Qhep and its distribution between Qha and Qpv is determined by the hepatic arterial resistance, the intra- and prehepatic portal resistance, and Qpv. Qpv is not intrinsically regulated per se. The portal venous resistance Rpv is low since about 25 per cent of cardiac output passes through a pressure gradient of 4 to 5 mmHg between the portal and hepatic veins. This low resistance is also about a tenth of the resistance through the splanchnic organs. Qpv depends on the outflow of the extrahepatic splanchnic organs and not of the liver itself ( ,RlC,h§rdSg.D..,.19.8.2). Finally, Qpv is not autoregulated (i.e. the relationship between pressure and flow is linear, and reactive hyperemia is absent). The principal intrinsically regulated variable is portal venous pressure ( Richards.o.n 1982), with Rpv modifying flow to maintain a relatively constant Ppv. Ppv depends primarily on the degree of constriction or dilatation of the mesenteric and splanchnic arterioles and on intrahepatic resistance. During low Qpv states, high Rpv tends to maintain Ppv relatively constant whereas, in the presence of a high Qpv, a decrease in Rpv would prevent the deleterious effect of an increase in Ppv on mesenteric venous drainage.
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