ABSTRACT
OBJECTIVE: To investigate the effect and mechanism of propofol on the spinal cord apoptosis associated with aortic cross-clamping in rabbits. METHODS: Twenty-four rabbits were randomly divided into sham operation group (A), ischemia/reperfusion group (B) and propofol group (C). In group B and C, the infrarenal aorta was clamped for 40 minutes followed by 7 days reperfusion. Ten minutes before clamping, group C was given propofol 5 mg/kg intravenously and continued at a rate of 20 mg x kg(-1)x h(-1) until unclamping. The aorta was not clamped in group A. The plasma concentrations of malondialdehyde (MDA) and superoxide dismutase (SOD) were determined at 10 minutes before clamping (C-10), before unclamping (C40), at 60 minutes (R60) and on the 7th day (R7 d) unclamping. Apoptotic spinal cord cells and expressions of Bax, Bcl-2 protein were measured by immunohistochemical technique. RESULTS: (1)The concentrations of MDA after ischemia and reperfusion in group B were increased significantly compared with C-10 and those in group A (P<0.05 or P<0.01), which in group C were significantly lower than those in group B (P<0.05), but not in group A. Changes in SOD activity were opposite to those in MDA contents in various groups. (2)The expressions of Bax protein in group B were significantly increased compared with those in group A (P<0.05), while the expression of Bcl-2 protein decreased. In group C, Bax protein expression was markedly lower than those in group B and higher than those in group A (P<0.01 and P<0.05), the expression of Bcl-2 was higher than those in groups B and A (both P<0.01). (3)The number of apoptosis cells in group B was much higher than that in group A, which in group C was much lower than that in group B, but higher than that in group A. (4)The ratio of paralysis in group C was significantly lower than that in group B with a high neurologic score (both P<0.01). CONCLUSION: Propofol can reduce the spinal cord apoptosis associated with aortic cross-clamping in rabbits. The possible mechanism is related to the effect of decreasing Bax expression, increasing Bcl-2 expression, and enhancing antioxidation.
