A preliminary account of these findings was presented at the Third International Symposium on Alcohol and Aldehyde Metabolizing Systems, Toronto, Canada, July 1979.
Effects of Chronic Ethanol Administration on 02 Consumption in Whole Body and Perfused Liver of the Rat
Article first published online: 1 FEB 2008
Alcoholism: Clinical and Experimental Research
Volume 5, Issue 2, pages 192–197, March 1981
How to Cite
Schaffer, W. T., Denckla, W. D. and Veech, R. L. (1981), Effects of Chronic Ethanol Administration on 02 Consumption in Whole Body and Perfused Liver of the Rat. Alcoholism: Clinical and Experimental Research, 5: 192–197. doi: 10.1111/j.1530-0277.1981.tb04887.x
- Issue published online: 1 FEB 2008
- Article first published online: 1 FEB 2008
- Received for publication September 3, 1980; revised manuscript received November 10, 1980; accepted November 14, 1980.
The effects of chronic ethanol consumption on thyroid hormone levels and the rates of whole animal and perfused liver oxygen consumption were determined to test the hypothesis that alcoholic liver damage is a result of thyroid mediated liver hypermetabolism (L. Videla, J. Bernstein, and Y. Israel: Biochem. J, 134: 507–514, 1973). Whole animal minimal oxygen consumption, a sensitive indicator of the effects of thyroid hormone (W. D. Denckla: J. Clin. Invest, 53:572–581, 1974) was unchanged in rats maintained 3 wk on a liquid diet containing 34% of the calories as ethanol (2.49 ± 0.06 ml of O2/min/1O0 g of fat-free body weight) when compared to animals fed an equicaloric sucrose containing liquid diet (2.61 ± 0.20 ml of 02/min/100 g of fat-free body weight) or Purina chow (2.50 ± 0.12 ml of O2/min/100 g of fat-free body weight). Ethanol treatment lowered serum thyroxine (5.09 ± 0.20 pg/100 ml) compared to sucrose-fed control rats (7.66 ± 0.40 pg/100 ml), while serum triiodothyronine was unaffected (59.3 ± 4.0 compared to 66.9 ± 3.1 ng/100 ml for controls). Measurement of O2 consumption in the isolated perfused rat liver showed no significant difference after chronic treatment with the ethanol diet compared to either the sucrose or chow control diets. Infusion of 10-7 M norepinephrine into the perfusion medium resulted in an approximately 22% increase in O2 consumption in ethanol-fed animal and sucrose controls, while a 31 % increase was observed for sucrose-treated animals given 10 μg of T3/kg of body weight/day for 3 wk. These data indicate that T3 potentiates the ability of norepinephrine to increase O2 consumption. The data presented give no support to the concept that chronic ethanol ingestion results in hyperthyroidism or liver hypermetabolism and, consequently, the rationale for treatment of alcoholic hepatitis with the antithyroid drug, propylthiouracil, is incorrect (H. Orrego, H. Ka-lant, Y. Israel, et al.: Gastroenterology, 76:105–115, 1979).