McDonough K H, Henry J J
Department of Physiology, Louisiana State University Medical Center, New Orleans 70112.
Am J Physiol. 1991 Jun;260(6 Pt 2):H1857-63. doi: 10.1152/ajpheart.1991.260.6.H1857.
Chronic alcoholism causes a cardiac contractile dysfunction which, in rats, may occur after 6 mo to 1 yr of alcohol consumption. Sepsis, on a more acute basis, can also induce intrinsic cardiac dysfunction. We tested the hypothesis that 2 mo of chronic alcohol feeding, while not directly causing overt depression of the myocardium, might sensitize the heart to a known cardiac stress, i.e., sepsis. We proposed that sepsis, induced in an alcoholic animal, would cause a more severe myocardial depression than in a nonalcoholic rat. Thus rats were fed a liquid diet with 36% of the total calories as alcohol for 8-10 wk and were then anesthetized and received an injection of live Escherichia coli (approximately 10(10) E. coli) through a dorsal subcutaneous catheter followed by a second dose approximately 5 h later. The following day, hearts were removed and, using the isolated working heart preparation, intrinsic contractile performance was assessed by generating ventricular function curves. Four groups of animals were studied. Hearts from the nonalcoholic-nonseptic group and the alcoholic-nonseptic group showed identical cardiac work (cardiac output x peak systolic pressure at the highest preload was 6,113 +/- 324 and 5,955 +/- 406 ml.min-1.mmHg-1, respectively). Work in the nonalcoholic-septic and the alcoholic-septic groups was decreased by 30 and 50%, respectively (4,806 +/- 478 vs. 2,917 +/- 435 ml.min-1.mmHg-1 at the highest preload). Thus 2 mo chronic alcohol consumption caused no overt cardiac dysfunction by itself but did exacerbate the myocardial injury induced by sepsis.
慢性酒精中毒会导致心脏收缩功能障碍，在大鼠中，饮酒6个月至1年后可能会出现这种情况。脓毒症在更急性的情况下，也可诱发心脏内在功能障碍。我们检验了这样一个假设：持续2个月的慢性酒精喂养，虽然不会直接导致心肌明显抑制，但可能会使心脏对一种已知的心脏应激即脓毒症敏感。我们提出，在酒精性动物中诱发的脓毒症，会比在非酒精性大鼠中导致更严重的心肌抑制。因此，给大鼠喂食一种液体饮食，其中36%的总热量来自酒精，持续8 - 10周，然后将其麻醉，并通过背部皮下导管注射活的大肠杆菌（约10¹⁰个大肠杆菌），约5小时后再注射第二剂。第二天，取出心脏，使用离体工作心脏标本，通过生成心室功能曲线来评估心脏内在收缩性能。研究了四组动物。非酒精性非脓毒症组和酒精性非脓毒症组的心脏显示出相同的心脏功（在最高前负荷下的心输出量×收缩压峰值分别为6,113±324和5,955±406 ml·min⁻¹·mmHg⁻¹）。非酒精性脓毒症组和酒精性脓毒症组的心脏功分别降低了30%和50%（在最高前负荷下分别为4,806±478和2,917±435 ml·min⁻¹·mmHg⁻¹）。因此，持续2个月的慢性酒精摄入本身不会导致明显的心脏功能障碍，但确实会加重脓毒症诱导的心肌损伤。
