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右美托咪定或(和)舒芬太尼预处理对浸水束缚应激大鼠急性胃黏膜损害的影响 被引量:6

Effects of dexmedetomidine on sufentanil pretreatment rats with acute gastric mucosal lessions induced by water-immersion-restraint stress
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摘要 目的:探讨右美托咪定(DEX)预处理或(和)舒芬太尼(SUF)预处理对浸水束缚应激(WIRS)大鼠急性胃黏膜损害的影响。方法:30只Wistar大鼠随机分成正常对照组(NC组,n=6)、WIRS对照组(WC组,n=6)、DEX预处理组(DP组,n=6)、SUF预处理组(SP组,n=6)、DEX复合SUF预处理组(DSP组,n=6)。DP组:腹腔注射7.5μg/kg10min后进行WIRS;SP组:腹腔注射10μg/kg2min后进行WIRS;DSP组:腹腔注射7.5μg/kg DEX8min后再注射SUF10μg/kg,2min后进行WIRS;以等容积生理盐水腹腔注射后10min进行WIRS作为WC组。所有实验大鼠于WIRS6h后给予10%水合氯醛3mL/kg腹腔注射麻醉,剖腹取出全胃后先进行胃液pH测定、胃黏膜损伤指数(GI)评定,然后按要求留取胃黏膜组织标本以检测胃黏膜组织超氧化物歧化酶(SOD)、丙二醛(MDA)、髓过氧化物酶(MPO)和一氧化氮合酶(NOS)的含量和病理学检查。结果:DEX预处理后,MDA、MPO升高幅度都较WC组明显降低,pH、SOD下降幅度明显减少,GI和胃黏膜损伤病理改变较WC组减轻(P﹤0.05),但NOS的变化没有统计学意义(P﹥0.05);与SP组比较,DSP组SOD、MDA、GI、pH、MPO、NOS的变化无统计学意义(P﹥0.05)。结论:DEX预处理可有效减轻WIRS诱发的急性胃黏膜损伤,其确切机制尚不清楚,可能与控制伤害性应激反应、降低氧化应激、降低胃酸和抑制炎症反应有关,但并没有使舒芬太尼对胃黏膜损伤的保护作用增强。 Objectives To explore the effects of dexmedetomidine on sufentanil pretreatment rats with acute gastric mucosal lesions induced by water-immersion-restraint stress.Methods Thirty wistar rats were randomly assigned to normal control group(Group NC,n = 6);WIRS controlled group(Group WC,n = 6,intraperitoneal infusion of saline 10 min before WIRS);DEX pretreatment group(Group DP,n = 6,intraperitoneal infusion of dexmedetomidine at 7.5 μg/kg 10 min before WIRS);SF pretreatment group(Group SP,n = 6,intraperitoneal infusion of sufentanil at 10μg/kg 2 min before WIRS);DEX and SF pretreatment group(Group DSP,n = 6,intraperitoneal infusion of dexmedetomidine at 7.5μg/kg 10 min and intraperitoneal infusion of sufentanil at 10μg/kg 2 min before WIRS).All rats were anesthetized by intraperitioneal injection of 10% chloral hydrate 6h after WIRS.Then the whole stomach was removed and the gastric pH,SOD,MDA,MPO and NOS levels were measured.The gastric mucosal lesion index(GI) was assessed and gastric mucosal tissues underwent pathological examination.Results The increased range of MDA and MPO,the decreased range of pH and SOD,GI and pathological changes of gastric mucosal damage in the DP group were significantly lower than those in the WC group(P 0.05),but the change of NOS was not statistically significance(P 0.05).Compared with the SP group,the various of SOD,MDA,UI,pH,MPO,NOS in DSP group have no significant change(P 0.05).Conclusions Dexmedetomidine pretreatment can effectively reduce the stress-induced acute gastric mucosal injury,and the mechanism may be related to control harmful stress response,reduce oxidative stress,reduce gastric acid and inhibit the inflammatory response,but it did not enhance the protective effect of sufentanil on acute gastric mucosal injury.
出处 《实用医学杂志》 CAS 北大核心 2012年第9期1432-1434,共3页 The Journal of Practical Medicine
基金 广东省自然科学基金资助项目(编号:S2011010003373) 江苏省高校省级重点实验室开放课题资助项目(编号:KJS09002)
关键词 溃疡 右美托咪定 舒芬太尼 Ulcer Dexmedetomidine Sufentanil
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  • 1杨新春,刘宇,王乐丰,葛永贵,王红石,李惟铭,徐立,崔亮,徐琳,王铁,刘胜辉,贾慧敏.心脏缺血后适应减轻急性心肌梗死再灌注损伤临床研究[J].中国介入心脏病学杂志,2006,14(6):323-326. 被引量:21
  • 2刘胜辉,杨新春,范谦.缺血后处理对大鼠缺血再灌注心肌细胞凋亡的影响[J].中国组织工程研究与临床康复,2007,11(8):1450-1452. 被引量:6
  • 3Zhao ZQ, Corvera JS, Halkos ME, et al. Inhibition of myocardial injury by isehemic posteonditioning during reperfusion: comparison with isehemie preconditioning[J]. Am J Physiol Heart CirePhysiol, 2003, 85.. H579--H588.
  • 4Galagudza M, Kurapeev D, Minasian S, et al. Ischemic postcon-ditioning: brief ischemia during reperfusion converts persistent ventricular fibrillation into regular rhythm [J]. Eur J Cardiothorac Surg, 2004, 25: 1006--1010.
  • 5Staat, Rioufol, Plot C,et al. Post conditioning the human heart[J]. Circulation, 2005, 112: 2143-2148.
  • 6Kin H, Zatta AJ, Lofye MT, et al. Postconditioning reduces infarct size via adenosine receptor activation by endogenous adenosine [J]. Cardiovascular Res, 2005, 67: 124--133.
  • 7Argaud L, Gateau-Roesch O, Raisky O, et al. Post-conditioning inhibits mitochondrial permeability transition [J]. Circulation, 2005, 111: 194-197.
  • 8Tsang A, Hausenloy DJ, Mocanu MM, et al. Postconditioning: a form of "modified reperfusion" protects the myocardium by activating the phosphatidylinositol 3 -- kinase-- Akt pathway [J]. CircRes, 2004, 95: 230--232.
  • 9Lefer AM, Camplell B, Skin YK, et al. Simvastatin preserves the ischemia reperfusion myocardium in nomoeholesterolemic rat hearts [J]. Circulation, 1999, 100 (2) : 178-184.
  • 10Heinrichs, Jahn, Suda T, et al. Selective stimulatory actions of corticotrophin-releasing factor ligands on correlates of energy baiance [J]. Physiol Behav, 2001,74(5) :201-202.

