Superoxide dismutase and catalase in protection of cardiopulmonary bypass-induced cardiac dysfunction and cellular injury
- PMID: 9191502
Superoxide dismutase and catalase in protection of cardiopulmonary bypass-induced cardiac dysfunction and cellular injury
Abstract
Background: 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.
Methods: 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.
Results: 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.
Conclusions: 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.
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