中醫用活血化瘀的方法來治療腦中風已有很久的歷史，補陽還五湯是活血化瘀的代表方劑，雖然它已被廣泛的使用來治療腦中風，但對它的療效至今尚未做客觀的評估，而且至今它的作用機轉仍然不清，因此本研究的目的是建立局部腦梗塞的動物模型來探討補陽還五湯的效用及機轉。將總共53隻重量300-350克的雄性Sprague-Dawley（SD）大鼠分成實驗一（35隻）和實驗二（18隻）。實驗一分成5組，每組7隻如下：1) Sham組：開腦暴露兩側頸總動脈及右側中大腦動脈，但沒有阻斷血流；2)控制組：同時阻斷兩側總頸動脈和右側中大腦動脈的血流90分鐘，然後再灌流24小時；3)實驗組A：同控制組，但血流阻斷前先連續七天每日口服補陽還五湯0.73克; 4)實驗B：同實驗A組，但口服補陽還五湯0.15克；5)對照組：同實驗組A，但口服PBS溶液1 ml。再灌流後，先觀察它們的神經狀態並根據神經缺損的程度從grade 0-3劃分為四個等級，然後將它們犧牲取腦﹐並作成2 mm的冠狀切片，經2,3,5-Triphenyl-tetrazolium chloride染色後取從前額葉算起前六片﹐將它們放置於影像分析系統中計算腦梗塞面積的比率，根據各組間神經狀態和腦梗塞面積比率的差異，來探討補陽還五湯對局部腦梗塞的效用。實驗二分成3組，每組6隻如下：1)Sham組：開腦暴露它們兩側的頸總動脈和右側的中大腦動脈，但沒有阻斷血流；2)控制組：阻斷兩側的頸總動脈及右側中大腦動脈血流；3)實驗組：同控制組，但於血流阻斷前連續七天每日口服補陽還五湯0.73克。血流阻斷前和阻斷後90分，以及再灌流30和120分鐘分別從右側股動脈導管採取0.5 ml的血液，測量一氧化氮（NO）的濃度。結果顯示腦血流阻斷前連續口服七天補陽還五湯0.73克∕日和0.15克∕日能減少缺血－再灌流損傷在大鼠的腦梗塞面積和神經缺損。發現連續口服七天補陽還五湯0.73克∕日組在腦血流阻斷前及後90分鐘不會改變血中的NO濃度，而血液再灌流30分鐘後，動脈血中實驗組的NO濃度增加，但再灌流120分鐘後動脈血中實驗組的NO濃度減少。 結論是補陽還五湯能減少缺血－再灌流損傷大鼠的腦梗塞面積，以及改善神經缺損，因此推論前治療補陽還五湯可以使用在人類腦梗塞的急性期。另外，補陽還五湯不改變正常生理狀態下的NO濃度，而當缺血90分鐘後再灌流30分鐘，補陽還五湯能增加NO的濃度，而再灌流120 分鐘，補陽還五湯能減少動脈血中的NO濃度，因此推論補陽還五湯至少部份是經由調節NO來減少缺血－再灌流損傷的腦梗塞面積和神經缺損。; The method of quick the blood and dispelled stasis is widely used to treat cerebrovascular accident (CVA) for a period of longtime in the traditional Chinese medicine. In these Medical formulas, Bu-Yang-Huan-Wu Tang (BYHWT) is the most famous one and has been widely used to treat CVA. However, nobody understands its therapeutic effect and action mechanisms. Therefore, the aim of the present study is to investigate the effect and mechanisms of BYHWT by using an animal model on focal cerebral infarct. A total of fifty-three male Sprague-Dawley (SD) rats weighting 300 to 350 g were used and divided into experiment one (n=35) and experiment two (n=18). Experiment one was divided into 5 groups of 7 rats as follows: 1) Sham group: both common carotid and right middle cerebral arteries were exposed but the blood flows did not be blocked. 2) Control group: rats block the blood flows of both common carotid and right middle cerebral arteries for 90 min before 24 hrs reperfusion. 3) Experiment A group: the method is identical to the control group but continuously feeds BYHWT 0.73 g/day for 7 days prior to the blood flows blocked. 4) Experiment B group: the method is identical to experiment A group but using BYHWT 0.15 g/day. 5) Contrast group: the method is identical to experiment A group but using PBS solution 1 ml/day. After reperfusion, the neurological status was observed and recorded from grade 0-3 according to the degree of neurological deficits. The rat brains then were removed and made 2 mm thickness coronal slices. The ratio of infarct area was calculated after 2,3,5-Triphenyl-tetrazolium chloride staining. We compared the neurological status and the ratio of infarct area among the groups to investigate the effect of BYHWT on focal cerebral infarct. Experiment two was divided in to 3 groups of 6 rats as follows: 1) Sham group: both common carotid and right middle cerebral arteries were exposure but the blood flows did not block. 2) Control group: rats block the blood flows of both common carotid and right middle cerebral arteries. 3) Experiment group: the method is identical to the control group but continuous uses oral administration of BYHWT 0.73 g/day for 7 days prior to the blood flows blocked. The blood samples were respectively taken from right femoral arterial catheter with 0.5 ml before and 90 min after blocking the cerebral blood flows and 30 min and 120 min after reperfusion. The results indicate that continuous using oral administration with BYHWT 0.73 g/day and 0.15 g/day for 7 days prior to the blood flows blocked can decrease the ratio of cerebral infarct and neurological deficit area in ischemia-reperfusion injured rats. In addition, continuously feeding BYWHT 0.73 g/day for 7 days prior to the blood flows blocked, the concentration of NO in artery was no changes, whereas the concentration of NO increased in BYWHT group after 30 min reperfusion
