropic abnormalities in heart failure." European Heart Journal 11, suppl A (April 2, 1990): 27–31. http://dx.doi.org/10.1093/eurheartj/11.suppl_a.27.

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Weiss, S. M., and D. A. Saint. "Riluzole is Positively Inotropic and Positively Lusitropic." Heart, Lung and Circulation 18 (2009): S303. http://dx.doi.org/10.1016/j.hlc.2009.05.458.

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Seri, Istvan. "Inotrope, Lusitrope, and Pressor Use in Neonates." Journal of Perinatology 25, S2 (April 21, 2005): S28—S30. http://dx.doi.org/10.1038/sj.jp.7211316.

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15

Slinker, Bryan K., Henry W. Green, Yiming Wu, Robert D. Kirkpatrick, and Kenneth B. Campbell. "Relaxation effect of CGP-48506, EMD-57033, and dobutamine in ejecting and isovolumically beating rabbit hearts." American Journal of Physiology-Heart and Circulatory Physiology 273, no. 6 (December 1, 1997): H2708—H2720. http://dx.doi.org/10.1152/ajpheart.1997.273.6.h2708.

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Because it is not known whether ejection influences the negative effect of the Ca2+-sensitizing drugs on ventricular relaxation, we extended our previous analysis of stress-dependent relaxation in isovolumic beats to encompass ejecting beats and evaluated the relationships between both the time of onset of relaxation and the rate of relaxation and wall stress in a broader analysis framework. Furthermore, because the sites of action of the Ca2+-sensitizing drugs CGP-48506 and EMD-57033 may be different, and thus CGP-48506 may have fewer adverse effects on resting muscle length or force, we compared these two drugs to test the hypothesis that CGP-48506 would have less effect than EMD-57033 on relaxation in the isolated buffer-perfused rabbit heart. This analysis of stress-dependent relaxation in both ejecting and isovolumic beats readily differentiates between the negative lusitropic effect of 2 × 10−6 M EMD-57033, the negligible lusitropic effect of 6 × 10−6 M CGP-48506, and the positive lusitropic effect of 1.25 × 10−6 M dobutamine. Furthermore, comparison of the effect of the two Ca2+-sensitizing drugs in ejecting versus isovolumic contractions shows that CGP-48506 affects relaxation differently in ejecting contractions than it does in isovolumic contractions, whereas EMD-57033 affects relaxation similarly in both ejecting and isovolumic contractions.

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Stein, B., S. Bartel, U. Kirchhefer, S. Kokott, E. G. Krause, J. Neumann, W. Schmitz, and H. Scholz. "Relation between contractile function and regulatory cardiac proteins in hypertrophied hearts." American Journal of Physiology-Heart and Circulatory Physiology 270, no. 6 (June 1, 1996): H2021—H2028. http://dx.doi.org/10.1152/ajpheart.1996.270.6.h2021.

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The aim of this study was to examine the mechanism(s) underlying the reduced isoproterenol-induced positive inotropic and lusitropic effects in hypertrophied hearts. Chronic beta-adrenergic stimulation (2.4 mg isoproterenol.kg-1. day-1 for 4 days) induced cardiac hypertrophy by 33 +/- 2% in rats. A parallel downregulation of phospholamban (PLB) and sarcoplasmic reticulum Ca2(+)-ATPase (SERCA2) protein expression by 49 and 40%, respectively, was observed, whereas troponin I (TNI) and C protein remained unchanged. In papillary muscles from chronically beta-adrenergically stimulated rats, the isoproterenol-induced positive inotropic and lusitropic effects, as well as adenosine 3',5'-cyclic monophosphate (cAMP) accumulation, were attenuated compared with those in control animals. Acute exposure to isoproterenol induced phosphate incorporation into PLB, TNI, and C protein of 48 +/- 4.6, 55 +/- 5.0, and 27 +/- 4.9 pmol/mg homogenate protein, respectively, in control animals. In the hypertrophied hearts, phosphate incorporation into PLB was reduced by 76%, whereas phosphate incorporation into TNI or C protein remained unchanged. In conclusion, chronic beta-adrenergic stimulation reduced the isoproterenol-stimulated positive inotropic and lusitropic effects in papillary muscles, which were accompanied by 1) diminished cAMP formation, 2) attenuation of cAMP-mediated PLB phosphorylation, and 3) downregulation of PLB and SERCA2 protein.

