| Objective: To observe the effect of hypoxia preconditioning on cerebral ischemia in rats with hypoxia preconditioning,and to further guide clinical drug administration.Methods: 30 male Wistar rats,weighing 250-300 grams,were randomly divided into five groups,divided into normal control group(n=6)and hypoxia group(n=6),ischemia reperfusion group,ischemia reperfusion group(10min 7 days(n=6)were observed in hippocampal neurons of ischemia reperfusion 20min)group: 1 days(n=6)(no large striatal spiny neurons observed);and hypoxia preconditioning + ischemia reperfusion group(n=6 group),hypoxia model: confined box continuous inlet 8%O2 + 92%N2 gas mixture 1 hours;cerebral ischemia model preparation: 10% chloral hydrate(350mg/kg Wt)intraperitoneal injection of anesthesia.The middle of the neck incision,separated on both sides of the common carotid artery about 1cm,the ischemic device to the common carotid artery,to avoid vascular compression and blood flow blocked,simple suture incision.The rats were fixed on the positioning system on the occipital transverse incision,exposed flank holes first cervical plate and the transverse plate,using bipolar electric coagulation needle two flank holes in coagulation of the vertebral artery,the incision was sutured after the animal is fully awake,move the cages at night,fasting,animal behavior normal,no obvious brain injury.After 24 h,the 10 min or 20 min of the common carotid artery was clamped and closed,which resulted in transient global cerebral ischemia.The rats in ischemia after 30 ~ 60 s in a coma,the righting reflex disappeared,breathing,bilateral mydriasis,pain reflex,these symptoms persist in the ischemic process,which does not have these symptoms or symptoms of these failed to continue throughout the process of ischemia in rats with abandon.Lifting device clamping the ischemia ischemia 10 min or 20 min after the recovery of cerebral blood flow,the animal gradually regained consciousness began,there were no obvious obstacles,where after ischemia,epilepsy,paralysis,convulsions and other symptoms of the rats were abandoned.The expression of cPKC and cPKC protein was observed by immunohistochemistry after 24 h.Results: After cerebral ischemia,the expression of cPKC and cPKC protein in ischemic tissue were increased but the expression of cPKC was significantly decreased in hypoxic preconditioning group.Conclusion: Ischemic tissue after cerebral ischemia and the expression of cPKC around the cPKC protein expression may be associated with neural cell apoptosis,suggesting that cell signal transduction system abnormal pathophysiological process of nerve cell injury in cerebral ischemia.This may be the effect of hypoxia preconditioning on brain damage after focal cerebral ischemia in the brain.. |