Gilmour R F, Mallov S
Res Commun Chem Pathol Pharmacol. 1977 Oct;18(2):303-27.
Myocardial necrosis was produced in rats by the subcutaneous injection of a single dose of epinephrine (3 mg base/kg). The severity of the cardiac injury produced was assessed by visual inspection, determination of the release of LDH, CPK, GOT, and HBDH from isolated perfused hearts, and measurement of cardiac uptake of technetium-99m-methylene diphosphonate in vivo. Ethanol, given in doses of 0.5 to 6.0 gm/kg 15 minutes or two hours prior to epinephrine administration protected the hearts against the epinephrine-produced injury, the degree of protection increasing with dose. Investigations of possible mechanisms of action of ethanol indicated that the protective action of the latter does not appear to be due to a lowering of plasma free fatty acid levels, a reduction of cardiac contractility, a non-specific caloric effect, an interference with epinephrine-induced platelet aggregation, or ethanol-induced analgesia.
通过皮下注射单剂量肾上腺素(3毫克碱/千克)在大鼠中产生心肌坏死。通过肉眼检查、测定离体灌注心脏中乳酸脱氢酶(LDH)、肌酸磷酸激酶(CPK)、谷草转氨酶(GOT)和α-羟丁酸脱氢酶(HBDH)的释放以及测量体内心脏对锝-99m-亚甲基二膦酸盐的摄取来评估所产生的心脏损伤的严重程度。在给予肾上腺素前15分钟或两小时给予剂量为0.5至6.0克/千克的乙醇可保护心脏免受肾上腺素所致损伤,保护程度随剂量增加而增加。对乙醇可能的作用机制的研究表明,乙醇的保护作用似乎不是由于血浆游离脂肪酸水平降低、心脏收缩力降低、非特异性热量效应、干扰肾上腺素诱导的血小板聚集或乙醇诱导的镇痛作用。