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Harkin, Christopher P., Paul S. Pagel, Judy R. Kersten, Douglas A. Hettrick, and David C. Warltier. "Direct Negative Inotropic and Lusitropic Effects of Sevoflurane." Anesthesiology 81, no. 1 (July 1, 1994): 156–67. http://dx.doi.org/10.1097/00000542-199407000-00022.

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18

Bronzwaer, J. G. F., and W. J. Paulus. "Nitric oxide: the missing lusitrope in failing myocardium." European Heart Journal 29, no. 20 (May 13, 2008): 2453–55. http://dx.doi.org/10.1093/eurheartj/ehn393.

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Gueugniaud, Pierre-Yves, Jean-Luc Hanouz, Jean-Marc Martino, Yves Lecarpentier, Pierre Coriat, and Bruno Riou. "Interaction of Halogenated Anesthetics with Dobutamine in Rat Myocardium." Anesthesiology 90, no. 6 (June 1, 1999): 1663–70. http://dx.doi.org/10.1097/00000542-199906000-00023.

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Background Halogenated anesthetics potentiate the positive inotropic effects of alpha- and beta-adrenoceptor stimulations, but their interactions with dobutamine remain unknown. Methods The effects of halothane, isoflurane, sevoflurane, and desflurane (1 and 2 minimum alveolar concentration) on the inotropic responses induced by dobutamine (10(-8)-10(-4) M) were studied in rat left ventricular papillary muscles in vitro. Inotropic effects were studied under low (isotony) and high (isometry) loads. The authors also studied the lusitropic effects in isotonic (R1) and isometric (R2) conditions. Data are the mean percentage of baseline +/- SD. Results Dobutamine induced a positive inotropic effect (active isometric force: 185+/-36%, P < 0.001) and a positive lusitropic effect under low load (R1: 78+/-9%, P < 0.001), but not under high load (R2: 95+/-21%, not significant). Halothane, isoflurane, and sevoflurane did not modify the positive inotropic effect of dobutamine. Even in the presence of alpha-adrenoceptor blockade, isoflurane did not potentiate the positive inotropic effect of dobutamine. Desflurane significantly enhanced the positive inotropic effect of dobutamine (active isometric force: 239+/-35%, P < 0.001), but this potentiation was abolished by pretreatment with reserpine. In contrast to halothane, isoflurane, sevoflurane, and desflurane did not significantly modify the lusitropic effects of dobutamine. Conclusions Halogenated anesthetics, except desflurane, did not modify the positive inotropic effects of dobutamine. Desflurane enhanced the positive inotropic effect of dobutamine, but this effect was related to the desflurane-induced release in intramyocardial catecholamine stores.

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Mizuno, Ju, Hiromi Matsubara, Satoshi Mohri, Juichiro Shimizu, Shunsuke Suzuki, Takeshi Mikane, Junichi Araki, Kazuo Hanaoka, Robert Akins, and Shigeho Morita. "Half-logistic time constant: a more reliable lusitropic index than monoexponential time constant regardless of temperature in canine left ventricle." Canadian Journal of Physiology and Pharmacology 86, no. 3 (March 2008): 78–87. http://dx.doi.org/10.1139/y08-001.

