T Tsunoda1, K Ohnishi, H Tanaka. 1. First Department of Medicine, Chiba University School of Medicine, Japan.
Abstract
UNLABELLED: Changes of portal, superior mesenteric, and splenic venous flows, and portohepatic gradient (portal vein pressure minus free hepatic vein pressure) after a meal were studied in patients with cirrhosis using the duplex ultrasonic Doppler flowmeter, and portal and hepatic vein catheterizations after ingestion of 227 ml of 33% glucose solution (300 kcal). As a control, changes of portal venous flow and portohepatic gradient after drinking 227 ml of water, were studied. Portal and superior mesenteric venous flows increased significantly at 30 min after glucose intake, and they returned gradually to the basal values, whereas no significant postprandial change occurred in splenic venous flow. The sum of superior mesenteric and splenic venous flows was greater than the estimated portal venous flow before glucose intake, and the difference widened during post-prandial mesenteric hyperemia, indicating an increase of blood flow into the portal-systemic shunts. After glucose intake, portohepatic gradient elevated immediately, in parallel with an increase of portal venous flow, and these changes persisted for the 30 min studied; however, no significant change occurred in these parameters after drinking water. IN CONCLUSION: 1) In patients with cirrhosis, hyperemia occurs in the intestine but not in the spleen after glucose intake, and 2) postprandial mesenteric hyperemia causes an increase of portal venous inflow, portal-systemic collateral flow, portal venous flow, and an elevation of portohepatic gradient.
UNLABELLED: Changes of portal, superior mesenteric, and splenic venous flows, and portohepatic gradient (portal vein pressure minus free hepatic vein pressure) after a meal were studied in patients with cirrhosis using the duplex ultrasonic Doppler flowmeter, and portal and hepatic vein catheterizations after ingestion of 227 ml of 33% glucose solution (300 kcal). As a control, changes of portal venous flow and portohepatic gradient after drinking 227 ml of water, were studied. Portal and superior mesenteric venous flows increased significantly at 30 min after glucose intake, and they returned gradually to the basal values, whereas no significant postprandial change occurred in splenic venous flow. The sum of superior mesenteric and splenic venous flows was greater than the estimated portal venous flow before glucose intake, and the difference widened during post-prandial mesenteric hyperemia, indicating an increase of blood flow into the portal-systemic shunts. After glucose intake, portohepatic gradient elevated immediately, in parallel with an increase of portal venous flow, and these changes persisted for the 30 min studied; however, no significant change occurred in these parameters after drinking water. IN CONCLUSION: 1) In patients with cirrhosis, hyperemia occurs in the intestine but not in the spleen after glucose intake, and 2) postprandial mesenteric hyperemia causes an increase of portal venous inflow, portal-systemic collateral flow, portal venous flow, and an elevation of portohepatic gradient.