| The cerebral apoplexy (brain stroke) is a group lacks the blood and thehemorrhage damage symptom take the brain as the main clinicalmanifestation disease, Has the extremely high case fatality rate and crippling rate. In recent years, its disease incidence rate year by year rose, alreadybecame the world second big cause of death. The apoplexy on clinical is called the cerebral infarction, itspathology foundation is the atherosclerosis. Therefore, prevented the infarct volume, restores the brain to donate blood, the promotion stemdead stove peripheral blood circulation can prevent or the reducedapoplexy occurrence. Although many protective treatment measures, such as Chinese medical science and western medicine, against brain ischemia damage have been found, few of them show satisfactory curative effect. Therefore, prevention measures are gradually emphasized in the treatment of brain ischernia. Recently, a lot of studies have focused on preconditioning measures of brain ischemia. Numerous studies have demonstrated the neuropretective effects of isoflurane (Iso), which indicates Iso may also play an important role in perioperative neurological management. But emulsified isoflurance whether also does have the function in ischemic tolerance in brain. In this study, weevaluated the effects of emulsified isoflurane preconditioning Of neuroprotection against middle cerebral artery occlusion injury. To determine if emulsified isoflurance has protective effect on brain against focal ischemia-reperfusion injury in a rat middle cerebral artery occlusion (MCAO) model.(1) To determine if emulsified isoflurance has protective effect on brain against focal ischemia-reperfusion injury in rats. (2) The Possible mechanism if emulsified isoflurane preconditioning induces ischemic tolerance against brain injury produced by MCAO in rats.Experiment 1:OBJECTIVE To provide reasonable and practicable animal models for clinical cerebral ischernia research. METHOD Middle Cerebral Artery Occlusion (MCAO) were carried out on 40 male S-D rats by suture occlusion via infra artery methods. The animals were divided into 5 groups randomly and equally (n=8):group A with 60-min MCAO, group B with 120-min MCAO, group C with 150-min MCAO, group D with 180-min MCAO, group D with sham operation. The neurological outcomes were evaluated at 24 h after the reperfusion. After 24h of reperfusion the brain infarct volumes were measured. RESULTS Neurological dysfuctions and brain infarct volumes gradually increased from A to D, E group and A-D group was significance inThe NDS (P＜0.05). The infarct size A group was lower than B-D group (P＜0.05). B group, C group was lower than E group (P＜0.05). but there was no significance in brain infarct volume between group B and C. CONCLUSION 120-min-MCAO rats were perfect cerebral ischernia models.Experiment 2: OBJECTIVE To investigate if Emulsified isoflurane preconditioning induces delayed ischemic tolerance against neuronal damage produced by MCAO in rats. METHOD Sixty male SD rats weighing 250～300 g were anesthetized with intraperitoneal 10%Chloral bydrate 3.5ml/kg. Middle cerebral artery occlusion (MCAO) was performed by surgical exposure of common, internal and external carotid arteries through a longitudinal incision in the neck. A nylon filament (0.20-0.25mm in diameter) with rounded end was inserted into internal carotid carotid artery and threaded cranianlly until resistance was felt. The depth of insertion was about 18-20 mm. The animals were randomly divided intosix equal groups. sham operation group in which caritiod arteries into exposed but no MCAO was performed; ischemia group: the animals inhaled 100% O2 for 30min before the beginning of MCAO which was maintained for 2h; isoflurane group: 0.9%was inhaled for 30 min before the 2h MCAO. emulsified isoflurance group: 8% emulsified isoflurance 17ml/kg/h was inhaled for 30 min before the 2h MCAO; Propofol group: Propofol 7.5mg/kg was inhaled for 10 min before the 2h MCAO; triglyceride group: 30% triglyceride 17ml/kg/h was inhaled for 30 min before the 2h MCAO;. The neurologic deficit score (NDS) was evaluated 24 h after reperfusion and the infarct volume was calculated at 24 h following reperfusion. RESULTS Rectal temperature, PH, PaO2, PaCO2, blood pressure and blood glucose were controlled and not different among groups during preconditioning. The NDS of isoflurane group, emulsified isoflurance group and Propofol group was lower than ischemia group (P＜0.05). The infarct size, ischemia group was (227.5±18.15)mm3, isoflurane group, emulsified isoflurance group and Propofol group reduced the infarct size at the end of 24 h reperfusion. (P＜0.05), but there was no significant difference between emulsified isoflurance group and isoflurane group. CONCLUSIONS Inhalation of 8% emulsified isoflurance can protect brain form focal ischemia reperfusion injury to some extent in rats.
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