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Temperature changes influence cardiac diastolic function. The monoexponential time constant (tauE), which is a conventional lusitropic index of the rate of left ventricular (LV) pressure fall, increases with cooling and decreases with warming. We have proposed that a half-logistic time constant (tauL) is a better lusitropic index than tauE at normothermia. In the present study, we investigated whether tauL can remain a superior measure as temperature varies. The isovolumic relaxation LV pressure curves from the minimum of the first time derivative of LV pressure (dP/dtmin) to the LV end-diastolic pressure were analyzed at 30, 33, 36, 38, and 40 °C in excised, cross-circulated canine hearts. tauL and tauE were evaluated by curve-fitting using the least squares method and applying the half-logistic equation, P(t) = PA/[1 + exp(t/tauL)] + PB, and the monoexponential equation, P(t) = P0exp(–t/tauE) + P∞. Both tauL and tauE increased significantly with decreasing temperature and decreased with increasing temperature. The half-logistic correlation coefficient (r) values were significantly higher than the monoexponential r values at the 5 above-mentioned temperatures. This implies that the superiority of the goodness of the half-logistic fit is not temperature dependent. The half-logistic model characterizes the amplitude and time course of LV pressure fall more reliably than the monoexponential model. Hence, we concluded that tauL is a more useful lusitropic index regardless of temperature.

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Nwasokwa, O. N., and M. M. Bodenheimer. "Global analysis of myocardial isotonic shortening: comparison with isometric dynamics." American Journal of Physiology-Heart and Circulatory Physiology 260, no. 2 (February 1, 1991): H486—H498. http://dx.doi.org/10.1152/ajpheart.1991.260.2.h486.

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Although potentially analytically useful, a global empirical model of the myocardial isotonic curve, L(t), has not been described. We propose the following relation: L(t) = C(t/A)B-1e-(t/A)B, where A, B, and C are global parameters, L is length, and t is time. We evaluated this model in nine in situ canine papillary muscles studied with a servo-system to produce isotonic twitches at different isotonic forces (F). For each twitch, the parameters were determined by nonlinear curve fitting. The model fit the observed curves of L(t) closely, with the coefficient of determination being 0.995 +/- 0.002. C changed with F, but A and B varied little with F, averaging 0.262 +/- 0.021 s and 2.76 +/- 0.17, respectively. Our predictions that A reflects chronotropic, B reflects lusitropic, and C reflects heterotonic (different afterloads) and inotropic states were supported. Comparison done in five muscles showed that A was the same but B was higher for isotonic than for isometric twitches: 0.270 +/- 0.020 vs. 0.264 +/- 0.038 s (P = not significant) for A and 2.79 +/- 0.18 vs. 2.39 +/- 0.05 (P less than 0.008) for B. Dobutamine increased A but not B in isotonic twitches. Thus shortening is lusitropic but leaves no lusitropic reserve to be mobilized by dobutamine. The relation L(t) = C(t/A)B-1e-(t/A)B provides a framework that undergirds global analysis of myocardial shortening and enables comparison with isometric dynamics.

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Rozenberg, Sandrine, Sophie Besse, Benoît Vivien, Pierre Coriat, and Bruno Riou. "Myocardial Effects of Halothane and Isoflurane in Senescent Rats." Anesthesiology 97, no. 6 (December 1, 2002): 1477–84. http://dx.doi.org/10.1097/00000542-200212000-00020.

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Background Aging is associated with marked alterations in myocardial contraction and relaxation, whereas halogenated anesthetics depress myocardial contractility. However, their effects on aging myocardium are unknown. Methods Mechanical variables of left ventricular papillary muscles from adult and senescent rats (29 degrees C; pH 7.40; Ca2+ 1.0 or 0.5 mM; stimulation frequency, 12 pulses/min) were studied. The expression of genes coding for the alpha and beta-myosin heavy chain (MHC) and Ca2+ -ATPase of the sarcoplasmic reticulum (SR) were studied. The effects of halothane and isoflurane were studied. The inotropic effects were compared under low and high loads, using the maximum unloaded shortening velocity (Vmax) and maximum isometric active force (AF). The lusitropic effects were compared in isotonic and isometric conditions. Results Senescent rats had a decrease in contraction and relaxation velocities, associated with a reexpression of beta-MHC mRNAs and a decrease in SR Ca2+ -ATPase mRNAs. Halothane induced a lower negative inotropic effect in senescent rats (1.5 vol%, AF: 53 +/- 14% vs. 39 +/- 12% of baseline values; P < 0.01) whereas isoflurane induced a similar negative inotropic effect (1.5 vol%, AF: 81 +/- 7% vs. 87 +/- 7% of baseline values; NS). Halothane induced a negative lusitropic effect in isotonic conditions in adult, but not in senescent, rats. Conclusions The inotropic and lusitropic effects of halothane were less important in senescent than in adult rats, whereas the effects of isoflurane were similar. These differences are probably related to differences in SR function and in the effects of halogenated anesthetics on the SR.

