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己酮可可碱在急性心肌缺血动物模型中的心脏保护作用。

Cardioprotective actions of pentoxifylline in an animal model of acute myocardial ischaemia.

作者信息

Gallenkämper W, Rücker W, Schrör K

出版信息

Br J Pharmacol. 1984 Apr;81(4):575-81. doi: 10.1111/j.1476-5381.1984.tb16121.x.

Abstract

The action of pentoxifylline on some of the consequences of acute myocardial ischaemia was studied in cats in vivo. Occlusion of the left anterior descending coronary artery (LAD) for 5 h resulted in a significant elevation in the ST-segment of the ECG, a reduction in free platelet count in right atrial blood and a loss of creatine phosphokinase (CK) and cathepsin D activities in homogenates of the severely ischaemic myocardium as compared to non-ischaemic myocardium. Intravenous infusions of pentoxifylline (0.30 mg kg-1 min-1 for 1 h and 0.15 mg kg-1 min-1 for the remainder of the 5 h observation period, starting 0.5 h after LAD occlusion) significantly reduced the loss of enzymes from the ischaemic myocardium, prevented any further increase in the ST-segment and restored the platelet count to its control level. There were no significant changes in plasma immunoreactive 6-oxo-prostaglandin F1 alpha (6-oxo-PGF1 alpha) and thromboxane B2 (TXB2), although a tendency for a reduction in TXB2 levels was observed. Pentoxifylline seems to affect, beneficially, the myocardium in this animal model of acute myocardial ischaemia. The reason for this cardioprotective action remains to be elucidated. It is, however, noteworthy that the overall profile of action of pentoxifylline resembles that of PGI2 administration in this model.

摘要

在猫体内研究了己酮可可碱对急性心肌缺血某些后果的作用。结扎左冠状动脉前降支(LAD)5小时导致心电图ST段显著升高,右心房血中游离血小板计数减少,与非缺血心肌相比,严重缺血心肌匀浆中肌酸磷酸激酶(CK)和组织蛋白酶D活性丧失。静脉输注己酮可可碱(LAD结扎后0.5小时开始,以0.30mg kg-1 min-1输注1小时,在其余5小时观察期内以0.15mg kg-1 min-1输注)显著减少了缺血心肌中酶的丧失,防止ST段进一步升高,并使血小板计数恢复到对照水平。血浆免疫反应性6-氧代前列腺素F1α(6-氧代-PGF1α)和血栓素B2(TXB2)无显著变化,尽管观察到TXB2水平有降低趋势。在这个急性心肌缺血动物模型中,己酮可可碱似乎对心肌有有益影响。这种心脏保护作用的原因尚待阐明。然而,值得注意的是,在这个模型中,己酮可可碱的总体作用模式类似于给予前列环素(PGI2)的作用模式。

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