EFFECTS OF HALOTHANE, ENFLURANE, AND ISOFLURANE ON SKINNED RAT MYOCARDIUM ACTIVATED BY CA-2+
EFFECTS OF HALOTHANE, ENFLURANE, AND ISOFLURANE ON SKINNED RAT MYOCARDIUM ACTIVATED BY CA-2+
复制标题
DOI：
10.1152/ajpheart.1993.264.1.h224
复制
发表时间：
1993-01-01
影响因子：
--
通讯作者：
STEPHENSON, DG
中科院分区：
文献类型：
--
作者：
HERLAND, JS;JULIAN, FJ;STEPHENSON, DG
研究了氟烷（1.9 mM, 9.4 mM）、安氟烷（3.3 mM, 16.5 mM）和异氟烷（1.6 mM, 8.1 mM）对大鼠透性心肌制剂中最大Ca2+激活力和Ca2+敏感性的影响。在通过温和均质或皂苷（50杯/毫升，30分钟）渗透的制剂中，用2% Triton X-100进一步破坏肌膜导致最大力和Ca2+敏感性增加。当膜被机械破坏或皂化时，每种蒸汽剂都使心肌对Ca2+更敏感。在这些制剂中，氟烷降低了最大力，但不受安氟烷或异氟烷的影响。随着细胞膜被Triton完全破坏，先前观察到的由安氟烷引起的Ca2+敏感性增加减少，而由氟烷和异氟烷引起的Ca2+敏感性增加被消除，最大力被氟烷和异氟烷降低，但不受安氟烷的影响。这些结果表明，1)与细胞膜系统相关的成分通常调节哺乳动物心肌的力，2)氟烷、安氟烷和异氟烷对这些成分有复杂的影响。因此，这些结果可以解释这些药物对哺乳动物心肌的肌力作用的一些差异。
The effects of halothane (1.9 mM, 9.4 mM), enflurane (3.3 mM, 16.5 mM), and isoflurane (1.6 mM, 8.1 mM) on maximal Ca2+-activated force and Ca2+ sensitivity were studied in rat myocardial preparations rendered permeable by various methods. In preparations permeabilized either by mild homogenization or by saponin (50 mug/ml, 30 min), further disruption of the sarcolemma with 2% Triton X-100 resulted in increased maximal force and Ca2+ sensitivity. When membranes were mechanically disrupted or saponized, each vapor agent caused the myocardium to be more sensitive to Ca2+. In these preparations, maximal force was decreased by halothane but was not affected by enflurane or isoflurane. With cellular membranes completely disrupted by Triton, the previously observed increase in Ca2+ sensitivity caused by enflurane was reduced, whereas that caused by halothane and isoflurane was abolished and maximal force was decreased by halothane and isoflurane but was not affected by enflurane. These results indicate that 1) components associated with the cellular membrane systems normally modulate force in mammalian myocardium, and 2) halothane, enflurane, and isoflurane have complex effects on these components. These results therefore can explain some of the differences in inotropic effects that these agents exert on mammalian myocardium.