| pubmed-article:7307858 | pubmed:abstractText | Rats develop hyperglucagonemia after end-to-side portacaval shunt and also after splenocaval shunt. In this study, animals with mesocaval shunt were shown not to develop hyperglobulinemia or increased titers of lipopolysaccharide antibodies. It is currently thought that the hyperglobulinemia of cirrhosis results from diversion of immunogens past the liver into the systemic circulation with stimulation of sites of globulin synthesis. Since all procedures result in development of immune complexes in the systemic circulation, an alternative hypothesis was sought. It is proposed that the liver may regulate antibody production by the spleen but that this mechanism only operates if splenic venous blood passes through the liver. Portacaval shunt and splenocaval shunt result in diversion of splenic venous blood past the liver and, consequently, failure of regulation, while after mesocaval shunt, splenic venous blood still enters the liver and thus the regulatory mechanism could operate. | lld:pubmed |
