SummaryWe have studied the production of tissue-type plasminogen activator (t-PA) and type-1 plasminogen activator inhibitor (PAI-1) in liver of normal rats and in rats with mild cirrhosis induced by carbon tetrachloride inhalation, to demonstrate the production of these fibrinolytic components and their pathophysiologic role in the liver in vivo. Immunohistochemical study of paraffin-embedded liver sections and fibrin autography of frozen sections showed that the normal rat liver produces very little t-PA or PAI-1. On the contrary, striking t-PA activity and both t-PA and PAI-1 antigens were observed in the cirrhotic liver. Both t-PA and PAI-1 in plasma were also markedly increased in the cirrhotic rats. Because the hepatocyte can internalize t-PA or PA/PAI-1 complexes from circulation, Northern blot analysis of the total liver RNA was performed to demonstrate the endogenous synthesis of t-PA and PAI-1 in the liver. Although the normal liver hardly expresses either t-PA or PAI-1 mRNA, striking t-PA and PAI-1 mRNA expression was observed in the liver of rats with mild cirrhosis.These data demonstrate that t-PA and PAI-1 production is strongly upregulated in the liver in rats with mild cirrhosis. These fibrinolytic components, whose production is closely associated with liver failure, may play important roles in the regulation of hepatocyte proliferation and liver regeneration in vivo.
Four cases of enormous shunt between portal and hepatic veins (portal-hepatic venous shunt) are reported with special reference to sonographic and portographic findings. Ultrasonography, an examination for screening, delineated a snail-like anechoic area in the liver, its connection with the portal and hepatic veins, and marked dilatation of the veins connecting with the shunt. Transarterial or percutaneous transhepatic portography, a method for definitive diagnosis, demonstrated large pooling of the contrast medium flowing from the dilated portal branch and subsequent visualization of the hepatic vein. The etiology and prognosis are unknown at present. The most likely pathogenesis for this shunt seemed to be a congenital anomaly, namely, persistence of the omphalomesenteric venous system. With recent advances in and the more frequent use of real-time ultrasonography, detection of this kind of vascular abnormality will doubtless increase.
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