| Recent years, an increasing frequency of perioperative cerebral ischemia is expected. To avoid neurological deterioration after surgery and general anesthesia, especially in high-risk patients, it is important to provide appropriate anesthesia management and prevention. Numerous studies have demonstrated the neuropretective effects of isoflurane (Iso), which indicates Iso may also play an important role in perioperative neurological management. Electro acupuncture (EA) is widely used in the treatment of cerebrovascular diseases. Recent studies found EA given before cerebral ischemia also produces neuroprotection againt ischemic injury. This study was designed to investigate the neuropretective effect of Iso and EA pretreatment against cerebral ischemia and its possible mechanism.Objectivel.To investigate the role of sodium channel in the neuroprotection inducedby repeated Iso pretreatment 2.To investigate the role of adenosine Al receptor and intracellular Ca2+ inthe acute neuroprotection induced by Iso pretreatment 3.To investigate the time course of cerebral ischemic tolerance induced by-6-EA and its possible mechanism.Method1. Role of sodium channel in the delayed phase of neuroprotective effect induced by preconditioning with IsoRats were randomly assigned to four groups: Control Group, animals received no treatment; Lidocaine Group, animals were administered with lidocaine once a day for 5 days; animals in Iso Group and Lidocaine +Iso Group received 1.5% Iso Ih per day for 5 days, while those in the Iso+Lidocaine Group received lidocaine before each Iso pretreatment. 24h after the last pretreatment, transient middle cerebral artery occlusion (MCAO, 120min) was induced. The neurological outcome was evaluated at 24h after reperfusion. The infarct volume was then assessed with TTC staining after the neurological outcome evaluation.2. Role of adenosine AI receptor antagonist in the rapid tolerance against focal cerebral ischemia induced by Iso anesthesiaRats were randomly assigned into five groups: Control animals exposed to 98% oxygen for Ih; animals in Iso, DMSO+Iso and DPCPX+Iso groups exposed to 1.5% Iso in oxygen for Ih, while in DPCPX+Iso group, 8-cyclopentyl-l,3-dipropulxanthine (DPCPX) was intraperitoneally administered before Iso exposure. In DMSO+Iso group, dimathyl sulfoxide (DMSO), the solvent of DPCPX, was intraperitoneally administered before Iso exposure. Animals in DPCPX group received DPCPX intraperitoneally without Iso pretreatment. One hour after the treatment, the MCAO was induced for 120 min. neurologic deficit scores and brain infarct volumes were evaluated after 24h reperfusion.3.1nfluence of isoflurance preconditioning and adenosine on intracellular Ca2+ during cerebral ischemia/reperfusion (I/R) injury-7-Animals in I/R, Iso and DPCPX+Iso groups received 120min MCAO followed with 2h reperfusion. Animals in Iso and DPCPX+Iso groups also received 60min Iso pretreatment Ih before MCAO. DPCPX was given to animals in DPCPX+Iso group before Iso pretreatment. After 2h reperfusion all the animals was decapitated and the brains were cut into slices with the use of vibratome. Intracellular Ca2+ was investigated using Laser Confocal Scanning Microscope.4. The time-course of cerebral ischemic tolerance induced by pretreatment with EAAnimals were randomly divided into 6 groups: Animals in control group received no treatment, and animals in groups EA1-5 received EA at the Baihui acupoint for 30 min at 1/2, 1, 2, 3, and 24h before focal cerebral ischemia (MCAO, 120min). The neurological outcome and infarct volume was evaluated at 24h after reperfusion.S.Role of adenosine AI receptor in the rapid ischemic tolerance induced by pretreatment with EAAnimals were randomly assigned into five groups: control group, DPCPX group, EA group, DMSO+EA group, and DPCPX+EA group. Animals in control and DPCPX groups received saline(l mg ?kg-1) or DPCPX (1 mg ?kg-1) 3h before MCAO. Animals in EA, DMSO+EA, and DPCPX+EA groups received saline(lml ?... |
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