[The relationship between the activity of phospholipase A2 and acute hypoxic pulmonary arterial pressure].
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.
Li
H P
HP
Department of Respiratory Internal Medicine, Affiliated Hospital of Guangdong Medical College, Zhanjiang.
He
J L
JL
Quan
C J
CJ
Ding
J S
JS
D000818:Animals; D015232:Dinoprostone / Q000097:blood; D005260:Female; D006976:Hypertension, Pulmonary / Q000201:enzymology* / Q000209:etiology / Q000378:metabolism; D000860:Hypoxia / Q000150:complications / Q000503:physiopathology; D008297:Male; D010741:Phospholipases A / Q000378:metabolism*; D054467:Phospholipases A2; D010972:Platelet Activating Factor / Q000378:metabolism; D011897:Random Allocation; D051381:Rats; D017207:Rats, Sprague-Dawley; D013929:Thromboxane B2 / Q000097:blood
D010972:Platelet Activating Factor; D013929:Thromboxane B2; D010741:Phospholipases A; D054467:Phospholipases A2; D015232:Dinoprostone