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现已有大量资料证明在心肌缺血部位释放前列腺素,包括PGE_1、PGE、PGF_(2α),但其生理意义尚不完全清楚。已经证明外源性PGE_1的输入,有降低全身动脉血压,减轻心脏的后负荷,并能减低冠脉阻力,增加冠脉血流量等广泛的血液动力学作用。Riemersma证明了PGE_1能明显地减低异丙肾上腺素引起冠状动脉结扎犬心外膜心电图ST段抬高,并同时降低血浆游离脂肪酸(FFA)的浓度,从而减轻异丙肾上腺素引起的心肌损伤。Ogletr-ee也曾证明PGE_1和PGE_2能阻止心肌缺血时心肌酶的释放,如肌酸磷酸激酶(CPK)和组织蛋白酶等,减少心肌缺血时血浆CPK的浓度,因此很多学者提出PGE_1可能对缺血心肌
There is a lot of data to prove the release of prostaglandins, including PGE_1, PGE and PGF_ (2α) in myocardial ischemia, but its physiological significance is not fully understood. It has been demonstrated that the input of exogenous PGE 1 has a wide range of hemodynamic effects such as lowering systemic arterial pressure, reducing cardiac post-load, reducing coronary resistance and increasing coronary blood flow. Riemersma demonstrated that PGE 1 can significantly reduce isoproterenol-induced ST segment elevation in the epicardial coronary artery ligation dog while reducing the concentration of plasma free fatty acid (FFA), thereby reducing isoproterenol-induced myocardial damage. Ogletr-ee also demonstrated that PGE_1 and PGE_2 can prevent the release of myocardial enzymes during myocardial ischemia, such as creatine phosphokinase (CPK) and cathepsin, to reduce the concentration of plasma CPK during myocardial ischemia, many scholars have suggested that PGE_1 may be Ischemic myocardium