Blanck T J, Runge S, Stevenson R L
Department of Anesthesiology and Critical Care Medicine, Johns Hopkins University, Baltimore, Maryland 21205.
Anesth Analg. 1988 Nov;67(11):1032-5.
The effect of halothane concentration on the binding of the calcium antagonist, [3H] nitrendipine (3HNTP), to rat and rabbit heart membranes was examined in vitro because it has been hypothesized that one mechanism by which halothane depresses cardiac contractility is by interfering with Ca2+ channel function. Membranes were incubated for 90 minutes in a closed system with 3HNTP and increasing concentrations of halothane. The amount of 3HNTP bound to membranes was quantified by radioligand binding technique and liquid scintillation counting. It was found in both the rat and rabbit cardiac membranes that halothane (0.4-2.0%) caused a dose-dependent decrease in specific 3HNTP binding (P less than 0.0001). The decrease in 3HNTP binding caused by halothane was also found to be reversible. These results indicate that halothane interferes with one property of the Ca2+ channel and suggest that this may be one possible mechanism for the negative inotropic action of halothane.
由于有假说认为氟烷降低心肌收缩力的一种机制是通过干扰钙离子通道功能，因此在体外研究了氟烷浓度对钙拮抗剂[3H]尼群地平（3HNTP）与大鼠和兔心脏膜结合的影响。将膜在封闭系统中与3HNTP和浓度不断增加的氟烷一起孵育90分钟。通过放射性配体结合技术和液体闪烁计数对与膜结合的3HNTP量进行定量。在大鼠和兔心脏膜中均发现，氟烷（0.4 - 2.0%）导致特异性3HNTP结合呈剂量依赖性降低（P小于0.0001）。还发现氟烷引起的3HNTP结合减少是可逆的。这些结果表明氟烷干扰了钙离子通道的一种特性，并提示这可能是氟烷负性肌力作用的一种可能机制。
