Mechanisms of brain injury with deep hypothermic circulatory arrest and protective effects of coenzyme Q10.

Sixteen dogs, divided randomly into a control group and coenzyme Q10 group (10mg/kg, intraperitoneally before the operation), underwent deep hypothermic circulatory arrest with cardiopulmonary bypass, as is done clinically. At four time points cerebral cortex and cerebrospinal fluid specimens were collected to study free radical formation, energy metabolism, and ultrastructure. During cardiopulmonary bypass cerebral electron spin resonance spectra and malondialdehyde contents were progressively higher than before bypass, especially at the 60 minutes of circulatory arrest and 30 minutes of reperfusion (p1 < 0.01, p2 < 0.05). In the coenzyme Q10 group at the latter two time points, they had increased less than in the control group at same time points (p1 < 0.02, p2 < 0.005). Adenosine triphosphate content in the cortex during bypass decreased gradually from the prebypass level (p1 < 0.02, p2 = p3 < 0.001), while lactate in cerebrospinal fluid increased (p1 < 0.05, p2 = p3 < 0.001). In the coenzyme Q10 group, adenosine triphosphate at the latter two time points was greater than that in the control group (p1 = p2 < 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 minutes of circulatory arrest and more seriously abnormal at 30 minutes of reperfusion. In the coenzyme Q10 group the abnormality was obviously reduced. The results suggest that oxygen-derived free radicals and abnormal energy metabolism might play critical roles in brain ischemia/reperfusion injury. Coenzyme Q10 could protect the brain by improving cerebral metabolism.