| ObjectiveSome operations such as repair of thoraco-abdominal aortic aneurysms requiring transient occlusion of the descending thoracic aorta leading to spinal cord ischemia reperfusion injury (SCII). Paraplegia is a devastating complication of the operations. To protect spinal cord function , therefore,is very important. Heme-oxygenase 1 (HO-1) is the inducible isoform of the rate-limiting enzyme in the degradation of heme to bilirubin, ferritin and carbon monoxide (CO) and have significant anti-inflammatory function. Recently it was reported that HO-1 had protective effect on ischemia reperfusion injury(SCI). This study was aimed to explore the changes of HO-1 expression at pre- and postischemia spinal cord in rats and to clarify the function of propofol on the changes.MethodsMale Sprague Dawley (SD) rats were used as experimental spinal cord ischemia reperfusion injury animal model. 126 male SD rats were randomly divided into two groups: 6 for sham operation group(S,n=6) and 120 for experimental groups. Experimental groups, including ischemia/reperfusion group(I/R, n=30), hemin group(I/R+H,n=30), propofol group(I/R+P,n=30)and propofol preconditioning group(I/R+PP,n=30),were scheduled to undergo 40 min abdominal aorta occlusion by clamping while the sham operation group underwent only separating abdominal aorta without occlusion.At the beginning of reperfusion , hemin(I/R+H group, 100mg /kg) and propofol (I/R+P group, 40mg/kg) were administered intraperitoneally while S group and I/R group with 10ml/kg saline. 40mg/kg propofol was administered intraperitoneally to I/R+PP group before spinal cord ischemia. Five observation phase points were selected in each experimental group at postreperfusion 2h, 4h, 8h, 16h and 24h respectively. immunohistochemistry was employed to examine HO-1 expression in spinal cord. Plasma superoxide dismutas(SOD) , serum malonyldialdehyed (MDA) , creatine kinase(CK) , creatine kinase-BB(CK-BB) were...
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