Background: Renal ischemia/reperfusion injury is a common pathohysiological change on clinic. It is proved that propofol has a certain effect on anti-hypoxia injury, but its effect on apoptosis pathways is still unclear. Objective: To observe the local changes of hemodynamics and expressions of the key protein in endogenetic-mitochondrion signaling apoptosis pathways, and to verify the protective effect of propofol on renal function of rats in during renal transplantation. Design: Randomized controlled animal study. Setting: Department of Anesthesiology, Tiantan Hospital affiliated to Capital University of Medical Sciences; Department of Anesthesiology, Friendship Hospital affiliated to Capital University of Medical Sciences. Materials: The experiment was carried out at the Animal Experimental Center of Beijing Friendship Hospital from January to April 2005. Forty male adult Lewis rats from inbred line were divided into three groups according to randomly digital table, including sham operation group (n=8), mere renal transplantation group (8 donators, 8 receptors) and renal transplantation + propofol group (8 donators, 8 receptors). Propofol was provided by Astrazeneca Company, Italian (batch number CG414). Methods: (1) Establishment of models of renal transplantation: Donator rats in mere renal transplantation group were anesthetized to routinely obtain kidney which was repaired in vitro. Receptor rats were anesthetized with the same way. Left kidney war resected and suffered from xenoma repal transplantation in situ. Twenty-five minutes ago, donators were intravenously injected with 1 mL/kg ringer lactate solution, and receptors were successively infused with 2.5 mL /(kg·h) ringer lactate solution at 15 minutes before opening renal vessel. Rats in renal transplantation + propofol group were treated with the same way mentioned above. However, at the same time point, donators were infused with 20 mg/kg propofol and receptors were infused with 1 mg /(kg · min) propofol in renal transplantation+ propofol group. Rats in sham operation group did not suffer from renal transplantation, but induced ischemia of left kidney. Then, blood was reperfused at 1 hour after ischemia. (2) Hemodynamics was observed with Doppler blood ultrasound technique, and blood velocity of renal vein was detected with ultrasonic probe which was fixed at local vessels after repenetration of auto- and foreign vessels. Expressions of Bcl-2, Bax, caspase 3 and cytochrome C were detected in endogenetic-mitochondrion signaling apoptosis pathways with the method of Western Blot. Main Outcome Measures: (1) Hemodynamic changes; (2) effect of propofol on expressions of apoptosis-pathways protein during renal transplantation. Results: (1) Hemodynamic changes: Blood velocity of renal vein of donators was not significantly different in mere renal transplantation group and renal transplantation + propofol group from that in sham operation group (P > 0.05); but blood velocity of renal vein of receptors was decreased in all three groups [(7.33±0.42), (5.79±0.38), (4.46±0.43) cm/s; P < 0.05]. (2) Effect of propofol on expressions of apoptosis-pathways protein during renal transplantation: As compared with those in sham operation group, expression of Bcl-2 protein was decreased in mere renal transplantation group, but expressions of Bax, cytochrome C and caspase 3 were increased. As compared with those in mere renal transplantation group, expression of Bcl-2 protein was increased in renal transplantation + propofol group, but expressions of Bax, cytochrome C and caspase 3 were decreased. Conclusion: Propofol can decrease the blood velocity of renal vein, inhibit the expressions of relative proteins in endogenetic-mitochondrion signaling apoptosis pathways induced by cold ischemia/reperfusion injury, and protect renal function of rats during renal transplantation.