在全世界，腦中風是導致死亡與殘障最重要的起因；一般而言，引發一個短暫性局部大腦缺血的狀況，由於興奮性毒素神經傳遞物質的釋放、鈣離子內流入神經元、自由基的產生、脂質過氧化和蛋白質的退變，可能會因而導致不可逆性的細胞損傷及神經行為的功能不良，許多證據指出對於大腦缺血性傷害的發病機制乃因鈣離子經由依賴電位調控的NMDA通道與L及N型電位調控的鈣離子通道內流所致；而在症狀開始後的3小時內，靜脈注射給予血栓溶解劑，是治療急性缺血性腦中風首要有效的治療方針，但是，直到現在血栓溶解劑在腦中風開始後，靜脈內給予大於3小時尚還不被認可，因出血的危險性會隨著時間的增加而增加，然而，大部份病人到達醫院時已經太晚，以致於不能獲得最大的效益，因此，發現其它有效的神經保護藥劑，對於保護缺血的腦部而言則是必需的。
　　本研究發現Mg2+各種藥理學上的作用可能是有效的，包括：抑制興奮性神經傳遞物質的釋放、阻斷依賴電位調控的NMDA通道與阻擋L及N型電位調控的鈣離子通道，這些機制則會使顱內的小動脈及小靜脈呈現血管擴張現象，而在腦血管擴張後，由於腦血流量的增加，可能會因而減少腦損傷的程度；在此篇研究中，將研究在短暫性局部大腦缺血的模型中，以具神經保護效能之MgSO4劑量(750μmol/Kg)於再灌流的同時進行頸動脈內灌注，看其是否可增進電生理及神經行為的功能；而以臨床上的觀點而言，對於經過治療後的中風病人，其行為功能上的復原比降低腦損傷的程度更為重要。
　　在材料與方法方面，選用23隻Sprague-Dawley的公鼠，體重在250-300克間，以1-2%的halothane混合於70%的N2O和30%的O2中進行麻醉，由右股動脈插管以計測生理參數，中大腦動脈阻塞手術的過程，則利用頸動脈內塞入縫線之方法，將右中大腦動脈的起始部位阻塞，產生局部缺血(90分鐘)現象，而縫線移除，也就是血液再灌流的開始，於20分鐘內將事前所配製的葯物由頸動脈內灌注入大白鼠體內；另外，用Laser-Doppler flowmetry來監測每側大腦半球SI及SII的局部腦皮質血流量；體感覺誘發電位則是以誘發電位量測系統針對上下肢SI部位進行記錄；而神經行為測試則是以神經學評估系統來做評估；最後，使用TTC染色腦切片再以電腦影像分析系統來量化腦損傷的程度。
　　從結果顯示出於再灌流後的72小時，由控制組缺血側的上下肢皮質領域所記錄到的體感覺誘發電位P1-N1振幅，降低至原始值的18%及26%；相對而言，以MgSO4治療的大白鼠，其P1-N1振幅則可明顯的提升至24%及40%；另外，MgSO4可改善感覺及運動神經行為上的結果，分別是33%及25%，且也可降低皮質及紋狀體的梗塞體積之大小，分別是40%；總之，在短暫性局部大腦缺血及再灌流後，使用magnesium作延緩治療有助其電生理及神經行為的改善與減少腦損傷的程度。

　　Cerebral stroke is a leading cause of death and disability worldwide. In general, transient focal cerebral ischemia that occurs during cerebrovascular surgery may result in irreversible cell damage and neurobehavioral dysfunction due to the release of excitotoxic neurotransmitters, influx of calcium ions into neurons, free radical generation, lipid peroxidation, and protein degradation. Much evidence implicates the influx of calcium ions via the N-methyl-D-aspartate (NMDA) receptor complex in the pathogenesis of cerebral ischemic injury. Intravenous thrombolysis within 3 hr after symptoms onset represents the first therapeutical approach that can effectively treat acute ischemic stroke. Until now, thrombolysis has not been approved for intravenous administration ＞3 hr after stroke onset because the risk of hemorrhage increases with time. However, most patients arrive at the hospital too late to receive the maximum benefit. Thus an effective neuroprotective agent is needed to protect ischemic brain after thrombolytic therapies.
　　Mg2+ has a variety of pharmacological actions that may be beneficial in the treatment of acute ischemic stroke. Neuroprotective mechanisms of Mg2+ include blockade of L- and N-type voltage-operated calcium channels, inhibition of excitatory neurotransmitter release, and blockade of voltage-dependent NMDA channels. These mechanisms show a dose-dependent vasodilation of intracranial arterioles and venules. Mg2+ may decrease the size of brain infarct due to increase cerebral blood flow after cerebral vasodilation. In the current study, we investigate whether delayed treatment with magnesium sulfate (MgSO4；750μmol/Kg ia) could improve electrophysiology and neurobehavioral function in the transient focal cerebral ischemia model. Improvement of functional outcome is more important than reduced brain damage with regard to stroke patients through treatment.
　　At 72 hr after the onset of reperfusion, the amplitude of somatosensory evoked potentials (SSEP) recorded from ischemic fore- and hindpaw cortical fields decreased to 18% and 26% of baselines in vehicle-injected rats. Respectively, the amplitude of SSEP recorded from cerebral ischemia rats treated with MgSO4 improved to 24% and 40% of baselines. In addition, MgSO4 improved sensory and motor neurobehavioral outcomes by 33% and 25%, and reduced cortical and striatal infarct sizes by 40%. In conclusion, delayed treatment with magnesium could improve electrophysiology and neurobehavioral outcomes and reduce brain damage after cerebral ischemia-reperfusion.

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