These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: Rates of protein synthesis in different regions of the normotensive and hypertrophied heart in response to acute alcohol toxicity.
    Author: Siddiq T, Richardson PJ, Morton J, Smith B, Sherwood RA, Marway JS, Preedy VR.
    Journal: Alcohol Alcohol; 1993 May; 28(3):297-310. PubMed ID: 8352841.
    Abstract:
    The objective of study was (a) to investigate whether protein synthesis in different regions of the heart (i.e. left and right atria, left and right ventricles) expressed equal sensitivity to acute ethanol dosage, and (b) to ascertain whether concomitant cardiac abnormalities (i.e. experimental hypertrophic heart disease) exacerbated these responses. Acute ethanol dosage (75 mmol/kg body weight, i.p.) to mature male Wistar rats reduced the fractional rate of protein synthesis (ks, %/day) in all regions (atria and ventricles) of the normal and overloaded (30 days aortic constricted) hearts. The responses in ks were variable. In normal heart, the atrial tissues showed a slightly greater decrease in ks (approx. -30%) when compared to the ventricular regions (approx -20%). The most pronounced effects occurred in the hypertrophied left ventricular tissues where the depressive effects of ethanol on the rate of protein synthesis were potentiated in the presence of hypertrophy (ks reduced by approx 40%). Other regions of the overloaded heart did not show additional sensitivity to the effects of ethanol on protein synthesis in the presence of chronic hypertension. In conclusion, the deleterious effects of ethanol on the left ventricle are additive in the presence of chronic hypertrophy. These results may have important implications for other cardiac abnormalities where there is also concomitant ethanol exposure.
    [Abstract] [Full Text] [Related] [New Search]