The mean blood pressure in the portal vein is approximately 10 mm Hg, while the mean blood pressure in the hepatic artery is around 90 mm Hg. The resistance of the vessels upstream to the hepatic sinusoid capillaries is significantly higher than that of the downstream vessels. As a result, the pressure in the sinusoid capillaries is only slightly higher (about 2 or 3 mm Hg) than that in the hepatic veins and inferior vena cava. The liver has a much greater ratio of presinusoidal to postsinusoidal resistance compared to other vascular beds. Therefore, drugs and interventions that alter presinusoidal resistance have minimal impact on pressure in the sinusoid capillaries and fluid exchange across the sinusoidal wall. However, changes in hepatic and central venous pressure are almost fully transmitted to the hepatic sinusoid capillaries, significantly influencing the transsinusoidal exchange of fluids.

In terms of flow regulation, blood flow in the portal venous and hepatic arterial systems have an inverse relationship. When blood flow is reduced 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 does not have autoregulation. When portal venous pressure and flow increase, resistance either remains constant or decreases. On the other hand, the hepatic arterial system is autoregulated, and adenosine may be involved in adjusting blood flow in this system.

The liver maintains a relatively constant oxygen (O2) consumption because it efficiently extracts O2 from hepatic blood. As the rate of O2 delivery to the liver varies, the liver compensates by adjusting the fraction of O2 extracted from the blood. The structure of the liver facilitates O2 extraction, as the presinusoidal vessels at the acinar center and the postsinusoidal vessels at the periphery of the acinus are sufficiently distant to prevent countercurrent exchange of O2, unlike what occurs in an intestinal villus.

The sympathetic nerves constrict the presinusoidal resistance vessels in the portal venous and hepatic arterial systems. However, the neural effects on the capacitance vessels are more significant. The liver contains approximately 15% of the total blood volume in the body. Under appropriate conditions, such as in response to hemorrhage, about half of the hepatic blood volume can be rapidly expelled by constricting the capacitance vessels. This makes the liver an important blood reservoir in humans.

When central venous pressure is elevated, as in congestive heart failure, large amounts of plasma water diffuse from the liver into the peritoneal cavity, leading to the accumulation of fluid in the abdomen known as ascites. Extensive fibrosis of the liver, as seen in hepatic cirrhosis, significantly increases hepatic vascular resistance and raises pressure in the portal venous system. This increase in capillary hydrostatic pressure through the splanchnic circulation results in extensive fluid transudation into the abdominal cavity. The pressure may also rise substantially in other veins that anastomose with the portal vein. For example, the esophageal veins may enlarge considerably to form esophageal varices, which can rupture and cause severe, often fatal internal bleeding. To prevent these serious problems associated with elevated portal pressure in cirrhosis of the liver, a surgical anastomosis (portacaval shunt) is often inserted between the portal vein and the inferior vena cava to lower portal venous pressure.
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.