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LORELL, B. "Diastolic (lusitropic) failure of the ischaemic and hypertrophied heart." Journal of Molecular and Cellular Cardiology 23 (July 1991): S33. http://dx.doi.org/10.1016/0022-2828(91)90617-u.

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Marchini, Timoteo, Verónica D'Annunzio, Mariela L. Paz, Lourdes Cáceres, Mariana Garcés, Virginia Perez, Deborah Tasat, et al. "Selective TNF-α targeting with infliximab attenuates impaired oxygen metabolism and contractile function induced by an acute exposure to air particulate matter." American Journal of Physiology-Heart and Circulatory Physiology 309, no. 10 (November 15, 2015): H1621—H1628. http://dx.doi.org/10.1152/ajpheart.00359.2015.

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Inflammation plays a central role in the onset and progression of cardiovascular diseases associated with the exposure to air pollution particulate matter (PM). The aim of this work was to analyze the cardioprotective effect of selective TNF-α targeting with a blocking anti-TNF-α antibody (infliximab) in an in vivo mice model of acute exposure to residual oil fly ash (ROFA). Female Swiss mice received an intraperitoneal injection of infliximab (10 mg/kg body wt) or saline solution, and were intranasally instilled with a ROFA suspension (1 mg/kg body wt). Control animals were instilled with saline solution and handled in parallel. After 3 h, heart O2 consumption was assessed by high-resolution respirometry in left ventricle tissue cubes and isolated mitochondria, and ventricular contractile reserve and lusitropic reserve were evaluated according to the Langendorff technique. ROFA instillation induced a significant decrease in tissue O2 consumption and active mitochondrial respiration by 32 and 31%, respectively, compared with the control group. While ventricular contractile state and isovolumic relaxation were not altered in ROFA-exposed mice, impaired contractile reserve and lusitropic reserve were observed in this group. Infliximab pretreatment significantly attenuated the decrease in heart O2 consumption and prevented the decrease in ventricular contractile and lusitropic reserve in ROFA-exposed mice. Moreover, infliximab-pretreated ROFA-exposed mice showed conserved left ventricular developed pressure and cardiac O2 consumption in response to a β-adrenergic stimulus with isoproterenol. These results provides direct evidence linking systemic inflammation and altered cardiac function following an acute exposure to PM and contribute to the understanding of PM-associated cardiovascular morbidity and mortality.

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Gueugniaud, Pierre-Yves, Jean-Luc Hanouz, Benoit Vivien, Yves Lecarpentier, Pierre Coriat, and Bruno Riou. "Effects of Desflurane in Rat Myocardium." Anesthesiology 87, no. 3 (September 1, 1997): 599–609. http://dx.doi.org/10.1097/00000542-199709000-00021.

