Sudo R T, Zapata-Sudo G, Suarez-Kurtz G
Departamento de Farmacologia Básica e Clínica, Universidade Federal do Rio de Janeiro, Brazil.
Anesthesiology. 1990 Nov;73(5):958-63. doi: 10.1097/00000542-199011000-00025.
The effects of halothane or cooling on Ca2(+)-activated tensions and on the uptake and release of Ca2+ by the sarcoplasmic reticulum were investigated in chemically skinned fibers of the extensor digitorum longus muscle of adult rabbits. At 22 degrees C, halothane (greater than 0.46 mM) induced Ca2+ release from the SR of Ca2(+)-loaded skinned fibers that resulted in transient tensions. Higher concentrations of halothane (greater than 4.65 mM) reduced the steady-state accumulation of Ca2+ in the SR at 22 degrees C. Cooling (to less than 10 degrees C) elicited transient contractures (cooling-induced contractures [CC]) in Ca2(+)-loaded skinned fibers, despite the fact that the tensions elicited by adding Ca2+ to the bath were depressed at these low temperatures. The skinned fibers did not develop CCs at 12-16 degrees C. Halothane cooling contractures could be elicited at these temperatures by exposing the fibers to halothane concentrations that failed to elicit Ca2+ release at 22 degrees C. The halothane cooling contractures were blocked by procaine but not by lidocaine. It was concluded that these contractures resulted from a synergistic interaction between halothane and cooling that stimulates Ca2+ release from, and reduces Ca2+ uptake by, the sarcoplasmic reticulum.
在成年兔趾长伸肌的化学去皮纤维中,研究了氟烷或冷却对Ca2(+)-激活张力以及对肌浆网摄取和释放Ca2+的影响。在22℃时,氟烷(大于0.46 mM)诱导Ca2(+)-负载的去皮纤维的肌浆网释放Ca2+,导致短暂张力。更高浓度的氟烷(大于4.65 mM)在22℃时降低了肌浆网中Ca2+的稳态积累。冷却(至低于10℃)在Ca2(+)-负载的去皮纤维中引发短暂挛缩(冷却诱导挛缩[CC]),尽管在这些低温下向浴中添加Ca2+所引发的张力降低。去皮纤维在12 - 16℃时未出现CC。在这些温度下,通过将纤维暴露于在22℃时未能引发Ca2+释放的氟烷浓度,可引发氟烷冷却挛缩。氟烷冷却挛缩被普鲁卡因阻断,但未被利多卡因阻断。得出的结论是,这些挛缩是由氟烷和冷却之间的协同相互作用引起的,这种相互作用刺激了肌浆网释放Ca2+并减少了其对Ca2+的摄取。