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REPERFUSION INDUCED FREE RADICAL FORMATION FOLLOWING GLOBAL ISCHEMIA

Although O2 derived free radical mechanisms have been implicated to cause cerebral damage associated with ischemia, free radicals have not been measured in this situation. In this study the production of free radicals was evaluated in rats exposed to global. Ischemia and reperfusion. Male Sprague Dawley rats pretreated with the spin trap phenyl-t-butyl nitrone (1.5 ml, 0.1 M; IP) were anesthetized with sodium pentobarbital (65 mg/kg). After tracheostomy, ventilation was controlled to maintain PaCO2 35-40 mmHg and supplemental o2 was administered to achieve a PO2 of 100-200 mmHg. Jugular vein and tail artery catheters were placed and the great vessels were exposed through a median sternotomy. After paralysis (succinylcholine, 4 mg/kg; iv) and anticoagulation (heparin 150 U/kg; iv) one group of animals was designated as sham operated controls and another made ischemic by cross clamping the ascending aorta and inferior vena cava. At the end of 8 min clamps were released and systemic acidosis was treated with sodium bicarbonate (3 mEq/kg). Immediately after ischemia or 15 min after reperfusion the animals were killed and brains removed for lipid extraction and detection of free radicals by electron spin resonance. Our spectra are consistent with large accumulation of free radicals in animals exposed to ischemia and not in sham operated controls (500% increase) or non-reperfused animals. We conclude that free radicals are generated by the brain in response to 8 min of global ischemia and reperfusion. Supported by 20020 & HL 32134.