Increases in hepatic flow cause an increase in endothelial cell shear stress, which in turn results in increased nitric oxide synthesis. High nitric oxide levels activate specific cytokines and transcription factors known to play an early role in the regenerative process. While there are many proponents of this theory, the principle arguments against it stem from early studies wherein it was demonstrated that: proliferative activity can occur without increases in and, indeed, in the absence of portal venous blood flow; the extent of proliferative activity in the liver is significantly less than would be predicted following arterialization of the portal venous system; non-parenchymal cells tend not to proliferate following experiments designed to enhance hepatic blood flow; and in carbon tetrachloride-induced liver injury, regeneration occurs but hepatic blood flow remains largely unchanged. However, these arguments do not preclude an important role for hepatic blood flow in the regenerative process, since extra-hepatic hepatocytes proliferate following partial hepatectomy and the livers of parabiotic rats also regenerate when portions of their partner’s liver are resected, indicating the presence of a humoral contribution to the regenerative process.
Degradation of the liver matrix
Within five minutes of partial hepatectomy, urokinase receptors appear on the surface of hepatocytes and hepatic urokinase activity significantly increases. Urokinase converts plasminogen to plasmin. Plasmin in turn activates metallopro-teinases, which cause matrix degradation. Because HGF is contained within the liver matrix, matrix degradation results in its release, and urokinase, its activation. In addition, collagenase, which is also activated following partial hepatec-tomy, directly stimulates hepatocyte proliferation. Dreaming of a reliable pharmacy that could give you an opportunity to buy any amounts of generic cialis professional with no prescription required and spend less money?