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目的观察自拟中风补血引接方对急性缺血性脑血管病(AICD)患者血清血栓素B2(TXB2)及6-酮前列腺素F1α(6-Keto-PGF1α)的影响,初步探讨中风补血引接方治疗AICD的机制。方法将符合纳入标准的90例AICD病患者随机分为试验组和对照组各45例。对照组予西医常规治疗,试验组在此基础上加服中风补血接引方,每日1剂。2组均治疗7 d。治疗前后采用脑卒中临床神经功能缺损程度评分量表进行神经功能缺损评分,判断临床疗效;分别于治疗前及治疗第3、7日空腹静脉采血,检测TXB2及6-Keto-PGF1α含量。结果治疗第7日,2组患者神经功能缺损评分均较治疗前明显降低(P<0.01),试验组明显低于对照组(P<0.05);治疗组总有效率(93.30%)优于对照组(84.40%),差异有统计学意义(P<0.05)。治疗第3日,2组患者血清TBX2水平及TXB2/6-Keto-PGF1α(T/P)值较治疗前明显降低(P<0.01),6-Keto-PGF1α显著增高(P<0.01);第7日2组患者血清TXB2水平及T/P值较第3日明显降低(P<0.01),6-Keto-PGF1α显著增高(P<0.01),第3、7日试验组血清TXB2水平及T/P值低于对照组(P<0.01),6-Keto-PGF1α高于对照组(P<0.01,P<0.05)。结论抑制血小板过度活化、调节T/P失调是中风补血引接方治疗AICD的作用机制之一。
Objective To observe the effects of Zhongfeng Xuexue Recipe on serum TXB2 and 6-Keto-PGF1α in patients with acute ischemic cerebrovascular disease (AICD) AICD mechanism of treatment. Methods Ninety patients with AICD who met the inclusion criteria were randomly divided into trial group and control group with 45 cases each. The control group was routinely treated with western medicine. On the basis of this, the experimental group was given a stroke supplement of blood, one dose per day. Both groups were treated for 7 days. Before and after treatment, the score of clinical neurological deficit score of stroke was used to evaluate the neurological deficit to judge the clinical curative effect. The levels of TXB2 and 6-Keto-PGF1α were detected before fasting and on the 3rd and 7th day of treatment respectively. Results On the 7th day after treatment, the score of neurological deficit in both groups was significantly lower than that before treatment (P <0.01), and the experimental group was significantly lower than the control group (P <0.05). The total effective rate (93.30%) in the treatment group was better than that in the control group Group (84.40%), the difference was statistically significant (P <0.05). On the third day after treatment, the levels of serum TBX2 and TXB2 / 6-Keto-PGF1α (T / P) in the two groups were significantly lower than those before treatment (P <0.01) and 6-Keto-PGF1α Serum TXB2 level and T / P ratio in the two groups on the 7th day were significantly lower than those on the 3rd day (P <0.01), while 6-Keto-PGF1α was significantly increased (P <0.01) / P value was lower than the control group (P <0.01), 6-Keto-PGF1α was higher than the control group (P <0.01, P <0.05). Conclusions Inhibition of platelet over-activation and regulation of T / P imbalance is one of the mechanisms of stroke and blood lead in treating AICD.