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Background The cardiovascular effects of desflurane have been investigated in several in vivo animal and human studies. To determine the possible contributions of myocardial depression, the effects of desflurane on various contractile parameters in isolated cardiac papillary muscles were compared with those of isoflurane and halothane. Methods The effects of desflurane, isoflurane, and halothane (0.5-2.5 minimum alveolar concentration [MAC]) were studied in rat left ventricular papillary muscles (29 degrees C; pH 7.40; stimulation frequency, 12 pulses/min). The inotropic effects were compared under low (isotony) and high (isometry) loads, using the maximum unloaded shortening velocity (Vmax) and maximum isometric active force (AF). The lusitropic effects were compared in isotonic and isometric conditions. Results Desflurane has no significant inotropic effect (AF at 2.5 MAC: 95 +/- 11% of control values; NS) in contrast with halothane and isoflurane (AF at 2.5 MAC: 37 +/- 14 vs. 65 +/- 10%, respectively; P < 0.05). After alpha- and beta-adrenoceptor blockade or pretreatment with reserpine, desflurane induced a negative inotropic effect (AF at 2.5 MAC: 83 +/- 11 vs. 89 +/- 8%, respectively) that was not significantly different from that of isoflurane (AF at 2.5 MAC: 80 +/- 12%). Halothane induced a negative lusitropic effect under low load, which was significantly greater than those of isoflurane and desflurane. In contrast to halothane, isoflurane and desflurane induced no significant lusitropic effect under high load and did not modify postrest potentiation. These results suggest that desflurane did not impair sarcoplasmic reticulum function. Conclusions When compared with isoflurane, desflurane induced a moderate positive inotropic effect related to intramyocardial catecholamine release. After adrenoceptor blockade, desflurane induced a negative inotropic effect comparable with that induced by isoflurane.

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Ramaswamykanive, H., D. Bihari, and T. R. Solano. "Myocardial Depression Associated with Pneumococcal Septic Shock Reversed by Levosimendan." Anaesthesia and Intensive Care 35, no. 3 (June 2007): 409–13. http://dx.doi.org/10.1177/0310057x0703500316.

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Levosimendan is a myocardial calcium sensitiser and potassium-ATP channel opener. Levosimendan has been used in critically ill patients in various conditions to support myocardial function as an inotrope, lusitrope and vasodilator. We report the use of levosimendan in a patient with invasive streptococcal septic shock.

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Hettrick, DA, PS Pagel, JR Kersten, JP Tessmer, and &NA; Warltier. "NEGATIVE INOTROPIC AND LUSITROPIC EFFECTS OF ETOMIDATE IN CARDIOMYOPATHIC DOGS." Anesthesia & Analgesia 86, Supplement (February 1998): 69S. http://dx.doi.org/10.1097/00000539-199802001-00069.

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28

Ishizaka, Tomomichi, Yu Yoshimatsu, Tomomi Sugiura, Yu Maeda, Katsuyoshi Chiba, and Kazuhiko Mori. "Trastuzumab-induced negative chronotropic and lusitropic effects in cynomolgus monkeys." Journal of Pharmacological and Toxicological Methods 105 (September 2020): 106755. http://dx.doi.org/10.1016/j.vascn.2020.106755.

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29

Lowes, Robert, Lee Woodson, Javier Villanueva-Meyer, and Mali Mathru. "A72 LUSITROPIC FUNCTION IS PRESERVED DURING PROPOFOL ANESTHESIA IN HUMANS." Anesthesiology 87, Supplement (September 1997): 72A. http://dx.doi.org/10.1097/00000542-199709001-00072.

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30

Perez, N. G., Alicia Mattiazzi, and H. E. Cingolani. "Lusitropic changes induced by acid base alterations in cat papillary muscles." Archives Internationales de Physiologie, de Biochimie et de Biophysique 101, no. 3 (January 1993): 233–37. http://dx.doi.org/10.3109/13813459309046481.

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31

Bronzwaer, Jean G. F., Jacques Goldstein, Francis Wellens, George Jambroes, and Walter J. Paulus. "Lusitropic function of the cardiac allograft: Loading and inactivation dependent effects." Journal of the American College of Cardiology 17, no. 2 (February 1991): A365. http://dx.doi.org/10.1016/0735-1097(91)92424-k.

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32

Wei, Bin, Hongguang Wei, and J. P. Jin. "Dysferlin deficiency blunts β-adrenergic-dependent lusitropic function of mouse heart." Journal of Physiology 593, no. 23 (November 2, 2015): 5127–44. http://dx.doi.org/10.1113/jp271225.

