B Shi1, Z Yang. 1. Department of Surgery Tongji Hospital, Tongji Medical University, Wuhan 430030, China.
Abstract
OBJECTIVE: To investigate the vascular lesion and its mechanisms in spleen in patients with portal hypertension. METHODS: 28 specimens of spleen from portal hypertension patients and 10 from normal controls were stained by HE and Masson Trichrome to study their vascular pathological lesions. The proteins of PCNA, and Flt-1 were analyzed by immunohistochemistry. The mRNAs of VEGF and bFGF were also identified with in situ hybridization. RESULTS: Various vascular lesions occurred, such as sclerosis endangitis fibrosis and endothelial cell damage. The proteins of PCNA, and Flt-1 were intensively immunostained in portal hypertension spleens compared with normal controls. The mRNAs of VEGF and bFGF were highly expressed, but weakly in controls. CONCLUSIONS: (1) Vascular lesion of spleen is one part of portal hypertensive vascular lesions. (2) The mechanisms of these lesions are due to the changes of microcirculation and hemodynamics, immune disorders, increasing growth factors such as VEGF, Flt-1 and bFGF both at protein and transcription levels.
OBJECTIVE: To investigate the vascular lesion and its mechanisms in spleen in patients with portal hypertension. METHODS: 28 specimens of spleen from portal hypertensionpatients and 10 from normal controls were stained by HE and Masson Trichrome to study their vascular pathological lesions. The proteins of PCNA, and Flt-1 were analyzed by immunohistochemistry. The mRNAs of VEGF and bFGF were also identified with in situ hybridization. RESULTS: Various vascular lesions occurred, such as sclerosis endangitis fibrosis and endothelial cell damage. The proteins of PCNA, and Flt-1 were intensively immunostained in portal hypertension spleens compared with normal controls. The mRNAs of VEGF and bFGF were highly expressed, but weakly in controls. CONCLUSIONS: (1) Vascular lesion of spleen is one part of portal hypertensive vascular lesions. (2) The mechanisms of these lesions are due to the changes of microcirculation and hemodynamics, immune disorders, increasing growth factors such as VEGF, Flt-1 and bFGF both at protein and transcription levels.