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心房利钠因子可保护离体工作的缺血大鼠心脏免受血管紧张素II的作用。

Atrial natriuretic factor protects the isolated working ischaemic rat heart against the action of angiotensin II.

作者信息

Linz W, Schölkens B A, Albus U, Petry P, Breipohl G, Knolle J

机构信息

Hoechst AG, Frankfurt/Main, Federal Republic of Germany.

出版信息

J Hypertens Suppl. 1988 Dec;6(4):S339-41. doi: 10.1097/00004872-198812040-00105.

DOI:10.1097/00004872-198812040-00105
PMID:2977176
Abstract

The interaction between atrial natriuretic factor [synthetic human ANF-(103-126)] and angiotensin II (Ang II) and its influence on reperfusion arrhythmias, cardiodynamics, enzyme loss and metabolic changes were investigated in isolated ischaemic working rat hearts. Acute regional myocardial ischaemia was induced by coronary artery occlusion which was associated with ventricular fibrillation. Perfusion with 1 X 10(-9) mol/l Ang II markedly aggravated these arrhythmias. Perfusion with 1 X 10(-7) mol/l ANF, in contrast, gave protection against ventricular fibrillation and prevented Ang II-induced aggravation of ventricular fibrillation. Atrial natriuretic factor improved cardiodynamics, in particular, during reperfusion, whereas Ang II impaired cardiodynamics and increased the release of creatine kinase and lactate dehydrogenase. These adverse effects of Ang II were absent when ANF was simultaneously perfused. Compared with control hearts, myocardial tissue levels of glycogen, ATP and creatine phosphate were increased in hearts perfused with either ANF or ANF plus Ang II, whereas lactate levels decreased. Perfusion with Ang II alone led to deterioration in these metabolic parameters. These results in isolated working rat hearts suggest that ANF protects against the consequences of ischaemia and reperfusion and that functional antagonism between ANF and Ang II may contribute to this.

摘要

在离体缺血工作大鼠心脏中,研究了心房利钠因子[合成人ANF-(103-126)]与血管紧张素II(Ang II)之间的相互作用及其对再灌注心律失常、心脏动力学、酶损失和代谢变化的影响。冠状动脉闭塞诱导急性局部心肌缺血,其与心室颤动相关。用1×10(-9)mol/l Ang II灌注显著加重了这些心律失常。相反,用1×10(-7)mol/l ANF灌注可预防心室颤动,并防止Ang II诱导的心室颤动加重。心房利钠因子改善了心脏动力学,特别是在再灌注期间,而Ang II损害了心脏动力学并增加了肌酸激酶和乳酸脱氢酶的释放。当同时灌注ANF时,Ang II的这些不良反应消失。与对照心脏相比,用ANF或ANF加Ang II灌注的心脏中,心肌组织中的糖原、ATP和磷酸肌酸水平升高,而乳酸水平降低。单独用Ang II灌注导致这些代谢参数恶化。这些在离体工作大鼠心脏中的结果表明,ANF可预防缺血和再灌注的后果,并且ANF与Ang II之间的功能拮抗作用可能对此有贡献。

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