MECHANISMS OF BRAIN INJURY WITH DEEP HYPOTHERMIC CIRCULATORY ARREST AND PROTECTIVE EFFECTS OF COENZYME Q(10)

Sixteen dogs, divided randomly into a control group and coenzyme Q(10) group (10mg/kg, intraperitoneally before the operation), underwent de ep hypothermic circulatory arrest with cardiopulmonary bypass, as is d one clinically. At four time points cerebral cortex acid cerebrospinal fluid specimens were collected to study free radical formation, energ y metabolism, and ultrastructure. During cardiopulmonary bypass cerebr al electron spin resonance spectra and malondialdehyde contents were p rogressively higher than before bypass, especially at the 60 minutes o f circulatory arrest and 30 minutes of reperfusion (p(1) < 0.01, p(2) < 0.05). In the coenzyme Q(10) group at the latter two time points, th ey had increased less than in the control group at same time points (p (1) < 0.02, p(2) < 0.005). Adenosine triphosphate content in the corte x during bypass; decreased gradually from the prebypass level (P-1 < 0 .02, P-2 = P-3 < 0.001), while lactate in cerebrospinal fluid increase d (p(1) < 0.05, p(2) = p(3) < 0.001). In the coenzyme Q(10) group, ade nosine triphosphate at the latter two time points was greater than tha t in the control group (p(1) = p(2) < 0.05), while the lactate changes were not significantly different from control at each time point (all p > 0.05). Ultrastructure of the cortex was normal before bypass and almost normal during bypass, but it was obviously abnormal at 60 minut es of circulatory arrest and more seriously abnormal at 30 minutes of reperfusion. In the coenzyme Q(10) group the abnormality was obviously reduced. The results suggest that oxygen-derived free radicals and ab normal energy metabolism might play critical roles in brain ischemia/r eperfusion injury. Coenzyme Q(10) could protect the brain by improving cerebral metabolism.