Ethanol-induced increase in portal hepatic blood flow: Interference by anesthetic agents

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Abstract
While a number of studies show that acute oral administration of ethanol results in increases in liver blood flow, a large body of evidence has also been presented in which such an effect is not observed. To shed light on this discrepancy, we have studied in rats, a number of variables that might modulate or inhibit the effect of ethanol. These included the use of three anesthetic agents studied at two different times after anesthetic administration and the effect of animal age, gender, batches and seasonal variation. Portal blood flows were determined by the radiolabeled microsphere method in 12 separate experiments in awake rats. Ethanol given at doses ranging from 0.5 to 4.0 gm per kg consistently increased portal vein blood flow by approximately 50% (42.2 ± 3.5 to 63.4 ± 6.5 ml per min per kg). The interexperiment variation was 2.4 to 3.0%, showing remarkable consistency, typical of an all-or-none effect at the doses employed. On the other hand, the ethanol-induced increase in portal blood flow was completely suppressed by ketamine (75 mg per kg), thiopental (50 mg per kg) and fentanyl (15 μg per kg) when given 15 min prior to blood flow determinations. This suppression was dependent on the dose and duration of anesthesia. These anesthetic agents had no effect on basal hepatic arterial or portal blood flows. Ethanol or the anesthetics were without effects on hepatic artery blood flow. Neither gender, weight (150 to 350 gm) nor animal batch had effect on the response to ethanol. Similarly, there was no effect of seasonal variation. The increase in portal vein blood flow following a dose of 2 gm per kg of ethanol disappeared only after 6 hr when blood levels of ethanol had decreased to concentrations below 3 mM. The consistency, under nonpathological conditions, of an increase in portal blood flow by ethanol is of interest because, as ethanol also increases liver oxygen consumption, an increment in oxygen delivery induced by ethanol could play a compensatory role preventing the occurrence of hypoxic liver damage.
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