Key result
Halothane and sevoflurane increased elastic stiffness during relaxation when extracellular Ca(2+) was increased to match control peak force, suggesting a direct effect on cross bridges.
Halothane and sevoflurane appear to have a direct effect on cross bridges in ferret ventricular myocardium, as evidenced by increased elastic stiffness during relaxation.
Hypothesis-generating for volatile anesthetic effects on myocardial stiffness; leaves open validation in human models.
The effects of halothane, isoflurane, and sevoflurane on elastic stiffness, which reflects the degree of cross-bridge attachment, were studied in intact cardiac muscle. Electrically stimulated (0.25 Hz, 25 degrees C), isometrically twitching right ventricular ferret papillary muscles (n = 15) at optimal length (L(max)) were subjected to sinusoidal length oscillations (40 Hz, 0.25- 0.50% of L(max) peak to peak). The amplitude and phase relationship with the resulting force oscillations was decomposed into elastic and viscous components of total stiffness in real time. Increasing extracellular Ca(2+) concentration in the presence of anesthetics to produce peak force equal to control increased elastic stiffness during relaxation, which suggests a direct effect of halothane and sevoflurane on cross bridges.
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Bartunek et al. (2002) studied Intact cardiac muscle (ferret ventricular myocardium) (n=15). Halothane, isoflurane, and sevoflurane vs. Control was evaluated on Elastic stiffness during relaxation. Halothane and sevoflurane increased elastic stiffness during relaxation when extracellular Ca(2+) was increased to match control peak force, suggesting a direct effect on cross bridges.
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