Lung ischemic preconditioning could reduce normothermic rabbit lung ischemia-reperfusion injury. The possible mechanisms are increased production of endogenous A II and reduced formation of oxygen free radicals during lung ischemia for 60 minutes followed by reperfusion for 60 minutes.
Our results indicate that IPC elicits brain ischaemic tolerance and mitochondrial protection by activating the CB1R, which provides a new mechanism for IPC-induced neuroprotection against cerebral ischaemia.
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