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33

Abrol, Neha, Pieter P. de Tombe, and Seth L. Robia. "Acute Inotropic and Lusitropic Effects of Cardiomyopathic R9C Mutation of Phospholamban." Journal of Biological Chemistry 290, no. 11 (January 15, 2015): 7130–40. http://dx.doi.org/10.1074/jbc.m114.630319.

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34

Salgado, Helio C., Géssica M. Simões, Valter J. Santana Filho, Valdo J. Dias da Silva, Maria Cristina O. Salgado, and Rubens Fazan. "NEGATIVE INOTROPIC AND LUSITROPIC EFFECTS OF INTRAVENOUS AMIODARONE IN CONSCIOUS RATS." Clinical and Experimental Pharmacology and Physiology 34, no. 9 (September 2007): 870–75. http://dx.doi.org/10.1111/j.1440-1681.2007.04676.x.

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35

KAPELKO, V. "Lusitropic control of the heart: Dependence on phosphocreatine pathway in cardiomyocytes." Journal of Molecular and Cellular Cardiology 23 (July 1991): S78. http://dx.doi.org/10.1016/0022-2828(91)90749-c.

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36

Schwinger, Robert H. G., Michael Böhm, and Erland Erdmann. "Inotropic and lusitropic dysfunction in myocardium from patients with dilated cardiomyopathy." American Heart Journal 123, no. 1 (January 1992): 116–28. http://dx.doi.org/10.1016/0002-8703(92)90755-k.

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37

BRONZWAER, J. "Lusitropic and diastolic effects of different types of brief myocardial ischemia." Journal of Molecular and Cellular Cardiology 23 (July 1991): S32. http://dx.doi.org/10.1016/0022-2828(91)90613-q.

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38

Petroff, Martin Vila, Cecilia Mundiña-Weilenmann, Leticia Vittone, Gladys Chiappe de Cingolani, and Alicia Mattiazzi. "Lusitropic effects of α- and β-adrenergic stimulation in amphibian heart." Molecular and Cellular Biochemistry 141, no. 2 (December 1994): 87–95. http://dx.doi.org/10.1007/bf00926171.

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39

Rozenberg, Sandrine, Sophie Besse, Julien Amour, Benoît Vivien, Benoît Tavernier, and Bruno Riou. "Effects of Desflurane in Senescent Rat Myocardium." Anesthesiology 105, no. 5 (November 1, 2006): 961–67. http://dx.doi.org/10.1097/00000542-200611000-00017.

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Background The myocardial negative inotropic effects of desflurane are less pronounced than those of other halogenated anesthetics, partly because of intramyocardial catecholamine store release. However, the effects of desflurane on aging myocardium are unknown, whereas aging is known to be associated with an attenuation of catecholamine responsiveness. Methods The effects of desflurane (1.9-9.3 vol%) were studied in left ventricular papillary muscle of adult and senescent rats (29 degrees C; 0.5 mm Ca; stimulation frequency 12 pulses/min). The inotropic effects were compared under low and high loads, using the maximum unloaded shortening velocity and maximum isometric active force, and without or with alpha- and beta-adrenoceptor blockade. Results Desflurane induced a moderate positive inotropic effect in adult rats but a negative inotropic effect in senescent rats. After alpha- and beta-adrenoceptor blockade, desflurane induced a comparable negative inotropic effect in adult and senescent rats. No lusitropic effect under low load was observed, whereas desflurane induced a slight but significant positive lusitropic effect under high load similar between the two groups of rats. This positive effect was abolished by adrenoceptor blockade. Conclusion The authors' study suggests that desflurane does not induce significant intramyocardial catecholamine release in senescent myocardium, a result that should be integrated in the well-known alteration in the catecholamine response during aging.

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40

Tamiya, Kouichi, Toshiyuki Beppu, and Kazuaki Ishihara. "Double-exponential curve fitting of isometric relaxation: a new measure for myocardial lusitropism." American Journal of Physiology-Heart and Circulatory Physiology 269, no. 4 (October 1, 1995): 1. http://dx.doi.org/10.1152/ajpheart.1995.269.4.1-a.

