Basic Research
Copyright ©2006 Baishideng Publishing Group Co., Limited. All rights reserved.
World J Gastroenterol. May 7, 2006; 12(17): 2737-2741
Published online May 7, 2006. doi: 10.3748/wjg.v12.i17.2737
Splenic vasculopathy in portal hypertension patients
Tao Li, Ji-Yuan Ni, Yan-Wu Qi, Hai-Yang Li, Tong Zhang, Zhen Yang
Tao Li, Ji-Yuan Ni, Yan-Wu Qi, Hai-Yang Li, Tong Zhang, Zhen Yang, Department of Hepatic Surgery, Tongji Hospital, Tongji medical College, Huazhong University of Science and Technology, Wuhan 430030, Hubei province, China
Supported by National Natural Science Foundation of China, No. A30170920
Correspondence to: Zhen Yang, Department of Hepatic Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, 13 Hangkong Road, Wuhan 430030, Hubei province, China. litaoforgood@tom.com
Telephone: +86-27-83663502 Fax: +86-27-83622624
Received: September 14, 2005
Revised: October 1, 2005
Accepted: October 26, 2005
Published online: May 7, 2006
Abstract

AIM: To investigate the interaction between portal hypertension, splanchnic hyperdynamic circulation and splanchnic vasculopathy by observing splenic arterial and venous pathological changes and the ro1e of extra-cellular matrix in the pathogenesis of portal hypertensive vasculopathy by measuring the expression of type Ι and type III procollagen mRNA in splenic venous walls of portal hypertensive patients.

METHODS: Morphological changes of splenic arteries and veins taken from portal hypertensive patients (n = 20) and normal controls (n = 10) were observed under optical and electron microscope. Total RNA was extracted and the expression of type Ι and type III procollagen mRNA in splenic venous walls of portal hypertensive patients (n = 20) was semi-quantitatively detected using reverse transcription-polymerase chain reaction (RT-PCR).

RESULTS: Under optical microscope, splenic arterial intima was destroyed and internal elastic membrane and medial elastic fibers of the splenic arterial walls were degenerated and broken. Splenic venous intima became remarkably thick. Endothelia1 cells were not intact with formation of mural thrombus. The tunica media became thickened significantly due to hypertrophy of smooth muscles. Fibers and connective tissues were increased obviously. Under electron microscope, smooth muscle cells of the splenic arteries were degenerated and necrotized. Phenotypes of smooth muscle cells changed from constrictive into synthetic type. Red blood cells and platelets accumulated around the damaged endothelial cells. Synthetic smooth muscle cells were predominant in splenic veins and their cytoplasma had plentiful rough endoplasmic reticulum ribosomes and Golgi bodies. Along the vascular wall, a lot of collagen fibers were deposited, the intima was damaged and blood components accumulated. There was no significant difference in the expression of type I procollagen mRNA in splenic venous wall between the patients with portal hypertension and those without portal hypertension (P > 0.05), but the expression of type III procoagen mRNA was significantly stronger in the patients with portal hypertension than in those without portal hypertension (P < 0.01).

CONCLUSION: Type III procollagen and collagen might be important extra-cellular matrix resulting in neointimal formation and vascular remodeling in the pathogenesis of portal hypertensive vasculopathy. The pathological changes in splenic arteries and veins exist in portal hypertension patients. There might be an interaction between portal hypertension, splanchnic hyperdynamic circulation and splanchnic vasculopathy.

Keywords: Portal hypertension; Splanchnic hyperdy-namic circulation; Splanchnic vasculopathy