期刊文献+

舒芬太尼预处理对大鼠烫伤后早期脂质过氧化和一氧化氮合酶活力的影响 被引量:2

The early effects of sulfentanyl pretreatment on NOS and lipoperoxidation in rats after thermal trauma
下载PDF
导出
摘要 目的:观察舒芬太尼预处理对大鼠烫伤后早期脂质过氧化和NOS的影响。方法:SD大鼠40只,随机分为假烫伤组(S组,n=10),烫伤组(B组,n=10),舒芬太尼预处理组(SUF组,n=10),纳络酮拮抗组(NAL组,n=10)。大鼠以94℃热水致伤18s,复制大鼠30%体表面积Ⅲ°烫伤,观察烫伤后6h血浆超氧化物歧化酶活性(SOD)和丙二醛(MDA)含量以及10%心肌组织匀浆测定一氧化氮合酶(NOS)活力。结果:大鼠烫伤后血浆的MDA含量显著上升,SOD活性显著下降,NOS活力明显增强,舒芬太尼预处理组MDA水平较烫伤组和纳络酮拮抗组明显下降,但仍显著高于假烫伤组;血浆SOD活性较烫伤组和纳络酮拮抗组明显增加,但仍显著高于假烫伤组;10%心肌组织匀浆NOS的活力较烫伤组和纳络酮拮抗组明显降低,但明显高于假烫伤组。结论:舒芬太尼预处理烫伤大鼠可能通过抑制烫伤后脂质过氧化损伤和NOS活力以及保护SOD等抗氧化酶活性,减轻大鼠烫伤后过度的伤害性应激反应,保护各器官功能。 Objective To observe the effects of sulfentanyl pretreatment on nitric oxide synthase (NOS) and lipoperoxidation in rats after thermal trauma. Methods Forty Sprague-Dawley rats were divided into four groups with 10 of each, including sham-burn group (Group S); burn group (Group B), in which rats had third– degree burns over 30% total body surface area (TBSA); sulfentanyl pretreatment group (Group SUF); and naloxone group. Serum superoxide dismutase (SOD) activity and malondialdehyde (MDA) content were detected, so was NOS activity in myocardial tissues. Results SOD activity was reduced but MDA content and NOS activity were increased significantly in Group B. Sulfentanyl pretreatment increased lower activities of SOD and NOS and decreased highter MDA content induced by severe thermal trauma. Naloxone pretreatment mostly antagonized the protective role of sulfentanyl in the rats. Conclusions Sulfentanyl pretreatment can relieve excessive stress reaction due to thermal trauma in rats by suppressing lipoperoxidation damage and NOS activity and by protecting SOD activity.
出处 《实用医学杂志》 CAS 北大核心 2010年第12期2109-2111,共3页 The Journal of Practical Medicine
基金 广东省科技计划项目(编号:2008B060600020) 广东省中医药局课题(编号:2008082)
关键词 烧伤 脂质过氧化 一氧化氮合酶 舒芬太尼 Burns Lipoperoxidation Nitric oxide synthase Sulfentanyl
  • 相关文献

参考文献9

二级参考文献42

  • 1王素敏,董玉枝,王薇,符云峰,刘福英,徐增年,刘树锋.胡桃抗衰老作用的实验研究[J].中国老年学杂志,1994,14(3):164-166. 被引量:28
  • 2[1]Baxter GF,Yellon DM.Time course of delayed myocardial protection after transient adenosine Al-receptor activation in the rabbit[J].J Cardiovasc Pharmacol,1997,29(5):631-638.
  • 3[2]Takano H,Tang XL,Bolli R.Differential role of KATP channels in late preconditioning against myocardial stunning and infarction in rabbits[J].Am J Physiol Heart Circ Physiol,2000,279(5):2350-2359.
  • 4[3]Gho BC,Schoemaker RG,van den Doel MA,et al.Myocardial protection by brief ischemia in non-cardiac tissue[J].Circulation 1996,94(9):2193-2200.
  • 5[4]Wada T,Penninger JM.Mitogen-activated protein kinases in apoptosis regulation[J].Oncogene,2004,23(16):2838-2849.
  • 6Fryer RM, Wang YG, Hsu AK, et al. Essential activation of PKC-δ in opioid-initiated cardioprotection. Am J Physiol Heart Circ Physiol 2001; 280(3 ):H1346 - 53.
  • 7Gross ER, Hsu AK, Gross GJ. Opioid-Induced Cardioprotection Occurs via Glycogen Synthase Kinase{beta} Inhibition During Reperfusion in Intact Rat Hearts. Circ Res 2004; 94(7): 960 -6.
  • 8Weil J, Eschenhagen T, Fleige G, et al. Localization of preproenkephalin mRNA in rat heart: selective gene expression in left ventricular myocardium. Am J Physiol Heart Circ Physiol 1998; 275:H378 - 84.
  • 9Shinmura K, Nagai M, Tamaki K, et al. COX-2-derived prostacyclin mediates opioid-induced late phase of preconditioning in isolated rat hearts. Am J Physiol Heart Circ Physiol 2002; 283(6): H2534 -43.
  • 10Cao ZP, Liu LJ, Van Winkle DM. Activation of δ- and-κopioid receptors by opioid peptides protects cardiomyocytes via KATP channels. Am J Physiol Heart Circ Physiol 2003; 285(3): H1032 - H9.

共引文献165

同被引文献10

引证文献2

二级引证文献6

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部