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Pages H393–H406: Kouichi Tamiya, Toshiyuki Beppu, and Kazuaki Ishihara. “Double-exponential curve fitting of isometric relaxation: a new measure for myocardial lusitropism.” Page H402: Figure 10 should appear as the following. (See PDF)

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41

Rosas, Paola Cecilia, Yang Liu, Mohamed Abdalla, Candice Thomas, David Kidwell, Rajesh Kumar, Kenneth Baker, et al. "PHOSPHORYLATED CARDIAC MYOSIN BINDING PROTEIN-C ENHANCES LUSITROPY." Journal of the American College of Cardiology 63, no. 12 (April 2014): A871. http://dx.doi.org/10.1016/s0735-1097(14)60871-8.

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42

Hefer, David, Ting Yi, Donald E. Selby, David E. Fishbaugher, Sarah M. Tremble, Kelly J. Begin, Prospero Gogo, et al. "Erythropoietin induces positive inotropic and lusitropic effects in murine and human myocardium." Journal of Molecular and Cellular Cardiology 52, no. 1 (January 2012): 256–63. http://dx.doi.org/10.1016/j.yjmcc.2011.10.005.

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43

Wu, Yiming, Elizabeth D. Luczak, Eun-Jeong Lee, Carlos Hidalgo, Jinying Yang, Zhan Gao, Jingdong Li, Xander H.T. Wehrens, Henk Granzier, and Mark E. Anderson. "CaMKII effects on inotropic but not lusitropic force frequency responses require phospholamban." Journal of Molecular and Cellular Cardiology 53, no. 3 (September 2012): 429–36. http://dx.doi.org/10.1016/j.yjmcc.2012.06.019.

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44

Al-Rubaiee, Mustafa, Pandu R. Gangula, Richard M. Millis, Robin K. Walker, Nsini A. Umoh, Valerie M. Cousins, Miara A. Jeffress, and Georges E. Haddad. "Inotropic and lusitropic effects of calcitonin gene-related peptide in the heart." American Journal of Physiology-Heart and Circulatory Physiology 304, no. 11 (June 1, 2013): H1525—H1537. http://dx.doi.org/10.1152/ajpheart.00874.2012.

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Previous studies have demonstrated positive-inotropic effects of calcitonin gene-related peptide (CGRP), but the mechanisms remain unclear. Therefore, two experiments were performed to determine the physiological correlates of the positive-inotropic effects of CGRP. Treatments designed to antagonize the effects of physiologically active CGRP1–37 included posttreatment with CGRP8–37 and pretreatment with LY-294002 (LY, an inhibitor of phosphatidylinositol 3-kinase), 17β-estradiol (E), and progesterone (P) were also used to modulate the effects of CGRP1–37. Experiment 1 was in vitro studies on sarcomeres and cells of isolated adult rat cardiac myocytes. CGRP1–37, alone and in combination with E and P, decreased sarcomere shortening velocities and increased shortening percentages, effects that were antagonized by CGRP8–37, but not by LY. CGRP1–37 increased resting intracellular calcium ion concentrations and Ca2+ influxes, effects that were also antagonized by both CGRP8–37 and LY. Experiment 2 was in vivo studies on left ventricular pressure-volume (PV) loops. CGRP1–37 increased end-systolic pressure, ejection fraction, and velocities of contraction and relaxation while decreasing stroke volume, cardiac output, stroke work, PV area, and compliance. After partial occlusion of the vena cava, CGRP1–37 increased the slope of the end-systolic PV relationship. CGRP8–37 and LY attenuated most of the CGRP-induced changes. These findings suggest that CGRP-induced positive-inotropic effects may be increased by treatments with estradiol and progesterone and inhibited by LY. The physiological correlates of CGRP-induced positive inotropy observed in rat sarcomeres, cells, and intact hearts are likely to reveal novel mechanisms of heart failure in humans.

