Leprán I, Lefer A M
Basic Res Cardiol. 1985 Mar-Apr;80(2):135-41. doi: 10.1007/BF01910460.
The effect of platelet-activating factor (PAF) was studied during the acute phase of myocardial ischemia in cats. PAF infusion (0.75 micrograms/kg/h for 4.5h) in anesthetized, open-chest cat decreased arterial blood pressure, but did not influence heart rate or biochemical indices of cell integrity. The same dose of PAF, however, started 30 min after coronary ligation, resulted in a significantly higher elevation of plasma creatine phosphokinase (CK) activity and a reduced CK content in the region of the ischemic myocardium. Treatment with the thromboxane A2 synthetase inhibitor, CGS-13080, significantly attenuated the PAF-aggravated ischemic cellular damage. These experiments suggest that hypoxia-generated PAF may contribute to the aggravation of myocardial ischemia, part of which appears to be due to PAF-induced release of thromboxane A2.
在猫心肌缺血急性期研究了血小板活化因子(PAF)的作用。在麻醉的开胸猫中输注PAF(0.75微克/千克/小时,持续4.5小时)可降低动脉血压,但不影响心率或细胞完整性的生化指标。然而,在冠状动脉结扎30分钟后给予相同剂量的PAF,可导致血浆肌酸磷酸激酶(CK)活性显著升高,且缺血心肌区域的CK含量降低。用血栓素A2合成酶抑制剂CGS-13080治疗可显著减轻PAF加重的缺血性细胞损伤。这些实验表明,缺氧产生的PAF可能导致心肌缺血加重,部分原因似乎是PAF诱导血栓素A2释放。