[The effect of glucagon on portal hemodynamics in patients with liver cirrhosis].
J Cervinka, M Kaláb, J Jedlicka, J Petrtýl, Z Mareček
Abstract
J Cervinka, M Kaláb, J Jedlicka, J Petrtýl, Z Mareček
Abstract
The authors assessed in 12 patients with compensated cirrhosis of the liver, portal hypertension and oesophageal varices, using a Doppler flowmeter Toshiba SAL 50A/SDL 01 under basal conditions, changes in the width, rate of blood flow and blood flow though the trunk of the portal vein before and after intravenous administration of 1 mg glucagon. The width of the trunk of the portal vein did not change significantly during assessment. A statistically significantly increased flow through the portal vein was recorded starting during the 5th minute, and it correlated with the increased velocity of the blood flow. The increased flow persisted to the 20th minute after glucagon administration. The drop of pressure in a wedged position assessed in the hepatic veins after administration of the drug was not significant, the pressure in the free hepatic vein increased insignificantly. On the whole the portohepatic gradient declined by 10.5%, the drop was not significant. Glucagon in pharmacological doses has an early onset of action even in cirrhotic subjects whereby the increased flow through the portal vein does not lead to a rise of the portohepatic gradient. Glucagon administration thus does not increase the risk of haemorrhage from oesophageal varices during acute fibroscopy of the oesophagus and stomach in patients with portal hypertension.
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The authors assessed in 12 patients with compensated cirrhosis of the liver, portal hypertension and oesophageal varices, using a Doppler flowmeter Toshiba SAL 50A/SDL 01 under basal conditions, changes in the width, rate of blood flow and blood flow though the trunk of the portal vein before and after intravenous administration of 1 mg glucagon. The width of the trunk of the portal vein did not change significantly during assessment. A statistically significantly increased flow through the portal vein was recorded starting during the 5th minute, and it correlated with the increased velocity of the blood flow. The increased flow persisted to the 20th minute after glucagon administration. The drop of pressure in a wedged position assessed in the hepatic veins after administration of the drug was not significant, the pressure in the free hepatic vein increased insignificantly. On the whole the portohepatic gradient declined by 10.5%, the drop was not significant. Glucagon in pharmacological doses has an early onset of action even in cirrhotic subjects whereby the increased flow through the portal vein does not lead to a rise of the portohepatic gradient. Glucagon administration thus does not increase the risk of haemorrhage from oesophageal varices during acute fibroscopy of the oesophagus and stomach in patients with portal hypertension.
Key concepts: Medicine, Cirrhosis, Portal venous pressure, Glucagon, Portal hypertension, Blood flow, Internal medicine, Hemodynamics