Weishaar R, Bertuglia S, Ashikawa K, Sarma J S, Bing R J
J Clin Pharmacol. 1978 Aug-Sep;18(8-9):377-87. doi: 10.1002/j.1552-4604.1978.tb02453.x.
This study was conducted to compare separately the chronic effects of high blood levels of ethanol and acetaldehyde on the metabolism of the heart. Levels of ethanol and acetaldehyde were altered by administration of either 4-methylpyrazole (4-MP), a potent alcohol dehydrogenase inhibitor, or pargyline (PAR), a monoamine oxidase inhibitor that markedly increases acetaldehyde levels in the blood following ethanol administration. Measurements were made in rats consuming ethanol for three to four weeks. Mitochondrial respiration, in vitro contractility of glycerinated heart muscle fibers, and myocardial protein synthesis were determined. As compared to animals receiving only ethanol, administration of either-4-methyl-pyrazole or pargyline plus ethanol resulted in more severe damage to mitochondrial respiration and myocardial protein synthesis. The data illustrate that both acetaldehyde and ethanol in high concentrations can cause severe damage to myocardial metabolism.
本研究旨在分别比较高血乙醇水平和乙醛水平对心脏代谢的慢性影响。通过给予4-甲基吡唑(4-MP,一种有效的乙醇脱氢酶抑制剂)或帕吉林(PAR,一种单胺氧化酶抑制剂,乙醇给药后可显著提高血液中乙醛水平)来改变乙醇和乙醛水平。对摄入乙醇三至四周的大鼠进行测量。测定线粒体呼吸、甘油化心肌纤维的体外收缩性和心肌蛋白合成。与仅接受乙醇的动物相比,给予4-甲基吡唑或帕吉林加乙醇会导致线粒体呼吸和心肌蛋白合成受到更严重的损害。数据表明,高浓度的乙醛和乙醇均可对心肌代谢造成严重损害。