Intracellular mechanism of action of isoflurane and halothane on striated muscle of the rabbit.

Studies were conducted on the effects of isoflurane and halothane on intracellular mechanisms of striated muscle contraction: Ca2+ activation of the contractile proteins and Ca2+ uptake and release from the sarcoplasmic reticulum. Functionally skinned muscle fibers (sarcolemma disrupted by homogenization) from isolated papillary muscle (PM), soleus (SL) (slow-twitch skeletal muscle), and adductor magnus (AM) (fast-twitch skeletal muscle) of rabbits were mounted on a photodiode tension transducer. They were immersed in control solution (saturated with N2), then in test solution (saturated with anesthetic-N2 mixture), and in control solution again. The following two studies were carried out: 1) in the study of Ca2+ -activated tension development of the contractile proteins, free Ca2+ concentration in the bathing solution was controlled by the use of a high EGTA (7 mM), and 2) in the study of Ca2+ uptake and release from the sarcoplasmic reticulum (SR), Ca2+ was loaded into the SR and released with caffeine and the resulting tension transients were measured. Isoflurane (1-4%) decreased (6-9%) the maximal Ca2+ -activated tension development in PM and SL but more in PM than in SL. In AM, however, isoflurane and halothane (1-3%) produced no change. Isoflurane decreased submaximal Ca2+ -activated tension development in PM, but effected no change in it in SL. Isoflurane and halothane increased the tension development in AM to the extent of producing a shift to the left in the pCa-tension curves of less than or equal to 0.1 pCa unit.(ABSTRACT TRUNCATED AT 250 WORDS)