Splenic vasculopathy in portal hypertension patients

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 I 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 I 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.

Figure 1

Changes of splenic arteries (A, B) and splenic veins (C, D) in patients with portal hypertension.

Figure 2

Ultrastructure of splenic artery (A, B) and splenic vein (C, D) in patients with portal hypertension.

Figure 3

Observation of splenic vein in patients with traumatic splenic rupture without liver cirrhosis (A), in patients with portal hypertension (B), and in patients with portal hypertension (C) under scanning electron microscope.

Figure 4

Observation of splenic artery in patients with traumatic splenic rupture without liver cirrhosis (A), in patients with portal hypertension (B), and in patients with portal hypertension (C) under scanning electron microscope.

Figure 5

Comparison of the expression intensity of type I (A) and type III (B) procollagen mRNA in splenic vein wall of patients with and without portal hypertension.

Figure 6

Expression of type III procollagen mRNA of splenic vein wall in patients with portal hypertension. Bands 1, 3, 5 and 7: control samples from patients without portal hypertension; Bands 2, 4, 6 and 8: samples from patients with portal hypertension.