[Effect of propofol on gastric mucosal injury after hemorrhagic shock and reperfusion in rabbits].

OBJECTIVE: To study the therapeutic effect and its mechanisms of propofol on gastric mucosal injury after hemorrhagic shock with reperfusion in rabbits. METHODS: Seventy-five New Zealand healthy adult male rabbits were randomly divided into 5 groups of 15 rabbits each: control group (S group), model group (M group), pre-ischemia group (P1 group), pre-reperfusion group (P2 group) and post-reperfusion group (P3 group). The hemorrhage reperfusion-gastric mucosal injury (HR-GMI) model was reproduced. In P1, P2 and P3 groups, propofol 5 mg/kg was injected intravenously 10 minutes before ischemia, reperfusion and 20 minutes after reperfusion respectively, then propofol 20 mgxkg(-1)xh(-1) was infused. In control and model groups, propofol was replaced with equal volume of normal saline. The ultrastructure change in gastric mucosa was examined, and the activity of superoxide dismutase (SOD) and contents of malondialdehyde (MDA) in serum and gastric mucosa were determined. RESULTS: (1) In M group, the most of the cristae and membranes of mitochondria in chief cells of gastric mucosa were fused or disappeared, with formation of vacuoles which induced vacuolization, and a part of membrane blended or disappeared, and degranulation appeared in rough endoplasmic reticulum in these cells. These changes in mitochondria and rough endoplasmic reticulum were mitigated in all propofol groups, especially in P1 group. (2) The activity of SOD was significantly decreased and the contents of MDA were obviously increased in serum and gastric mucosa in M group compared with those in S group (all P<0.01). The activity of SOD was significantly increased and the content of MDA was decreased in serum and gastric mucosa in all propofol groups compared with those in M group (P<0.05 or P<0.01). The activity of SOD was higher and the content of MDA was lower in P1 group than those in P3 group (both P<0.05). CONCLUSION: Propofol can attenuate the gastric mucosa injury by eliminating oxygen free radical and preventing its generation caused by hemorrhagic shock and reperfusion.