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去纤苷对猫急性心肌缺血的心脏保护作用。

Cardioprotective effects of defibrotide in acute myocardial ischemia in the cat.

作者信息

Niada R, Porta R, Pescador R, Mantovani M, Prino G

出版信息

Thromb Res. 1985 Apr 1;38(1):71-81. doi: 10.1016/0049-3848(85)90008-8.

Abstract

We investigated the effects of Defibrotide (D), a natural polydeoxyribonucleotide, on acute myocardial ischemia (AMI) in anesthetized cats. A permanent ligature was placed around the left anterior descending coronary artery (LAD) 12-14 mm from its origin. Ventricular fibrillation and death were exceptional and when they occurred the cats were not included in the evaluation. Pretreatment of cats with D, 32 mg Kg-1 h-1, i.v. infusion, maintained throughout the 5 h occlusion period, reduced AMI-ST segment increases and increased the diminished pressure-rate index (PRI). AMI-induced changes in lactate, ATP and CPK in ischemic tissue were prevented by D. PGI2 gave the same results as D. Atenolol prevented the loss of myocardial CPK, but had no favourable effects on lactate and ATP in ischemic tissue. The beneficial effects of D in AMI reported here could be partly attributed to its ability to enhance PGI2 release from vascular walls; D might also relieve ischemia by improvement of local tissue oxygenation, energy supplies and platelet function by its ability to deaggregate platelet clumps.

摘要

我们研究了天然多脱氧核糖核苷酸去纤苷(D)对麻醉猫急性心肌缺血(AMI)的影响。在距左冠状动脉前降支(LAD)起始处12 - 14毫米处进行永久性结扎。室颤和死亡情况罕见,一旦发生,这些猫不纳入评估。以32毫克/千克·小时的剂量静脉输注D对猫进行预处理,在整个5小时的闭塞期持续给药,可减少AMI - ST段升高,并增加降低的压力 - 心率指数(PRI)。D可预防缺血组织中AMI诱导的乳酸、ATP和肌酸磷酸激酶(CPK)的变化。前列环素(PGI2)产生与D相同的结果。阿替洛尔可防止心肌CPK的丢失,但对缺血组织中的乳酸和ATP没有有益作用。本文报道的D对AMI的有益作用可能部分归因于其增强血管壁释放PGI2的能力;D还可能通过改善局部组织氧合、能量供应以及通过其解聚血小板团块的能力改善血小板功能来缓解缺血。

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