Pathological morphology alteration of the splanchnic vascular wall in portal hypertensive patients.
- Author:
Zhen YANG
1
;
Li ZHANG
;
Dapeng LI
;
Fazu QIU
Author Information
- Publication Type:Journal Article
- MeSH: Adult; Female; Humans; Hypertension, Portal; metabolism; pathology; Immunohistochemistry; Male; Microscopy, Electron; Muscle, Smooth, Vascular; pathology; ultrastructure; Nitric Oxide Synthase; metabolism; Nitric Oxide Synthase Type II; Splenic Artery; metabolism; pathology; ultrastructure; Splenic Vein; metabolism; pathology; ultrastructure; Veins; metabolism; pathology; ultrastructure
- From: Chinese Medical Journal 2002;115(4):559-562
- CountryChina
- Language:English
-
Abstract:
OBJECTIVETo investigate the pathological morphology alteration of the splanchnic vascular wall in portal hypertensive patients.
METHODSSplenic arteries, veins and gastric coronary veins from portal hypertensive patients (n = 50) were removed during esophagogastric devascularization with splenectomy and were observed under optic and electron microscopes. The expression of iNOS in the splenic artery wall was analysed with immunohistochemistry.
RESULTSThe internal elastic membrane and medial elastic fibers of the splenic artery wall were broken and degenerated. Atrophy, apoptosis and phenotypic changes were seen in smooth muscle cells of splenic arteries. Positive staining for iNOS was seen in the cytoplasm of smooth muscle cells and iNOS activity was elevated compared with the non-cirrhotic patients (P < 0.01). In the splenic and gastric coronary veins of cirrhotic patients, we found proliferative intima, extensive thrombi adhering to the venous wall, mimicked arteriosclerosis plaques accompanied with hypertrophy of smooth muscle cells, and thickened muscle fibers of veins with increase in extracellular matrix.
CONCLUSIONPortal hypertension may be complicated by splanchnic arterial and venous vasculopathy. There may be an interactive relationship among portal hypertension, splanchnic hyperdynamic disturbances and splanchnic vasculopathy in the pathogenesis of portal hypertension.