EFFECTS OF CEREBROPLEGIC SOLUTIONS DURING HYPOTHERMIC CIRCULATORY ARREST AND SHORT-TERM RECOVERY

Previous studies have. suggested that a simple crystalloid ''cerebropl egic'' solution may prolong the safe duration of hypothermic circulato ry arrest. We tested the hypothesis that pharmacologic modification of the cerebroplegic solution would further enhance cerebral protection. Forty-six 4-week-old miniature piglets underwent core cooling to 15 d egrees C nasopharyngeal temperature and 2 hours of hypothermic circula tory arrest. Twelve animals had a 50 ml/kg dose of saline infused into the carotid artery system at the onset of hypothermic circulatory arr est and repeat doses of 10 ml/kg every 30 minutes during arrest, Eleve n animals received the same initial and repeat doses of University of Wisconsin organ preservation solution and 10 received University of Wi sconsin solution with 7.5 mg/L of MK-801, an excitatory neurotransmitt er antagonist. In 13 control animals blood was partially drained from the piglet before 2 hours of circulatory arrest at 15 degrees C and no cerebroplegic solution was infused. All solutions were delivered at 4 degrees C. Brain temperature (n = 24) at the onset of hypothermic cir culatory arrest was 15.0 degrees +/- 0.1 degrees C (mean +/- standard error). Brain temperature after cerebroplegic infusion dropped to 13.0 degrees +/- 0.3 degrees C and stayed lower than brain temperature in the control group throughout the hypothermic circulatory arrest period . Recovery of cerebral adenosine triphosphate and intracellular pH det ermined by phosphorus 31 magnetic resonance spectroscopy (n = 22) was significantly improved by saline infusion and was further improved wit h University of Wisconsin solution and University of Wisconsin solutio n plus MK-801 (p < 0.001). Recovery of cerebral blood flow measured by microspheres (n = 24) also was augmented by University of Wisconsin s olution (p < 0.001) but not in the presence of MK-801. The vascular re sistance response to acetylcholine and nitroglycerin suggested that MK -801 has a direct vasoconstrictive effect. Recovery of cerebral oxygen consumption (n = 24) was increased by University of Wisconsin solutio n and University of Wisconsin solution with MK-801 (p = 0.002). Brain water content (n = 46) was significantly lower in all cerebroplegia-tr eated groups than in controls (p < 0.001). Conclusion: Cerebroplegia i mproves short-term recovery after 2 hours of circulatory arrest in hyp othermic piglets. Pharmacologic modification with University of Wiscon sin solution further improves the recovery of cerebral blood flow and metabolism. MK-801 does not augment the protective effects of Universi ty of Wisconsin solution and reduces the recovery of cerebral blood fl ow by a direct vascular action. Modified cerebroplegia may provide a n ovel approach to improved cerebral protection when prolonged hypotherm ic circulatory arrest is necessary.