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Yves Lecarpentier

Publications and source records attributed to Yves Lecarpentier.

20 records · Page 2Linked to original sources

The paradoxical positive inotropic effect of sevoflurane in healthy and cardiomyopathic hamsters.

UNLABELLED: We investigated the effects of sevoflurane (0.7 to 3.6 vol%) on inotropy and lusitropy in left ventricular papillary muscles of healthy hamsters and genetically induced cardiomyopathic (strain BIO 14.6) hamsters in vitro (29 degrees C, pH 7.40, Ca(2+) 2.5 mM, stimulation frequency three per minute) under low (isotony) and high (isometry) loads. Sevoflurane induced a moderate positive inotropic effect in healthy hamsters (maximum unloaded shortening velocity and isometric active force at 3.6 vol%: 115% +/- 12% and 128% +/- 21% of baseline values, respectively; P < 0.01) and in cardiomyopathic hamsters (maximum unloaded shortening velocity and isometric active force at 3.6 vol%: 115% +/- 20% and 124% +/- 31% of baseline values, respectively; P < 0.05). This positive inotropic effect did not differ between healthy and cardiomyopathic hamsters, even when sevoflurane concentrations were corrected for minimum alveolar anesthetic concentration values in each strain, and was unchanged after alpha- and beta-adrenoceptor blockade. After calcium-channel blockade, this positive inotropic effect was abolished in healthy hamsters but enhanced in cardiomyopathic hamsters. In both strains, sevoflurane induced a moderate negative lusitropic effect under low and high loads. IMPLICATIONS: A paradoxical moderate positive inotropic effect of sevoflurane was observed in hamster ventricular muscle. This effect was likely related to calcium channel interaction, because after calcium-channel blockade, it was abolished in healthy hamsters and enhanced in cardiomyopathic hamsters.

Administration, Inhalation↗

Mechanics of Relaxation of the Human Heart.

Rapid and complete relaxation is a prerequisite for cardiac output adaptation to changes in loading conditions, inotropic stimulation, and heart rate. In the healthy human heart, the rate and extent of relaxation depend mainly on actomyosin cross bridge dissociation and on left ventricular end-systolic volume, rather than on the afterload level.

Journal Article↗