Halothane, enflurane, and isoflurane decrease the number of crossbridge interactions in rabbit papillary muscle without altering actin-myosin ATPase kinetics.
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Animal data on myocardial crossbridge effects warrant caution before clinical extrapolation; leaves open relevance to human diastolic function under anesthesia.
The authors examined the effect of halothane, enflurane, and isoflurane on the dynamic stiffness of rabbit papillary muscles in Ba2+ contracture. Ca2+ was replaced by Ba2+ in order to constantly activate myofibrils. The dynamic stiffness of the contractured muscle was examined by exposing the muscle to sinusoidal length perturbations at frequencies of 0.05-30 Hz under two concentrations of anesthetic, approximately 0.5, and 1.5-2 mM, and at two Ba2+ concentrations, 0.5 and 1.5-2 mM. The anesthetics had no effect on the frequency (fmin) at which minimum stiffness occurred, but markedly decreased the stiffness modulus at high frequencies (Khi). The decrease in Khi was significant for all anesthetics at the P less than 0.05 level. Increasing the Ba2+ concentration from 0.5 to 1.5-2 mM in the presence of 0.5 mM of anesthetic resulted in a return of Khi to control levels. The authors conclude that halothane, enflurane, and isoflurane did not alter actin-myosin ATPase kinetics, because fmin was unchanged, but decreased the number of crossbridge interactions, because Khi was significantly decreased by all three anesthetics.
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Shibata et al. (1989) studied this question.
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