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[短暂性缺血作为心肌中调节冠状动脉生成改变建模的一个因素]

[Transient ischemia as a factor in modelling regulated coronarogenic alteration in the myocardium].

作者信息

Gatsura V V, Imatdieva R M

出版信息

Eksp Klin Farmakol. 1994 Nov-Dec;57(6):63-5.

PMID:7756970
Abstract

The purpose of the investigation was to determine the minimal duration of transient ischemia which would produce stable myocardial damage. The compression of the anterior branch of the rat left coronary artery during 5, 10, 15, and 20 minutes was used for this purpose. The sizes of necrotic and ischemic areas in the rat myocardium were determined by the differential indicator method and morphometrically 4 and 72 hours after transient ischemia. It was established that 15-min transient occlusion is the most suitable for the above purpose. The ratio of a necrotic to an ischemic area was almost the same 4 and 72 hours after transient occlusion (45.8 +/- 6.9 and 41.1 +/- 8.6%, respectively). An analysis of cardioprotective cytochrome C activity confirms that there is a phenomenon of injury-slowing interventions in the pharmacology of anti-ischemic compounds.

摘要

该研究的目的是确定可导致稳定心肌损伤的短暂缺血的最短持续时间。为此,采用对大鼠左冠状动脉前支进行5、10、15和20分钟的压迫。通过差异指示剂法并在短暂缺血后4小时和72小时进行形态计量学分析,测定大鼠心肌中坏死区和缺血区的大小。结果表明,15分钟的短暂闭塞最适合上述目的。短暂闭塞后4小时和72小时,坏死区与缺血区的比例几乎相同(分别为45.8±6.9%和41.1±8.6%)。对心脏保护细胞色素C活性的分析证实,在抗缺血化合物药理学中存在损伤减缓干预现象。

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