Mason D T, Spann J F, Miller R R, Lee G, Arbogast R, Segel L D
Eur J Cardiol. 1978 Jun;7(4):311-6.
The direct effects of 100, 300 and 500 mg/100 ml ethanol on contractility of isolated, supported right ventricular papillary muscles were evaluated from 10 normal or failing cat hearts. In isometrically contracting muscles, 500 mg% ethanol decreased maximum tension in normal and failing hearts from 7.1 to 4.3 g/mm2 (P less than 0.001) and 3.4 to 2.3 (P less than 0.01) respectively, and lowered maximum tension rise from 30.4 to 20.2 g/mm2/sec (P less than 0.001) and 10.2 to 0.8 (P less than 0.01), without alterations of time to peak tension. In isotonically contracting muscles, 500 mg% ethanol reduced contractile element velocity at 0.5 g/mm2 load in normal and failing ventricles from 1.27 to 0.97 L/sec (P less than 0.001) and 0.59 to 0.39 (P less than 0.001) respectively. Thus, clinically meaningful doses of ethanol clearly, exerted dose-related negative inotropic actions on both normal and failing myocardium, thereby indicating that ethanol ingestion may exacerbate heart failure in diseased hearts.
从10只正常或衰竭的猫心脏中评估了100、300和500mg/100ml乙醇对离体、有支撑的右心室乳头肌收缩性的直接影响。在等长收缩的肌肉中,500mg%乙醇使正常和衰竭心脏的最大张力分别从7.1降至4.3g/mm2(P<0.001)和从3.4降至2.3(P<0.01),并使最大张力上升速率从30.4降至20.2g/mm2/秒(P<0.001)和从10.2降至0.8(P<0.01),而达到峰值张力的时间没有改变。在等张收缩的肌肉中,500mg%乙醇使正常和衰竭心室在0.5g/mm2负荷下的收缩成分速度分别从1.27降至0.97L/秒(P<0.001)和从0.59降至0.39(P<0.001)。因此,具有临床意义剂量的乙醇对正常和衰竭心肌均明显产生剂量相关的负性肌力作用,从而表明摄入乙醇可能会加重患病心脏的心力衰竭。