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  • 1钟天安,王建奇,姚鹏飞,徐越,贾军,张浚.重型颅脑损伤后应激性溃疡防治与胃肠道感染的相关性及对策[J].中华神经医学杂志,2006,5(8):823-825. 被引量:36
  • 2姚树桥,孙学礼.医学心理学[M].北京:人民卫生出版社.2009.73-97.
  • 3陈怡,朱长清,董胜翔,归茜,茅益民,曾民德,韩英,黄仲義,王青,白文元,吕晓萍,冯子坛,韩真.罗沙替丁治疗消化性溃疡或急性胃黏膜病变引起上消化道出血的临床研究[J].中国全科医学,2007,10(18):1511-1513. 被引量:10
  • 4Kocoglu H, Karaaslan K, Gonca E, et al. Preconditioning effects of dexmedetomidine on myocardial ischemia/reperfusion injury in rats [J]. Curent Therapeutic Research, 2008,69 (2) : 150-158.
  • 5Kocoglu H, Ozturk H, Ozturk H, et al. Effect of dexmedetomidine on isehemia-reperfusion injury in rat kidney: A histopathologic study [J ]. Renal Failure, 2009,31 ( 1 ) : 70- 74.
  • 6Ibacache M, Sanchez G, Dedrozo Z, et al. Dexmedetomidine preconditioning activates prosurvival kinases and attenuates regional ischemia/reperfusion injury in rat heart [J]. Biochimica et Biophysica Acta, 2012,1822(4) :537-545.
  • 7Sezer A, Memis D, Usta U, et al. The effect of dexmedetomidine on liver histopathology in a rat sepsis model: an experimental pilot study [J]. Ulus Travma Aci Cerrahi Derg, 2010, 16(2) : 108-112.
  • 8Okada H, Kurita T, Mochizuki T, et al. The cardioprotective effect of dexmedetomidinc on global ischaemia in isolated rat hearts [J]. Resuscitation, 2007,74(3) : 538-545.
  • 9Irani K. Oxidant signaling in vascular cell growth death and survival a review of the roles of reactive oxygens pecies in smooth muscle and endothelial cellini togentic and apoptotic signaling [J]. Circ Res, 2000,87(3):179-183.
  • 10Warren M C, Bump E A, Medeiros D, et al. Oxidative stress-induced apoptosis of endothelial cells [J]. Free Radic Res, 2000,29(6) :537-547.

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