The Effect of Ethanol Upon Systemic and Hepatic Blood Flow in Man

Stein, Samuel W.; Lieber, Charles S.; Leevy, Carroll M.; Cherrick, Gilbert R.; Abelmann, Walter H.

doi:10.1093/ajcn/13.2.68

Cited by 93 publications

(14 citation statements)

References 13 publications

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“…The present study first demonstrates that intragastric wine increases hepatic blood flow in conscious dogs and confirms the previous reports [1][2][3][4][5] where intravenous or intragas- trie ethanol increased hepatic blood flow. The peak blood ethanol levels were similar among intravenous ethanol (0.8 g/kg).…”

Section: Discussionsupporting

confidence: 92%

Effects of Ethanol and Wine on Hepatic Arterial and Portal Venous Flows in Conscious Dogs

Kogire¹,

Inoue²,

Sumi³

et al. 1992

Digestion

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The effects of ethanol and wine on hepatic arterial and portal venous flows were examined in conscious dogs. Ethanol was given intravenously or intragastrically, and red wine (ethanol: 14%) was given intragastrically over 30 min. Intravenous ethanol (0.8 g/kg) and intragastric ethanol (14% vol/vol) increased hepatic arterial flow, which remained elevated for 60 min after the cessation of ethanol administration. Ethanol also increased portal venous flow. Portal venous flow returned gradually toward basal levels after the cessation of intravenous ethanol infusion, whereas it remained elevated even after the cessation of intragastric ethanol. Intragastric wine increased hepatic arterial and portal venous flows. In contrast to intragastric ethanol, hepatic arterial flow continued to rise after the cessation of intragastric wine infusion, while portal venous flow returned toward basal levels. We conclude that, though both ethanol and wine increase hepatic blood flow, the responses of hepatic arterial and portal venous flows differ substantially among intravenous ethanol, intragastric ethanol and intragastric wine.

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Section: Discussionsupporting

confidence: 92%

Effects of Ethanol and Wine on Hepatic Arterial and Portal Venous Flows in Conscious Dogs

Kogire¹,

Inoue²,

Sumi³

et al. 1992

Digestion

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“…There has been controversy concerning the action of ethanol on splanchnic blood flow with some showing no effect (44)(45)(46) or even a decrease (47), whereas most studies reported an increase (6,(14)(15)(16)(17)(18)(19)(20). In general, unchanged or decreased flow was observed with low blood ethanol levels.…”

Section: Discussionmentioning

confidence: 99%

“…Under those conditions, a hyperadrenergic state (13) may contribute to the "hypermetabolic" state and increased oxygen utilization. Whether the latter occurs only in the withdrawal state or whether it also happens in the presence of alcohol was not clearly established, particularly since the ethanol-induced increase in oxygen consumption might be offset by an associated increase in splanchnic blood flow (6,(14)(15)(16)(17)(18)(19)(20). The present investigation was undertaken to address these various questions, particularly the issue whether decreased oxygen availability plays a significant role in alcoholinduced liver injury.…”

Section: Introductionmentioning

confidence: 98%

Impaired oxygen utilization. A new mechanism for the hepatotoxicity of ethanol in sub-human primates.

Lieber¹,

Baraona²,

Hernández‐Muñoz³

et al. 1989

J. Clin. Invest.

100

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The role of oxygenation in the pathogenesis of alcoholic liver injury was investigated in six baboons fed alcohol chronically and in six pair-fed controls. All animals fed alcohol developed fatty liver with, in addition, fibrosis in three. No evidence for hypoxia was found, both in the basal state and after ethanol at moderate (30 mM) or high (55 mM) levels, as shown by unchanged or even increased hepatic venous partial pressure of 02 and 02 saturation of hemoglobin in the tissue. In controls, ethanol administration resulted in enhanced 02 consumption (offset by a commitant increase in splanchnic blood flow), whereas in alcohol fed animals, there was no increase. At the moderate ethanol dose, the flow-independent 02 extraction, measured by reflectance spectroscopy on the liver surface, tended to increase in control animals only, whereas a significant decrease was observed after the high ethanol dose in the alcohol-treated baboons. This was associated with a marked shift in the mitochondrial redox level in the alcohol-fed (but not in control) baboons, with striking rises in splanchnic output of glutamic dehydrogenase and acetaldehyde, reflecting mitochondrial injury. Increased acetaldehyde, in turn, may aggravate the mitochondrial damage and exacerbate defective 02 utilization. Thus impaired 02 consumption rather than lack of 02 supply characterizes liver injury produced by high ethanol levels in baboons fed alcohol chronically.

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“…It has been suggested that the increase in liver blood flow following alcohol infusion results from cither a vasodi lator effect or from an increase in the number of vessels perfused [5,6]. In the present study, the increases in portal venous flow and liver blood flow following an infusion of 0.03 mg/g body weight/min alcohol would appear to result from splanchnic vasodilation since splanchnic vascular resistance was decreased while hepatic vascular resistance was un changed.…”

Section: Discussionmentioning

confidence: 46%

“…Clearly, there fore, the effects of alcohol on liver blood flow and portal venous flow are related to the rate of its administration. Previous studies have shown that alcohol either has no effect [1,4], increases [3,5,6] or decreases liver blood flow. In these studies, only one dose of alcohol was used but in each study the dose was dif ferent.…”

Section: Discussionmentioning

confidence: 99%

Effects of Alcohol on Hepatic Haemodynamics in the Rat

Jenkins¹,

Baxter²,

Devitt³

et al. 1986

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The effects of varying rates of alcohol infusion (0.015–0.12 mg/g body weight/ min) on hepatic haemodynamics were studied in male Wistar rats. An infusion of 0.015 mg/g body weight/min alcohol had no significant effect on portal pressure (PP) or wedged hepatic venous pressure (WHVP). However, increasing rates of infusion of alcohol (0.03–0.12 mg/g body weight/min) progressively increased PP and WHVP, the maximum increase in PP occurring following an infusion of 0.12 mg/g body weight/min (6.5 ± 0.5 – 10.3 ± 0.6 mm Hg). The effect of varying rates of alcohol infusion on portal venous flow and liver blood flow was biphasic. Thus following an infusion of 0.03 mg/g body weight/min alcohol, liver blood flow (40.6 ± 4.9–54.3 ± 5.8 ml/100g/min) and portal venous flow (28.6 ± 2.9–41.3 ± 4.1 ml/min) were increased. However, following infusions of 0.06 and 0.12 mg/g body weight/min alcohol, liver blood flow and portal venous flow were decreased. The results suggest that previous conflicting reports on the effects of alcohol on hepatic haemodynamics may be related to the dose of alcohol administered.

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The Effect of Ethanol Upon Systemic and Hepatic Blood Flow in Man

Cited by 93 publications

References 13 publications

Effects of Ethanol and Wine on Hepatic Arterial and Portal Venous Flows in Conscious Dogs

Effects of Ethanol and Wine on Hepatic Arterial and Portal Venous Flows in Conscious Dogs

Impaired oxygen utilization. A new mechanism for the hepatotoxicity of ethanol in sub-human primates.

Effects of Alcohol on Hepatic Haemodynamics in the Rat

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