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法舒地尔治疗急性脑梗死的疗效及对血清神经元特异性烯醇化酶的影响 被引量:6

Efficacy and effect of fasudil on clinical manifestations and serum neurospecific enolase in patients with acute cerebral infarction
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摘要 目的观察法舒地尔对急性脑梗死患者血清神经元特异性烯醇化酶(NSE)的影响以及临床疗效。方法将80例患者随机分为对照组和法舒地尔治疗组,测定患者治疗前后血清NSE含量、神经功能缺损评分以及Barthel指数(BI)。结果经法舒地尔治疗后10 d,患者血清NSE含量为(12±s 4)μg.L-1,神经功能缺损评分为(13±3)分,BI评分为(68±10)分。与对照组比较,治疗组血清NSE含量和临床神经功能缺损程度评分明显降低(P<0.05),BI评分明显升高(P<0.05)。结论血清NSE水平较好地反映了急性脑梗死的脑损伤程度。法舒地尔治疗可有效降低急性脑梗死患者血清NSE含量和神经功能缺损评分,促进临床神经功能的恢复。 AIM To observe the efficacy and effect of fasudil on clinical manifestations and serum neurospecific enolase(NSE) in the patients with acute cerebral infarction.METHODS Eighty patients with acute cerebral infarction were randomly divided into fasudil treatment group and control group.Before and after therapy,the levels of serum NSE were determined for the evaluation of neurological deficit and Barthel index(BI).RESULTS After therapy in the fasudil treatment group,the level of serum NSE was(12 ± s 4) μg·L-1,the total score of clinical neurological deficits was(13 ± 3) and the score of BI was(68 ± 10).Comparing with the control group,the levels of serum NSE and clinical neurological deficit were significantly lower(P 0.05),but the BI score was significantly higher(P 0.05).CONCLUSION The NSE level can rather be better reflected damage degree of acute cerebral infarction.Fasudil may decrease the level of serum NSE and clinical neurologic deficit score in patients with acute cerebral infarction.
出处 《中国新药与临床杂志》 CAS CSCD 北大核心 2010年第5期362-364,共3页 Chinese Journal of New Drugs and Clinical Remedies
关键词 脑梗死 法舒地尔 随机对照试验 神经元特异性烯醇化酶 brain infarction fasudil randomized controlled trials neurospecific enolase
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  • 1张曼,王文刚,曾定尹.法舒地尔对心力衰竭大鼠血流动力学和心肌细胞内钙离子浓度的影响[J].中国新药与临床杂志,2006,25(1):33-36. 被引量:17
  • 2各类脑血管疾病诊断要点[J].中华神经科杂志,1996,29(6):379-380. 被引量:33022
  • 3脑卒中患者临床神经功能缺损程度评分标准(1995)[J].中华神经科杂志,1996,29(6):381-383. 被引量:15750
  • 4罗洁,闵苏.新型脑、心血管活性药——法舒地尔[J].中国新药与临床杂志,2006,25(12):941-945. 被引量:47
  • 5KJOLLER L, HALL A. Signaling to Rho GTPases[J]. Exp Cell Res, 1999, 253(1): 166-179.
  • 6SETO M, SHINDO K, ITO K, et al. Selective inhibition of myosin phosphorylation and tension of hyperplastic arteries by the kinase inhibitor HA1077[J]. Eur J Pharmacol, 1995, 276 (1-2) : 27-33.
  • 7SOMLYO AP, SOMLYO AV. Ca^2+ sensitivity of smooth muscle and nonmuscle myosin Ⅱ : Modulated by G proeins, kinascs, and myosin phosphatase[J]. Physiol Rev, 2003, 83(4): 1325- 1358.
  • 8SHIBUYA M, HIAI S, SETO M, et al. Effect of fasudil in acute ischemic stroke: Results of a prospective placebo-controlled double-blind trial[J]. J Neurol Sci, 2005, 238(1-2): 31-39.
  • 9HITOMI A, IKEGAKI I, SUZUKI Y, et al. Hemoreological abnormalities in experimental cerebral ischemia and effects of protein kinase in hibitor on blood fluidity[J]. Life Sci, 2000, 67 (16) : 1929-1939.
  • 10KITAOKA Y, KUMAI T, LAM TIT, et al. Involvement of RheA and possible neuroprotective effect of fasudil, a Rho kinase inhibiter, in NMDA-induced neurotoxieity in the rat retina [J]. Brain Res, 2004, 1018(1): 111-118.

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