丁苯酞对急性脑梗死患者血浆脑型肌酸激酶同工酶、内皮素及降钙素基因相关肽的影响

The effect of butyiphthalide on plasma brain-type creatine kinase isoenzyme,endothelin andcalcitonin gene related peptide in patients with acute cerebral infarction

目的探讨丁苯酞与急性脑梗死患者血浆脑型肌酸激酶同工酶（CK．BB）、内皮素（ET）、降钙素基因相关肽（CGRP）的关系。方法60例急性脑梗死患者按随机数字表法分为常规治疗组和丁苯酞治疗组，每组30例。常规治疗组给予常规治疗，丁苯酞治疗组在常规治疗的基础上加用丁苯酞200mg，3次，d。两组均连续治疗7d。分别于治疗前后测定血浆CK．BB、ET、CGRP水平，并进行比较。结果两组治疗后血浆CK．BB、ET水平降低，CGRP水平升高，与治疗前比较差异有统计学意义（p〈0．01或〈0．05），并且丁苯酞治疗组治疗后血浆CK．BB、ET水平显著低于同期常规治疗组[（216．48±36．95）U／L比（333．07±54．03）U／L，（83．33±26．48）ns／L比（98．46±31．46）ng／L]，差异有统计学意义（P〈0．05），CGRP水平显著高于同期常规治疗组[（44．16±13．28）ng/L比（36．42±12．31）ng／L]，差异有统计学意义（P〈O．05）。结论丁苯酞能降低血浆酶活性，调节ET／CGRP平衡，并且具有扩脑动脉效应以拮抗ET，改善脑缺血、缺氧，从而起到保护脑细胞与血管内皮细胞的作用。

Objective To explore the correlation between butylphthalide and plasma brain-type ereatine kinase isoenzyme （CK-BB）, endothelin （ET）, calcitonin gene related peptide （CGRP） in patients with acute cerebral infarction （ACI）. Methods Sixty patients with ACI were divided into treatment group and control group with 30 cases each by random digits table method. Both groups received normal treatment continuously for 7 days, and butylphthalide of 200 mg was added to treatment group for 3 times per day. The levels of plasma CK-BB,ET and CGRP of two groups before and after treatment were measured andcompared. Results The levels of plasma CK-BB,ET of two groups both decreased significantly after treatment, but CGRP rose obviously. It showed significant differences before and after treatment of both groups （P 〈 0.01 or 〈 0.05 ）. The levels of plasma CK-BB, ET of treatment group after treatment were lower than those of control group in the same period [ （216.48 ± 36.95 ） U/L vs. （333.07 ± 54.03 ） U/L, （83.33 ± 26.48 ） ng/L vs. （98.46 ± 31.46） ng/L, P 〈 0.05 ]. The level of plasma CGRP of treatment group after treatment was significantly higher than that of control group in the same period [ （44.16 ± 13.28 ） ng/L vs. （36.42 ± 12.31 ） ng/L,P 〈0.05]. Conclusion Butylphthalide can reduce the plasma enzyme activity, balance ET and CGRP, extend the cerebral arteries to antagonize ET, improve cerebral ischemia and cerebral hypoxia,which can protect brain cells and endothelial cells.