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45

Konrad, D., A. Oldner, M. Wanecek, A. Rudehill, E. Weitzberg, B. Biber, G. Johansson, S. Häggmark, and M. Haney. "Positive inotropic and negative lusitropic effects of endothelin receptor agonism in vivo." American Journal of Physiology-Heart and Circulatory Physiology 289, no. 4 (October 2005): H1702—H1709. http://dx.doi.org/10.1152/ajpheart.00892.2004.

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The endothelin (ET) system is involved in the regulation of myocardial function in health as well as in several diseases, such as congestive heart failure, myocardial infarction, and septic myocardial depression. Conflicting results have been reported regarding the acute contractile properties of ET-1. We therefore investigated the effects of intracoronary infusions of ET-1 and of the selective ETB receptor-selective agonist sarafotoxin 6c with increasing doses in anesthetized pigs. Myocardial effects were measured through analysis of the left ventricular pressure-volume relationship. ET-1 elicited increases in the myocardial contractile status (end-systolic elastance value of 0.94 ± 0.11 to 1.48 ± 0.23 and preload recruitable stroke work value of 68.7 ± 4.7 to 83.4 ± 7.2) that appear to be mediated through ETA receptors, whereas impairment in left ventricular isovolumic relaxation (τ = 41.5 ± 1.4 to 58.1 ± 5.0 and t1/2 = 23.0 ± 0.7 to 30.9 ± 2.6, where τ is the time constant for pressure decay and t1/2 is the half-time for pressure decay) was ETB receptor dependent. In addition, intravenous administration of ET-1 impaired ventricular relaxation but had no effect on contractility. Intracoronary sarafotoxin 6c administration caused impairments in left ventricular relaxation (τ from 43.3 ± 1.8 to 54.4 ± 3.4) as well as coronary vasoconstriction. In conclusion, ET-1 elicits positive inotropic and negative lusitropic myocardial effects in a pig model, possibly resulting from ETA and ETB receptor activation, respectively.

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46

Kiely, David G., Robert I. Cargill, and Brian J. Lipworth. "Effects of Hypercapnia on Hemodynamic, Inotropic, Lusitropic, and Electrophysiologic Indices in Humans." Chest 109, no. 5 (May 1996): 1215–21. http://dx.doi.org/10.1378/chest.109.5.1215.

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47

Martino, JM, JL Hanouz, PY Gueugniaud, B. Vivien, B. Riou, and P. Coriat. "Mécanismes de l'effet lusitrope négatif de l'halothane sur le myocarde de rat." Annales Françaises d'Anesthésie et de Réanimation 16, no. 6 (September 1997): 817. http://dx.doi.org/10.1016/s0750-7658(97)86460-x.

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48

Groban, Leanne, Jewell Jessup, and Thomas Register. "EARLY ESTROGEN REPLACEMENT PREVENTS LUSITROPIC IMPAIRMENT FOLLOWING OVARIECTOMY IN MIDDLE-AGED CYNOMOLGUS MONKEYS." Journal of the American College of Cardiology 55, no. 10 (March 2010): A38.E369. http://dx.doi.org/10.1016/s0735-1097(10)60370-1.

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49

Burstein, Steven, Marc J. Semigran, G. William Dec, Charles A. Boucher, and Michael A. Fifer. "Positive inotropic and lusitropic effects of intravenous flosequinan in patients with heart failure." Journal of the American College of Cardiology 20, no. 4 (October 1992): 822–29. http://dx.doi.org/10.1016/0735-1097(92)90179-q.

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50

Amour, Julien, Xavier Loyer, Pierre Michelet, Aurélie Birenbaum, Bruno Riou, and Christophe Heymes. "Preservation of the Positive Lusitropic Effect of β-Adrenoceptors Stimulation in Diabetic Cardiomyopathy." Anesthesia & Analgesia 107, no. 4 (October 2008): 1130–38. http://dx.doi.org/10.1213/ane.0b013e3181806903.

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