Prasad K, Chan W P, Bharadwaj B
Department of Physiology, College of Medicine, University of Saskatchewan, Saskatoon.
Can J Cardiol. 1996 Oct;12(10):1083-91.
Cardiac dysfunction following cardiopulmonary bypass (CPB) is well known. Various possible sources for increased levels of oxygen free radicals (OFRs) exist during CPB and OFRs depress cardiac function. Postpump (following CPB) cardiac dysfunction may be due to increased levels of OFRs.
This study investigated the effects of cold crystalloid cardioplegia with and without superoxide dismutase (SOD) and catalase (CAT) on cardiac function (cardiac index [CI], left ventricular work index [LVWI]), cardiac contractility (+dp/dt, +dp/dt/PAW [pulmonary arterial wedge pressure], +dp/dt/LVEDP [left ventricular end-diastolic pressure]), diastolic compliance (-dp/dt), OFR-producing activity of polymorphonuclear leukocytes (PMNL-CL); creatine kinase (CK) and MB isoenzyme of CK (MBCK), malondialdehyde (MDA), and white blood cells (WBC) and PMNLs from coronary sinus blood; and lactate levels in arterial blood in anesthetized dogs at various times (up to 90 mins) of reperfusion following 90 mins of hypothermic ischemic cardiac arrest. The dogs were divided into three groups: group I, sham bypass; group II, cold crystalloid cardioplegic cardiac arrest; group III, similar to group II but received SOD and catalase treatment.
Postpump decreases in cardiac function, contractility and diastolic compliance were associated with increases in PMNL-CL activity, blood MDA, plasma CK and MBCK, and plasma lactate, and decreases in WBC and PMNLs. Prevention of postpump cardiac dysfunction (function and contractility) by SOD and CAT was associated with restoration in PMNL-CL activity, plasma CK and MBCK activity, and blood MDA towards control values although not complete. The levels of plasma lactate, total WBC and PMNLs were similar in group II and group III.
These results suggest that postpump depression of cardiac function and contractility could be due to increased levels of OFRs and that SOD and CAT scavengers of superoxide anion and hydrogen peroxide respectively may be effective in preventing postpump cardiac dysfunction.
体外循环（CPB）后心脏功能障碍众所周知。在CPB期间存在多种可能导致氧自由基（OFRs）水平升高的来源，而OFRs会抑制心脏功能。体外循环后心脏功能障碍可能归因于OFRs水平的升高。
本研究调查了含和不含超氧化物歧化酶（SOD）及过氧化氢酶（CAT）的冷晶体心脏停搏液对心脏功能（心脏指数[CI]、左心室作功指数[LVWI]）、心脏收缩力（+dp/dt、+dp/dt/PAW[肺动脉楔压]、+dp/dt/LVEDP[左心室舒张末期压力]）、舒张顺应性（-dp/dt）、多形核白细胞产生OFR的活性（PMNL-CL）；冠状动脉窦血中的肌酸激酶（CK）及其MB同工酶（MBCK）、丙二醛（MDA）、白细胞（WBC）和多形核白细胞；以及麻醉犬在低温缺血性心脏停搏90分钟后的不同再灌注时间（长达90分钟）动脉血中的乳酸水平的影响。犬被分为三组：第一组，假体外循环；第二组，冷晶体心脏停搏液心脏停搏；第三组，与第二组相似但接受SOD和CAT治疗。
体外循环后心脏功能、收缩力和舒张顺应性的降低与PMNL-CL活性、血MDA、血浆CK和MBCK以及血浆乳酸的升高，以及WBC和多形核白细胞的减少有关。SOD和CAT对体外循环后心脏功能障碍（功能和收缩力）的预防与PMNL-CL活性、血浆CK和MBCK活性以及血MDA恢复至对照值相关，尽管未完全恢复。第二组和第三组的血浆乳酸、总WBC和多形核白细胞水平相似。
这些结果表明，体外循环后心脏功能和收缩力的降低可能归因于OFRs水平的升高，并且分别作为超氧阴离子和过氧化氢清除剂的SOD和CAT可能有效预防体外循环后心脏功能障碍。
