Mohanlal R W, Wijnmaalen P, Mauve I, Zeeuwe P, van der Laarse A
Dept. Cardiology, University Hospital Leiden, The Netherlands.
Res Commun Chem Pathol Pharmacol. 1989 Jan;63(1):3-11.
Isolated rat hearts underwent low flow perfusion with a perfusion pressure of 15 mmHg for two hours followed by reperfusion at a perfusion pressure of 80 mmHg for two hours. In these severely damaged hearts we tested whether diltiazem (0.5 mg/l) administered during ischemia or during reperfusion had vasodilatory effects. Ischemia-induced progressive vasoconstriction was not influenced by the presence of diltiazem: during ischemia coronary vascular resistance (CVR) rose from 3.3 +/- 0.1 to 46.4 +/- 17.6 mmHg.ml-1.min in the diltiazem group and from 3.5 +/- 0.1 to 42.4 +/- 5.3 mmHg.ml-1.min in the control group (n.s.). If diltiazem was administered during reperfusion only CVR dropped from 45.7 +/- 9.2 to 4.4 +/- 1.1 mmHg.ml-1.min in the presence of diltiazem, and from 47.1 +/- 11.6 to 9.3 +/- 1.5 mmHg.ml-1.min in the control group (P less than 0.025). The disparity between diltiazem's effects during ischemia and reperfusion suggests a different mechanism of Ca2+-influx in vascular smooth muscle cells in ischemic and reperfused hearts: in reperfusion through the Ca2+-channels which are sensitive to calcium antagonists, and in ischemia through other channels, like the Na+/Ca2+ exchanger, or from intracellular calcium stores.
将离体大鼠心脏以15 mmHg的灌注压进行低流量灌注两小时，随后以80 mmHg的灌注压再灌注两小时。在这些严重受损的心脏中，我们测试了在缺血期或再灌注期给予地尔硫䓬（0.5 mg/l）是否具有血管舒张作用。缺血诱导的进行性血管收缩不受地尔硫䓬存在的影响：在缺血期，地尔硫䓬组的冠状动脉血管阻力（CVR）从3.3±0.1升高至46.4±17.6 mmHg·ml-1·min，对照组从3.5±0.1升高至42.4±5.3 mmHg·ml-1·min（无显著性差异）。仅在再灌注期给予地尔硫䓬时，地尔硫䓬存在时CVR从45.7±9.2降至4.4±1.1 mmHg·ml-1·min，对照组从47.1±11.6降至9.3±1.5 mmHg·ml-1·min（P<0.025）。地尔硫䓬在缺血期和再灌注期作用的差异表明，缺血和再灌注心脏血管平滑肌细胞中Ca2+内流的机制不同：再灌注时通过对钙拮抗剂敏感的Ca2+通道，缺血时通过其他通道，如Na+/Ca2+交换体或细胞内钙库。
