Chahine R, Mateescu M A, Roger S, Yamaguchi N, de Champlain J, Nadeau R
Department of Physiology, Université de Montréal, (Qué.), Canada.
Can J Physiol Pharmacol. 1991 Oct;69(10):1459-64. doi: 10.1139/y91-218.
The potentially injurious effects of oxygen-derived free radicals (OFR) on the myocardium can be prevented in part by pretreatment with OFR scavengers or antioxidants. Since ceruloplasmin (CP) has been shown to possess potent antioxidant activity and scavenge a variety of OFR in vitro, we have undertaken to study its protective effects against myocardial injury induced by OFR. CP was freshly purified by a fast method that minimized proteolytic enzyme degradation. Free radicals were generated by the electrolysis (10 mA DC current for 1 min) of a Krebs-Henseleit solution perfusing an isolated rat heart preparation under constant pressure conditions. CP (0.25 microM) afforded 80 and 63% protection (n = 8, p less than 0.05), respectively, against the deleterious effects of electrolysis-induced OFR on left ventricular pressure and coronary flow. The increase in left ventricular end diastolic pressure used here as an index of heart failure did not occur in the presence of 0.25 microM CP. Moreover, CP significantly reduced the increase of norepinephrine washout in the effluent perfusate after electrolysis suggesting a protection against free radical-induced injury to sympathetic nerve endings.
氧衍生自由基（OFR）对心肌的潜在有害作用可通过用OFR清除剂或抗氧化剂进行预处理部分预防。由于已证明铜蓝蛋白（CP）具有强大的抗氧化活性并能在体外清除多种OFR，我们已着手研究其对OFR诱导的心肌损伤的保护作用。CP通过一种快速方法进行新鲜纯化，该方法可最大限度减少蛋白水解酶的降解。在恒压条件下，通过对灌注离体大鼠心脏标本的Krebs-Henseleit溶液进行电解（10 mA直流电流，持续1分钟）来产生自由基。CP（0.25微摩尔）分别对电解诱导的OFR对左心室压力和冠状动脉血流的有害作用提供了80%和63%的保护（n = 8，p < 0.05）。在此用作心力衰竭指标的左心室舒张末期压力升高在存在0.25微摩尔CP时未出现。此外，CP显著降低了电解后流出灌注液中去甲肾上腺素洗脱的增加，表明对自由基诱导的交感神经末梢损伤有保护作用。
