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Visualization and Analysis of Blood Flow and Oxygen Consumption in Hepatic Microcirculation: Application to an Acute Hepatitis Model
Published on: August 4, 2012
Hepatic artery hemodynamics in acute viral hepatitis
1Department of Pathophysiology, University of Medicine and Pharmacy, Iaşi, Romania.
In order to evaluate the effect of the acute viral hepatitis on arterial blood flow we performed duplex Doppler US on 30 patients with acute viral hepatitis (AVH) and compared the results with those obtained on 20 normal volunteers. Hepatic artery flow (HAF) was significantly increased with the patients suffering from acute viral hepatitis. The data obtained show that the increase of arterial blood flow is not always associated with the increase of arterial velocities. We could put in evidence the presence of the hepatic artery response to altered portal blood flow (arterial buffer) during a AVH. If the increase of HAF is absolutely necessary for recovery from hepatitis, excessive increase of HAF seems to increase the time of recovery. In our study, the evolution of acute viral hepatitis was good when the HAF values did not exceed 65% of liver supply. The increase of arterial blood flow over 65% seems to limit the portal supply of the liver and in this way the amounts of regenerating substances which bathe the liver cells. The HAF value plays an important role in acute viral hepatitis evolution, so that the exploration of HAF and hepatic artery velocities may be a reliable examination in order to monitor the evolution of this disease.
In order to evaluate the effect of the acute viral hepatitis on arterial blood flow we performed duplex Doppler US on 30 patients with acute viral hepatitis (AVH) and compared the results with those obtained on 20 normal volunteers. Hepatic artery flow (HAF) was significantly increased with the patients suffering from acute viral hepatitis. The data obtained show that the increase of arterial blood flow is not always associated with the increase of arterial velocities. We could put in evidence the presence of the hepatic artery response to altered portal blood flow (arterial buffer) during a AVH. If the increase of HAF is absolutely necessary for recovery from hepatitis, excessive increase of HAF seems to increase the time of recovery. In our study, the evolution of acute viral hepatitis was good when the HAF values did not exceed 65% of liver supply. The increase of arterial blood flow over 65% seems to limit the portal supply of the liver and in this way the amounts of regenerating substances which bathe the liver cells. The HAF value plays an important role in acute viral hepatitis evolution, so that the exploration of HAF and hepatic artery velocities may be a reliable examination in order to monitor the evolution of this disease.
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