Nagao T, Vanhoutte P M
Center for Experimental Therapeutics, Baylor College of Medicine, Houston, TX 77030.
J Cereb Blood Flow Metab. 1993 May;13(3):498-502. doi: 10.1038/jcbfm.1993.64.
Isometric tension and membrane potential were measured to determine the electrophysiological events occurring during anoxia in the isolated canine basilar artery. Anoxia induced transient contractions which were inhibited by the Ca(2+)-channel inhibitor, diltiazem, and were abolished in Ca(2+)-free solution. Anoxic contractions were accompanied by membrane depolarizations, which were resistant to diltiazem. When matched contractions were obtained with anoxia and high K+, the level of membrane depolarization was smaller during anoxic contractions. These results support the importance of voltage-dependent Ca2+ influx in the generation of anoxic contractions in the canine basilar artery. However, membrane depolarization does not fully account for these anoxic contractions.
测量等长张力和膜电位，以确定在离体犬基底动脉缺氧期间发生的电生理事件。缺氧诱导短暂收缩，该收缩被钙通道抑制剂地尔硫卓抑制，且在无钙溶液中消失。缺氧收缩伴有膜去极化，其对地尔硫卓有抗性。当缺氧和高钾引起的收缩相匹配时，缺氧收缩期间的膜去极化水平较小。这些结果支持电压依赖性钙内流在犬基底动脉缺氧收缩产生中的重要性。然而，膜去极化并不能完全解释这些缺氧收缩。
