Mean blood pressure in the portal vein is approximately 10 mm Hg, and mean blood pressure in the hepatic artery is approximately 90 mm Hg. The resistance of the vessels upstream to the hepatic sinusoid capillaries is considerably greater than that of the downstream vessels. Consequently, the pressure in the sinusoid capillaries is only 2 or 3 mm Hg greater than that in the hepatic veins and inferior vena cava. The ratio of presinusoidal to postsinusoidal resistance is much greater in the liver than in almost any other vascular bed. Hence, drugs and other interventions that alter presinusoidal resistance usually affect pressure in the sinusoid capillaries and fluid exchange across the sinusoidal wall only slightly. However, changes in hepatic and central venous pressure are transmitted almost quantitatively to the hepatic sinusoid capillaries, and they profoundly affect the transsinusoidal exchange of fluids.
Regulation of Flow
Blood flow in the portal venous and hepatic arterial systems varies reciprocally. When blood flow is curtailed in one system, flow increases in the other but does not fully compensate for the decreased flow in the first system.
The portal venous system is not autoregulated. As portal Pv and flow are raised, resistance either remains constant or decreases. The hepatic arterial system is autoregulated, however, and adenosine may be involved in this adjustment of blood flow.
The liver tends to maintain constant O2 consumption because O2 extraction from hepatic blood is very efficient. As the rate of O2 delivery to the liver varies, the liver compensates by an appropriate change in the fraction of O2 extracted from blood. Such extraction is facilitated by the distance between the presinusoidal vessels at the acinar center and the postsinusoidal vessels at the periphery of the acinus (see
Fig. 17.43 ). The substantial distance between these types of vessels prevents countercurrent exchange of O2, in contrast to the countercurrent exchange that occurs in an intestinal villus.
The sympathetic nerves constrict the presinusoidal resistance vessels in the portal venous and hepatic arterial systems. Neural effects on the capacitance vessels are more important, however. The liver contains approximately 15% of the total blood volume of the body. In appropriate conditions, as in response to hemorrhage, approximately half of the hepatic blood volume can be rapidly expelled by constriction of the capacitance vessels (see also ). Hence, the liver is an important blood reservoir in humans.
Whencentralvenouspressureiselevated,asincongestiveheartfailure,largevolumesofplasmawaterdiffusefromtheliverintotheperitonealcavity;thisaccumulationoffluidintheabdomenisknownasascites. Extensivefibrosisoftheliver,asinhepaticcirrhosis,markedlyincreaseshepaticvascularresistanceandtherebyraisespressuresubstantiallyintheportalvenoussystem.Theconsequentincreaseincapillaryhydrostaticpressurethroughthesplanchniccirculationalsoleadstoextensivefluidtransudationintotheabdominalcavity.Thepressuremaylikewiserisesubstantiallyinotherveinsthatanastomosewiththeportalvein.Forexample,theesophagealveinsmayenlargeconsiderablytoformesophagealvarices.Thesevaricesmayruptureandleadtosevere,frequentlyfatalinternalbleeding.TopreventthesegraveproblemsassociatedwithelevatedportalPvincirrhosisoftheliver,ananastomosis(portacavalshunt)isofteninsertedsurgicallybetweentheportalveinandtheinferiorvenacavatolowerportalPv.