Desflurane induces only minor Ca2+ release from the sarcoplasmic reticulumof mammalian skeletal muscle

Background: Desflurane is a weaker trigger of malignant hyperthermia than i s halothane. There are very few data of the pathophysiologic background of this observation. Therefore, the authors' aim was to investigate the direct effect of desflurane on calcium release in skinned skeletal muscle fibers. Methods: For the measurements, single saponin-skinned muscle fiber preparat ions of BALB/c mice were used. For Ca2+ release experiments, liquid desflur ane at 0.6 and 3.5 mM was applied to weakly calcium-buffered solutions with no added Ca2+. Desflurane was diluted in strongly Ca2+-buffered solutions, with [Ca2+] between 3.0 and 24.9 mu M for [Ca2+]-force relations. Force tr ansients were transformed into Ca2+ transients based on the individual [Ca2 +]-force relations. As controls, 30 mM caffeine and equimolar sevoflurane w ere investigated in the same muscle fibers. Results: At 3.5 mM, desflurane induced peak force transients of 8 +/- 4% (m ean +/- SD) of maximal Ca2+-activated force (T-max). These peak values were significantly smaller than those in the presence of 3.5 mM sevoflurane (24 +/- 10% of T-max, P < 0.05), and 4 or 5 times smaller than previously repo rted Ca2+-release-induced force transients by equimolar halothane. Calculat ed peak Ca2+ transients derived from force transients and induced by 3.5 an d 0.6 mM desflurane were significantly smaller than those Induced by 30 mar caffeine. The [Ca2+]-force relation was shifted by desflurane, resulting i n a Ca2+-sensitizing effect. The maximal Ca2+-activated force was significa ntly increased by 0.6 mM desflurane in comparison with the control, with no added substance (P less than or equal to 0.05). Conclusion: Desflurane induces only slight Ca2+ release in skinned skeletal muscle fibers.