【作者】 李海峰；

【导师】 刘晓亮；

【作者基本信息】 吉林大学 ， 急诊医学， 2009， 硕士

【摘要】 心脏骤停是急诊医师经常遇到的危重症之一,其抢救成功率极低。近年来随着心肺复苏技术的发展,特别是自2000年国际心肺复苏及心血管急救指南颁布以来,心肺复苏作为一个理论或临床技能的热点问题已经引起国内医务工作者的关注。如何提高心肺复苏成功率,降低死亡率,并改善复苏后患者的预后,成为摆在广大急救医学工作者面前的一道巨大的难题。临床上,心跳骤停所给患者带来的损伤是全方位的,全系统的和致命的,这也决定心肺复苏过程是一个复杂系统的过程,为此国内外学者从不同的发病机制及不同发病阶段来部分地解决这道难题,相信随着一道道小的难题解决,这道巨大的难题也就随之迎刃而解。本次实验就是从缺血/再灌注损伤机制中的白细胞激活角度,来探讨白细胞激活在心肺复苏中的作用,并采用血必净来抑制白细胞激活,进而减轻细胞因子所给患者带来的损伤。实验达到了预期结果,并期望在不久的将来成为临床上提高复苏成功率,改善心脏骤停病人预后的有效方法和实验依据。结果提示:(1)心脏骤停复苏后大鼠心脑组织中IL-1β、TNF-α、ICAM-1、MMP-9、TGF-β1及p38MAPK的含量明显增多,而细胞因子IL-1β和TNF-α大量释放导致全身炎症反应综合征(SIRS)的发生。(2)血必净注射液能明显抑制等心脑中IL-1β、TNF-α、ICAM-1、MMP-9及p38MAPK的含量,升高TGF-β1含量。血必净对IL-1β、TNF-α、ICAM-1、MMP-9及p38MAPK的含量的抑制存在量-效关系,即大剂量较中、小剂量作用更为明显。(3)电镜观察大鼠心脑标本,血必净治疗组损伤性改变较模型组为轻,提示血必净对心脑等脏器有保护作用。本研究特点:立题方面:立题新颖,紧跟心肺脑复苏的研究前沿。研究工作:以成熟、可靠的方法为主,结果准确、可靠,结论严谨,理论及实践意义较大。更多还原

【Abstract】 Moer attention is payed how to enhence the survival rate and quality of life after CPCR of CA patient. In the past few years the role of inflammatory is valued in CPCR, the negative contribution of tumor necrosis factor–αand interleulin-1βhave been accredited generally after ischemic of cardia and brain. At the same time, orther cytokine(ICAM-1、MMP-9、TGF-β1) and p38MAPK were expressed and activated in CPCR, they promote each other and enhance damage of brain and cardia. Along with the development of the theories and the methods of CPCR, epinephrine has been administed as a drug essential for CPCR. Especially, high dose epinephine may enhance the success rate of resuscitation of sudden CA. However, many investigations were demonstrated that high dose epinephrine may result in more serious sequela and reduce the survival rate after CA. If the excessive inflammatory reaction are inhibited after CPCR, the success rate of resuscitation of sudden CA will been elevated. The motive of experiment①Content of cytokine (IL-1β、TNF-α、ICAM-1、 MMP-9、TGF-β1)、activated p38MAPK are observed in tissue of cardia and brain, thuough erect model of CPCR rats.②Contribution of cytokine (IL-1β、TNF-α、ICAM-1、MMP-9、TGF-β1)、activated p38MAPK and the ultrstructure in brain and cardia are observed after treatment with different dose of Xue bi jing.Methods Fifty Wistar rats(body weight 300±20g) were divided into five groups at random,ten rats each groups. Besides control guoup, the rest treat with routine method after AC.1.Control group: only to be intubatede, not choked. 2.Model group:to cause to happen model of AC, and treat with Sodium Chloride (5ml.Bid) aftet successful resuscitation.3, Little dose of xue bi jing group: to cause to happen model of AC, and treat with Xue bi jing (5ml/kg) diluted 5ml.i.vBid three day before resuscitation and one day aftet successful resuscitation . 4.Middle dose of xue bi jing group: to cause to happen model of AC, and treat with Xue bi jing (7.5ml/kg) diluted 5ml.i.vBid three day before resuscitation and one day aftet successful resuscitation . 5. High dose of xue bi jing group: to cause to happen model of AC, and treat with Xue bi jing (15ml/kg) diluted 5ml.i.vBid three day before resuscitation and one day aftet successful resuscitation .Results 1. Contents of cytokine ( IL-1β、TNF-α、ICAM-1、MMP-9、TGF-β1)、activated p38MAPK in cardia and brain of rats increase obviously after 24 hours resuscitation. 2.Xue bi jing significantly inhibit the quantitation of cytokine (IL-1β、TNF-α、ICAM-1、MMP-9)、activated p38MAPK expression from CPCR rats, dose decide effect. 3. Compare with contral group the ultrstructure of brain and cardia were damadged in orther groups, compare with contral group the level of cytokine ( IL-1β、TNF-α、ICAM-1、MMP-9、TGF-β1) and activated p38MAPK were increase significantly in the brain and cardia of model group.Conclusion 1. Contents of cytokine (IL-1β、TNF-α、ICAM-1、MMP-9、TGF-β1) and activated p38MAPK in cardia and brain of rats increase obviously after 24 hours resuscitation, and over increased cytokine(IL-1β、TNF-α、ICAM-1、MMP-9) and activated p38MAPK injure brain and cardia of rats.2. Xue bi jing significantly inhibit the quantitation of cytokine (IL-1β、TNF-α、ICAM-1、MMP-9) expression and activated p38MAPK from CPCR rats, increased TGF-β1, and lessen tissue damage.3. Xue bi jing significantly inhibit the quantitation of cytokine (IL-1β、TNF-α、ICAM-1、MMP-9) expression and activated p38MAPK from CPCR rats, dose decide effect, high dose xue bi jing reduce the damadge led by ischemia/reperfusion from CPCR rats more obvious than other dose.更多还原