| ObjectiveThere are several circumstances such as Carotid endarterectomy, acute ischemic stroke or cardiac arrest can lead to cerebral ischemia, the effect neuro-protection way is always the purpose of doctor purchase in this issue. Isoflurane reduces cerebral metabolic rate for oxygen, increased cerebral blood flow and in-tracranial pressure, but its well controlling characteristic is being increasingly used in clinical anesthesia. Some research have already verified that isoflurane improve neurological outcome after incomplete cerebral ischaemia, isoflurane and mild hypothermia not only similarly prevent hippocampal neuron death in an in vitro model of cerebral ischemia, but also prevents delayed cell death in an orga-notypic slice culture model of cerebral ischemia. But recently research find that isoflurane delays but does not prevent cerebral infarction in rats subjected to focal ischemia,its neuroprotection remains controversial. In this paper, we investigated through various aspects such as neuro electrophysiology, neuropathology, neuro - biochemical and neurologic behavior. In vivo middle cerebral artery occlusion (MCAO) models, we try to testify isoflurane neuroprotection by neurobe-havioral evaluations,infarct volume,amino acids detection and the expression of cerebral Bel - 2/Bax. An in vitro hippocampal slices preparation oxygen - glucose deprivation (OGD) was used to examine the action of isoflurane on electro-physiological and biochemical parameters during anoxia and reoxygen.Materials and Methods1 Experiments on focal cerebral ischemia in vivo1. 1 Focal cerebral ischemia models and experimental group Male adult SD rats weighing 280 -320g were anesthesized with 1% pentobarbital 40mg/kg,ip. Focal cerebral ischemia was induced by intraluminal MCAO technique described by Longa. Briefly, the left common carotid artery (CCA) , internal carotid artery (ICA) and external carotid arteries (ECA) was exposed through a midline cervical incision. EGA and CCA were ligated with a 3 - 0 suture. A 4 - cm length and 0. 25 - 0. 30mm width of a fishing line, whose tip had been rounded by heating near a flame , was introduced from the carotid bifurcation into the ICA until slight resistance was felt (20 to 22 mm) , thereby occluding the origin of the MCA,the animals putting length of fishing line less 10mm was excluded. Re-circulation of MCA was established 2h after MCAO by gentle withdrawal of the suture. The tympanic membrane temperature replacing the brain temperature was monitored by Spectramed instrument and maintained at 37 ~37. 5C by overhead heating lamp. The rats were randomly divided into four groups; In group I ,rats subjected to incision without occlusion. In group H ,rats inhaled 100% oxygen 30min before 2h ischemia and 60min reperfusion. In groups III and IV, rats inhalated 0. 8MAC and 1. 3 MAC isoflurane 30min before 2h ischemia and 60min reperfusion respectively.1. 2 Observed parameters The animals neurobehavioral evaluations were performed 3,22,70h after reperfusion of MCAO. Quantitative electroencephalogram (qEEG) and tympanic membrane temperature was monitored during ische-mia/reperfusion period. The size of the infarct was determined by examining 2 -mm - thick brain sections stained with triphenyltetrazolium chloride at 22 and 70h after reperfusion. The light and ultrastructural microscopy ( characteristics) of CA1 after 22h of reperfusion were studied. Concentrations of excitory amino acids ( EAA) and inhibitory amino acids (IAA ) in both cerebral cortex and hippocampus were measured with high - performance liquid chromatography (HPLC) system during 30,60,120min ischemia and 60min reperfusion. The animals were transcardially perfusion fixed with 4% paraformaldehyde. The brains were removed from the skull, postfixed overnight in the same fixative at4 ,After series dehytrate with 15% and 30% sucrose solution, Serial coronal sectionsof 32 m were made by cryosectioning and immunohistochemical analysis.2 Experiments on hippocampal slices in vitrO2.1 Hippocampal slices prep...
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