PURPOSE: The purpose of this study was to investigate hemodynamic changes in the hepatic artery after glucose ingestion. METHODS: We used color Doppler sonography to measure hemodynamic changes in the right hepatic artery and the right portal vein in response to glucose ingestion (225 ml, 300 kcal) in 25 healthy subjects and 25 patients with cirrhosis. RESULTS: In healthy subjects, the peak systolic and end-diastolic velocities in the right hepatic artery decreased (33 +/- 3% and 53 +/- 3%) from baseline velocities measured in the fasting state. The resistance index of the right hepatic artery and the velocity in the right portal vein in these subjects significantly (p < 0.01) increased (14 +/- 2% and 32 +/- 2%) from baseline values after glucose ingestion. Glucose ingestion produced significantly (p < 0.01) smaller changes in cirrhotic patients. The maximum decrease in the peak systolic and end-diastolic velocities in the right hepatic artery were 13 +/- 2% and 25 +/- 3% from baseline velocities, and the maximum increases in the resistance index of the right hepatic artery and the velocity in the right portal vein were 6 +/- 1% and 10 +/- 3% from baseline values. CONCLUSIONS: The decrease in blood flow velocity in the right hepatic artery after glucose ingestion is presumably a homeostatic mechanism to maintain constant hepatic perfusion. This reciprocal response was reduced in cirrhotic patients.
PURPOSE: The purpose of this study was to investigate hemodynamic changes in the hepatic artery after glucose ingestion. METHODS: We used color Doppler sonography to measure hemodynamic changes in the right hepatic artery and the right portal vein in response to glucose ingestion (225 ml, 300 kcal) in 25 healthy subjects and 25 patients with cirrhosis. RESULTS: In healthy subjects, the peak systolic and end-diastolic velocities in the right hepatic artery decreased (33 +/- 3% and 53 +/- 3%) from baseline velocities measured in the fasting state. The resistance index of the right hepatic artery and the velocity in the right portal vein in these subjects significantly (p < 0.01) increased (14 +/- 2% and 32 +/- 2%) from baseline values after glucose ingestion. Glucose ingestion produced significantly (p < 0.01) smaller changes in cirrhotic patients. The maximum decrease in the peak systolic and end-diastolic velocities in the right hepatic artery were 13 +/- 2% and 25 +/- 3% from baseline velocities, and the maximum increases in the resistance index of the right hepatic artery and the velocity in the right portal vein were 6 +/- 1% and 10 +/- 3% from baseline values. CONCLUSIONS: The decrease in blood flow velocity in the right hepatic artery after glucose ingestion is presumably a homeostatic mechanism to maintain constant hepatic perfusion. This reciprocal response was reduced in cirrhotic patients.