Penicillar arterioles of red pulp in residual spleen after subtotal splenectomy due to splenomegaly in cirrhotic patients: a comparative study.

BACKGROUND Following splenomegaly due to portal hypertension, pathologic characteristics include passive congestion and lymphoplasia. High venous pressure and hemodynamics can result in vascular proliferation and lymphoplasia, and promote splenic microcirculation and functional changes. The aim of this study was to determine the changes in penicillar arterioles (PAs) of red pulp in residual splenic tissue after subtotal splenectomy due to splenomegaly in cirrhotic patients to provide anatomic and physiologic evidence for reserved splenic surgery. METHODS Thirteen patients with splenomegaly due to portal hypertension, who were treated surgically, comprised the splenomegaly group. After 8 years, we obtained another specimen by puncture biopsy from the residual spleen group. We designated patients with splenic trauma as the control group. The morphology of PAs under light microscopy was facilitated by EVG staining and immunohistochemistry for CD34. Semi-thin sections were HE-stained. The ultrastructure of PA endothelial cells was observed under electron microscopy. RESULTS In the residual spleen group, diffuse distribution, tenuous elastic intima in the arterial wall, and continuity in PA of red pulp were seen under light microscopy. A significantly lower density and average cross-sectional area of PAs were observed in the residual spleen group compared with the splenomegaly and control groups (P < 0.01). A uniform mitochondrial matrix and a decreased number of ruptured cristae in PA endothelial cells were observed under electron microscopy. While there were some beneficial changes (splenic artery flow volume, portal venous diameter, and portal venous flow volume), the platelet and leucocyte counts were markedly increased in residual spleen. CONCLUSION Subtotal splenectomy can eliminate the factors which precipitate splenomegaly (portal hypertension), improve the reconstruction of splenic capillaries, correct hypersplenism, and restore normal splenic function.