磷脂酶A2活力与急性缺氧性肺动脉高压关系的探讨

通过动物实验探讨磷脂酶Ａ２及相关炎性介质在急性缺氧性肺动脉高压形成中的作用。３０只ＳＤ大鼠随机分为三组；正常对照组，缺氧组及缺氧加地塞米松组。均测定肺动脉压；缺氧３０ｍｉｎ后，取静脉血肺组织测定ＰＬＡ２活力，血小板活化因子，前列腺素Ｅ２，血栓素Ｂ２。

THE RELATIONSHIP BETWEEN THE ACTIVITY OF PHOSPHOLIPASE A_2 AND ACUTE HYPOXIC PULMONARY ARTERIAL PRESSURE

The action of phospholipase A2 (PLA2) and related inflammatory mediators on the fonnation of hypoxic pulmonary arterial hgnrtension was studied- 30 Sprague-Dawley rats were equally divided into three groups at random: normal control group, hypoic group and the group pretreated with dexamethasone plus hypoxia. The pulmonary arterial pressure (PAP) was measured by inserting a microcatheter into the pulmonary artery.Afer 30 min of hypoxia, the ctivity of PLA2, platelet achvating factor (PAF),prostaglandin E2 (PGE2) and thromboxane B2 (TXB2) were measured in blood and lung tissue, and it was found that the mean pulmonary arterial pressure (mPAP), the PLA2activity, PGE2 , TXB2 and PAF in blood and lung tissue were sighficanily increased; but pretreatment with dexamethasone relieved the changes mentioned above. In hypoxia, a positive correlations was found between the PLA2 activity and mPAP, PAF, PGE2, TXB2 respectively; positive correlations were also found between PAF, PGE2, TXB2 and mPAP. In conclusion, PLA2 induced the release of inflanunation mediators, Which may play roles in the formation of the acute hrpokie pulmonary arterial hypertension .