Portal Blood Flow in Cirrhosis of the Liver*

Abstract

Summary. Direct measurements of portal flow and pressure in a relatively large number of patients with cirrhosis show a marked reduction in flow associated with a nearly constant plateau of portal pressure. This lack of correlation indicates the complex relationships of resistances in the splanchnic, collateral, and hepatic circuits determining the division of the available splanchnic flow between the portal vein and the collateral pathways. Subtracting the measured portal flow from well-established estimates of total hepatic blood flow in cirrhosis suggests that the hepatic artery contributes more than onehalf of the blood perfusing the cirrhotic liver. There was no instance of retrograde portal flow during the preshunt measurements, although such reversal was frequent after side-to-side portacaval anastomosis. Attempting to explain the plateau of portal pressure in the face of an increasing outflow resistance presumably associated with progress of the disease, we postulate that an augmented inflow resistance to the splanchnic chamber reduces splanchnic flow in cirrhosis. End-to-side portacaval anastomosis did not return normal portal flow, although it decreased pressure to accepted control levels. The assumption is that most of the splanchnic blood was flowing through the shunt, leading to a high splanchnic resistance in the immediate postshunt status. If this resistance was previously elevated, as suggested by the plateau of portal pressure, the mechanism responsible for the elevation was not immediately deactivated after the shunt, and the true effect of the operation upon splanchnic flow may not be measurable at such time.Respiratory oscillations were a significant component of portal flow in cirrhosis before and after portacaval anastomosis, indicating the limitations of any steady state analysis of the circulatory derangement in cirrhosis. IntroductionBeginning with the original observations of Bradley, Ingelfinger, Groff, and Bradley (1), a body of evidence indicates a significant reduction in total hepatic blood flow in patients with cirrhosis of the liver. We have considerably less in-

Effective plasma volume in cirrhosis with ascites. Evidence that a decreased value does not account for renal sodium retention, a spontaneous reduction in glomerular filtration rate (GFR), and a fall in GFR during drug-induced diuresis

“…Hepatic blood flow was not measured in the present study because of poor hepatic extraction of Indocyanine green in patients with severe liver disease. Moreno et al, however, have made direct measurements of portal blood flow in an ascitic and a nonascitic group of patients with cirrhosis (19). Although there was an increase in mean hepatic blood flow in the nonascitic group as compared to the ascitic group (7.4 ±5.3 (SD) ml/min per kg vs. 4.9 ±5.3 (SD) ml/ min per kg) the difference was small when compared to normal (20.9 ±4.1 (SD) ml/min per kg).…”

Paraumbilical collateral veins on MRI as possible protection against portal venous thrombosis in candidates for liver transplantation

“…Although portal hypertension decreases flow to hepatic parenchyma regardless of the character of portosystemic shunting, a PUV allows this shunting to occur through the main PV, rather than away from it, thereby maintaining the volume and velocity of main PV flow, potentially preventing reduced main PV size and reducing the likelihood of main PV thrombosis [27]. In contrast, in the presence of a large splenorenal shunt, a portion of splenic venous blood is diverted into the shunt and subsequently causes a significant reduction of portal venous velocity and flow volume [28][29][30] shunt develops, as in all 3 of 119 patients with PUV who had PV size less than 1 cm or if ascites is present [32], as in 1 of 119 patient with PUV who had non occlusive thrombus in main PV.…”

Effect of Portal Venous Blood Flow Diversion on Portal Pressure

“…Moreno et al (1) and Burchell et al (9) have studied portal and hepatic arterial blood flow at laparotomy for portacaval anastomosis. They demonstrated an elevated setpoint for portal pressure of 40 cm of water since this pressure was found despite wide variation in portal blood flow (10). Attempts to correlate portal or hepatic arterial flow measured before or immediately after portacaval anastomosis with prognosis failed (9).…”

“…An abrupt compensatory increase in hepatic arterial flow has been documented during acute portal flow diversion at the creation of a portacaval anastomosis (7)(8)(9). These facts imply homeostatic activity of the splanchnic vascular system to maintain portal pressure and/or hepatic blood flow when portal blood flow decreases (10)(11)(12). To evaluate the splanchnic hemodynamic response to portal blood flow diversion, we studied the response ofportal pressure to acute incremental diversion of portal venous blood through a temporary extracorporeal umbilical vein to saphenous vein portal-systemic shunt (13).…”