Role of hormones in the mechanism of the swift increase in alcohol metabolism in the rat

Yuki, Takehiko; Bradford, Blair U.; Thurman, Ronald G.

doi:10.1016/s0091-3057(80)80011-6

Cited by 30 publications

(17 citation statements)

References 8 publications

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“…This was associated with an increase in blood catecholamine levels and was blocked by ␣ and ␤ adrenergic blocking agents as well as prior adrenectomy or hypophysectomy [8]. These studies indicate that acute ethanol increases the metabolic rate which increases the ethanol elimination rate [9] and that both thyroid hormone and adrenal cathecholamines participate in this process.…”

Section: Ethanol-induced Increase In O 2 Consumption Is Hormone Depenmentioning

confidence: 70%

“…Previous studies by Yuki et al [8] showed that an acute high dose of ethanol in rats, caused an increase in oxygen uptake in the perfused livers. This was associated with an increase in blood catecholamine levels and was blocked by ␣ and ␤ adrenergic blocking agents as well as prior adrenectomy or hypophysectomy [8].…”

Section: Ethanol-induced Increase In O 2 Consumption Is Hormone Depenmentioning

confidence: 95%

“…Catecholamines increase the metabolic rate in the liver when ethanol is fed acutely [8] and this response is ablated by ␤ adrenergic blockers, hypophysectomy or adrenalectomy. To determine if the elevation of the catecholamine levels seen at the peaks of the UAL cycle were important in producing hypoxic rats were fed propranolol with ethanol [25].…”

Section: What Are the Mechanisms Involved Which Cause Hypoxia At The mentioning

confidence: 99%

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The role of hypoxia in the pathogenesis of alcoholic liver disease

French

2004

Hepatology Research

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Section: Ethanol-induced Increase In O 2 Consumption Is Hormone Depenmentioning

confidence: 70%

Section: Ethanol-induced Increase In O 2 Consumption Is Hormone Depenmentioning

confidence: 95%

Section: What Are the Mechanisms Involved Which Cause Hypoxia At The mentioning

confidence: 99%

See 1 more Smart Citation

The role of hypoxia in the pathogenesis of alcoholic liver disease

French

2004

Hepatology Research

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“…It appears now that this phenomenon also involves alpha adrenergic receptors and elevated catecholamines levels. Adrenergic drugs are known to increase the metabolic rate (Yuki et al, 1980) and thus accelerate the ethanol elimination rate (Scola and Schwabe, 1980;Yuki et al, 1980) as was observed during the UAL cycle.…”

Section: Discussionmentioning

confidence: 87%

“…In acute ethanol feeding experiments, ethanol has been shown to increase the rate of O 2 consumption by the perfused liver (Yuki et al, 1980;Schaffer et al, 1981). This increase in O 2 consumption is blocked by intraperitoneal injection of the alpha blocker phenoxybenzamine or the beta blocker propranolol.…”

Section: Introductionmentioning

confidence: 98%

Catecholamines are involved in the mechanism of the urinary alcohol level cycle in rats fed ethanol intragastrically at a constant rate

French

et al. 2004

Life Sciences

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Ethanol-induced vasoconstriction causes focal hepatocellular injury in the isolated perfused rat liver

et al. 1992

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The role of microcirculation in the pathogenesis of alcoholic liver injury was investigated in isolated perfused livers from fed rats. Infusion of ethanol into the portal vein at concentrations ranging from 25 to 200 mmol/L increased portal pressure, which is an indicator of hepatic vasoconstriction, in a concentration-dependent fashion. Portal pressure started to rise immediately on initiation of ethanol load and remained at higher than basal levels throughout the period of ethanol infusion. Release of lactate dehydrogenase, an indicator of cell injury, into the effluent perfusate began to increase after 20 to 30 min of ethanol infusion and continued to increase until the end of the experiment (60 min after the initiation of ethanol infusion). The lactate dehydrogenase level in the effluent perfusate at 60 min was dependent on the ethanol concentration (0 mmol/L, 8 +/- 3 IU/L; 25 mmol/L, 22 +/- 3 IU/L; 50 mmol/L, 51 +/- 11 IU/L; 100 mmol/L, 60 +/- 7 IU/L; 200 mmol/L, 120 +/- 7 IU/L). Simultaneous infusion of sodium nitroprusside (100 mumol/L), a known vasodilator, inhibited significantly the ethanol-induced increases in portal pressure and lactate dehydrogenase release by abolishing hepatic vasoconstriction. In histological examinations focal hepatocellular necrosis, evidenced by trypan blue staining of cell nuclei, was detected predominantly in midzonal and pericentral areas of the liver lobule after 60 min of ethanol infusion. Change in portal pressure during 60 min of ethanol infusion correlated significantly with levels of lactate dehydrogenase after ethanol infusion (r = 0.82; p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

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Role of hormones in the mechanism of the swift increase in alcohol metabolism in the rat

Cited by 30 publications

References 8 publications

The role of hypoxia in the pathogenesis of alcoholic liver disease

The role of hypoxia in the pathogenesis of alcoholic liver disease

Catecholamines are involved in the mechanism of the urinary alcohol level cycle in rats fed ethanol intragastrically at a constant rate

Ethanol-induced vasoconstriction causes focal hepatocellular injury in the isolated perfused rat liver

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