The experimental study on pathological changes of pulmonary tissues in portal hypertensive rabbits with schistosomal cirrhosis.
- Author:
Yong-gui ZHOU
1
;
Zhen YANG
;
Dong-jian LI
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Disease Models, Animal; Endothelin-1; metabolism; Hypertension, Pulmonary; etiology; pathology; Liver Cirrhosis, Experimental; complications; Lung; metabolism; pathology; Male; Nitric Oxide Synthase; metabolism; Rabbits; Schistosomiasis; complications
- From: Chinese Journal of Surgery 2005;43(9):587-590
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo investigate the pathologic features of the pulmonary tissue in portal hypertensive rabbits with schistosomal cirrhosis, and to study the role of endothelin-1 (ET-1) and nitric oxide (NO) in pathogenesis of portal hypertensive pulmonary vasculopathy.
METHODSThe experimental group included 10 rabbits infected percutaneously with cercariae of Schistosomiasis Japonica. The control group included 10 normal rabbits. HE stain, Masson trichrome stain and transmission electron microscopy were applied to detect the pathologic features of the pulmonary tissue. The expression and distribution of endothelin-1 (ET-1) and nitric oxide synthase (NOS) in the lung tissues were analyzed by immunohistochemistry.
RESULTSAfter 120 d, the pathological morphology alteration of the pulmonary tissue was observed in the rabbits in experimental group. Both of ET-1 and NOS-containing cells were more abundant in distribution and expression in the lung tissue of experimental group than those of the control group. There was significant difference between the two groups in the parameter of area, lightness and gray level of ET-1 and NOS (P < 0.01).
CONCLUSIONSPulmonary pathologic changes occur in the portal hypertensive rabbits with schistosomal cirrhosis. ET-1 and NOS-containing cells are more abundant in pulmonary vessel of portal hypertension, then followed by dilation of intrapulmonary vessel. It is deduced that ET-1 and NO might play an important role in the pathogenesis of portal hypertensive pulmonary vasculopathy.