Li H P, He J L, Quan C J, Ding J S
Department of Respiratory Internal Medicine, Affiliated Hospital of Guangdong Medical College, Zhanjiang.
Sheng Li Xue Bao. 1997 Dec;49(6):685-9.
The action of phospholipase A2 (PLA2) and related inflammatory mediators on the formation of hypoxic pulmonary arterial hypertension was studied. 30 Sprague-Dawley rats were equally divided into three groups at random: normal control group, hypoxic group and the group pretreated with dexamethasone plus hypoxia. The pulmonary arterial pressure (PAP) was measured by inserting a microcatheter into the pulmonary artery. After 30 min of hypoxia, the activity of PLA2, platelet activating 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 PLA2 activity, PGE2, TXB2 and PAF in blood and lung tissue were significantly 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 inflammation mediators, which may play roles in the formation of the acute hypoxic pulmonary arterial hypertension.
研究了磷脂酶A2（PLA2）及相关炎症介质在缺氧性肺动脉高压形成中的作用。将30只Sprague-Dawley大鼠随机均分为三组：正常对照组、缺氧组和地塞米松预处理加缺氧组。通过将微导管插入肺动脉来测量肺动脉压（PAP）。缺氧30分钟后，检测血液和肺组织中PLA2、血小板活化因子（PAF）、前列腺素E2（PGE2）和血栓素B2（TXB2）的活性，发现血液和肺组织中的平均肺动脉压（mPAP）、PLA2活性、PGE2、TXB2和PAF均显著升高；但地塞米松预处理可缓解上述变化。在缺氧状态下，PLA2活性分别与mPAP、PAF、PGE2、TXB2呈正相关；PAF、PGE2、TXB2与mPAP之间也呈正相关。总之，PLA2诱导炎症介质释放，这可能在急性缺氧性肺动脉高压的形成中起作用。
