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钙拮抗剂对缺血后再灌注期间心脏去甲肾上腺素耗竭的抑制作用。

Inhibitory effect of calcium antagonists on the depletion of cardiac norepinephrine during postischemic reperfusion.

作者信息

Nayler W G, Sturrock W J

出版信息

J Cardiovasc Pharmacol. 1985 May-Jun;7(3):581-7. doi: 10.1097/00005344-198505000-00026.

Abstract

We have investigated whether Ca2+ antagonists of the dihydropyridine type (nifedipine, nisoldipine, and nitrendipine) attenuate or abolish the ischemia-reperfusion-induced depletion of the cardiac stores of norepinephrine (NE). The experiments were performed using isolated, Langendorff-perfused rat hearts. Ischemia (global) was induced for 15 or 60 min at 37 degrees C and was followed by normothermic reperfusion. Left ventricular NE content was assayed by high-performance liquid chromatography with electrochemical detection. The continued presence of nifedipine (0.03 microM), nisoldipine (0.03 microM), or nitrendipine (0.03 microM) before and after the ischemic episode abolished the loss of NE caused by 15 min but not 60 min of ischemia and reperfusion. Nifedipine, 0.03 microM, but not diltiazem, 0.24-1.22 microM, or verapamil, 0.22-1.09 microM, attenuated (p less than 0.05) NE depletion when added only on reperfusion.

摘要

我们研究了二氢吡啶类钙拮抗剂(硝苯地平、尼索地平及尼群地平)是否能减轻或消除缺血-再灌注引起的心脏去甲肾上腺素(NE)储备耗竭。实验采用离体的、Langendorff灌注大鼠心脏进行。在37℃诱导15或60分钟的(整体)缺血,随后进行常温再灌注。通过高效液相色谱-电化学检测法测定左心室NE含量。在缺血发作前后持续存在硝苯地平(0.03微摩尔)、尼索地平(0.03微摩尔)或尼群地平(0.03微摩尔)可消除15分钟而非60分钟缺血和再灌注所致的NE丢失。仅在再灌注时添加0.03微摩尔的硝苯地平而非0.24 - 1.22微摩尔的地尔硫䓬或0.22 - 1.09微摩尔的维拉帕米可减轻(p < 0.05)NE耗竭。

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