Vadas P, Hay J B
Can J Physiol Pharmacol. 1983 Jun;61(6):561-6. doi: 10.1139/y83-086.
This study examined the role of plasma phospholipase A2 (PLA2) in the mediation of the hypotension associated with experimental endotoxin shock in rabbits. Endotoxin shock was induced in rabbits, and mean arterial blood pressure and plasma PLA2 levels were monitored. Serial plasma PLA2 determinations over 5 h showed an 11-fold increase in circulating enzyme activity, and the rise in circulating enzyme activity was directly related to the fall in mean arterial blood pressure. Pretreatment of rabbits with glucocorticoids abrogated the hypotensive effect of endotoxin, and also inhibited a rise in plasma PLA2 activity. To determine if the rise in PLA2 activity was simply a mechanistically unrelated epiphenomenon, the effect of infusion of exogenous PLA2 (purified from the blood of rabbits in endotoxin shock) was investigated. Infusion of the exogenous enzyme into normal rabbits caused a fall in mean arterial blood pressure, and the rate of fall of blood pressure paralleled that induced by endotoxin itself. Treatment of the PLA2-active fraction, prior to infusion with the PLA2 inhibitor, p-bromophenacyl bromide, protected against this hypotensive effect. These data are consistent with the postulate that the endotoxin-induced release of massive amounts of PLA2 into the systemic circulation in rabbits contributes significantly to the hypotension associated with septic shock.
本研究探讨了血浆磷脂酶A2（PLA2）在介导兔实验性内毒素休克相关低血压中的作用。对兔诱导内毒素休克，并监测平均动脉血压和血浆PLA2水平。在5小时内连续测定血浆PLA2显示循环酶活性增加了11倍，且循环酶活性的升高与平均动脉血压的下降直接相关。用糖皮质激素预处理兔可消除内毒素的降压作用，同时也抑制血浆PLA2活性的升高。为了确定PLA2活性的升高是否仅仅是一种与机制无关的附带现象，研究了输注外源性PLA2（从内毒素休克兔血液中纯化）的作用。向正常兔输注外源性酶导致平均动脉血压下降，且血压下降速率与内毒素本身诱导的速率平行。在输注PLA2抑制剂对溴苯甲酰溴之前，对PLA2活性部分进行处理可预防这种降压作用。这些数据与以下假设一致，即内毒素诱导大量PLA2释放到兔的体循环中，对脓毒症休克相关的低血压有显著影响。
