三硝酸甘油而非自发一氧化氮供体可维持缺血兔心脏的心肌功能和细胞完整性。

I Woditsch, K Schrör
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引用次数: 2

摘要

langendorff灌注兔心脏进行2小时的全身低流量缺血,然后再灌注30分钟。这导致左心室舒张压明显升高,左心室肌酸磷酸激酶活性降低。早期再灌注时NO形成明显减少。在超氧化物歧化酶(20 U/ml)存在下,NO释放(氧合血红蛋白技术)完全正常化,表明超氧化物自由基使NO失活。三硝酸甘油(GTN)处理;30 μ m)可预防缺血引起的心肌组织损伤。0.3 μ m的SIN-1无效。这些数据表明GTN对心肌缺血有保护作用,而SIN-1没有。由此可见,NO生成部位可能是决定NO供体生物活性的重要因素。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Glyceryl trinitrate but not spontaneous NO donors preserve myocardial function and cell integrity in ischemic rabbit hearts.

Langendorff-perfused rabbit hearts were subjected to 2 h of global, low-flow ischemia followed by 30 min of reperfusion. This resulted in a marked increase of left ventricular enddiastolic pressure and a loss in left ventricular creatine phosphokinase activity. NO formation was significantly reduced in early reperfusion. In the presence of superoxide dismutase (20 U/ml), NO release (oxyhemoglobin technique) was completely normalized, indicating inactivation of NO by superoxide radicals. Treatment with glyceryl trinitrate (GTN; 30 microM) prevented ischemia-induced myocardial tissue injury. SIN-1 (0.3 microM) was ineffective. These data demonstrate a protective effect of GTN but not SIN-1 in myocardial ischemia. It is concluded that the site of NO generation may play an important role in determining the biological activity of NO donating substances.

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