Abstract

Mouse soleus and extensor digitorum longus muscles exposed to halothane concentrations (0.3-2.0%) that, at room temperature, have no effect on either resting or twitch tension, develop transient contractures when cooled to 2-10 degrees C. The halothane-cooling contractures (HCC) are reproducible and their amplitudes can be graded by both the halothane concentration and the temperature of cooling. Under identical conditions the HCC is significantly larger in soleus as compared to extensor digitorum longus muscles. The maximal HCC in soleus muscles (1-2% halothane, 2 degrees C) reaches 42% of the tetanic tension recorded at 24 degrees C; in extensor digitorum longus the maximum is 12% of tetanic tension. This difference is ascribed to the predominance of slow-twitch fibers in the soleus muscle. Neither membrane depolarization with high [K]0 solutions nor a short (2 min) exposure to Ca-free media inhibits the HCC. The contractures are depressed, however, when the muscles are preequilibrated for 30 min with Ca-free solutions; under these conditions, the muscle twitches and the caffeine-cooling contractures are also depressed. These effects are ascribed to partial depletion of the Ca content of the sarcoplasmic reticulum. The HCC is abolished by 4 mM procaine, partially inhibited by 4 to 10 mM procainamide and potentiated by 4 mM lidocaine, but it is not significantly affected by dantrolene (40 microM). It is proposed that the HCC results from synergistic interaction of halothane and low temperature inhibiting Ca-sequestration by the sarcoplasmic reticulum of the muscle fibers.(ABSTRACT TRUNCATED AT 250 WORDS)