Contribution of circulating platelet and leukocyte activation to primary pulmonary hypertension in rats.
- Author:
Hong-Qiang WANG
1
;
Xiao-Sheng HU
;
Jia-Wei ZHOU
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Blood Platelets; metabolism; Fibrinogen; metabolism; Hypertension, Pulmonary; blood; chemically induced; Leukocytes; physiology; Male; Monocrotaline; Platelet Aggregation; Platelet Count; Random Allocation; Rats; Rats, Sprague-Dawley
- From: Journal of Zhejiang University. Medical sciences 2008;37(3):250-256
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo evaluate the contribution of platelet and leukocyte activation in pathogenesis primary pulmonary hypertension (PPH).
METHODSPulmonary hypertension was induced by subcutaneous injection of 2% monocrotaline (MCT) in male Prague-Dawley (SD) rats. Blood samples were collected at the third week after MCT injection, and flow cytometry was used to determine the fibrinogen-binding platelet, CD11b expression on leukocyte and platelet-leukocyte aggregation.
RESULTThree weeks after MCT injection, rats exhibited higher right ventricular systolic pressure (RVSP) and mean pulmonary artery pressure(mPAP), as compared with controls. MCT induced vascular remodeling characterized by vascular medial wall thickening in pulmonary muscular arteries. The ratio of platelets fibrinogen binding was increased in rats 3 weeks after MCT injection than that of control group[(4.08 +/-1.59)% compared with (1.45 +/- 0.61)%, P<0.01]. CD11b expression in monocytes and neutrophils, but not in lymphocytes was increased significantly 3 weeks after MCT injection (P <0.01). Platelet-neutrophil aggregations increased in MCT injected rats as compared with controls (P <0.01).
CONCLUSIONRats of PPH model demonstrate enhanced circulating platelet and leukocyte activation, which may contribute to the pathogenesis of PPH.
