期刊文献+

创伤性休克大鼠血浆AM与NO变化的相关性实验研究 被引量:5

A Correlation Study on Changes of Plasma Adrenomedulin and Nitric Oxide in Rats with Traumatic Shock
原文传递
导出
摘要 目的 探讨创伤性休克时大鼠血浆肾上腺髓质素 (AM)和一氧化氮 (NO)的变化特点及相关性。方法 将 40只SD大鼠分为对照组 ( 10只 )、休克未复苏组 ( 10只 )、休克复苏组 ( 10只 )和氨基胍组 ( 10只 )。对照组 10只麻醉后插管 ;3 0只SD大鼠制作创伤性休克动物模型 ,双侧股骨干砸伤后并经股动脉放血至MAP3 5~ 45mmHg。休克复苏组血压维持 3 0min ,然后回输失血和等量的林格氏液。氨基胍组在复苏时静脉注射AG60mg/kg。观察休克前后血浆AM和NO浓度的动态变化。结果 大鼠创伤性休克后 ,血浆AM和NO水平均高于对照组 ,复苏后 0 5h达到高峰 ,氨基胍组两指标变化不明显 ,AM的变化与NO的变化呈正相关。结论 提示AM与NO在创伤性休克发生发展中起重要的调节作用 。 Objective To investigate the changes of plasma adrenomedulin(AM) and nitric oxide(NO) and their correlation in rats with traumatic shock. Methods 40 Sprague-Dawley rats were randomly divided into control group(n=10), traumatic shock without resuscitation group (n=10), traumatic shock with resuscitation group (n=10) and aminoguanidine group (n=10). 10 rats of control group only received intubation after anesthesia. The other 30 rats were made animal models of traumatic shock by crashing both femur shafts and doing bloodletting to mean arterial pressure of 35~45mmHg via femoral artery. Hypotention of rats in traumatic shock with resuscitation group were maintained 30min, and then the lost blood was returned, followed by an infusion of equal volume of Ringer's solutions. Rats of aminoguanidine group were given aminoguanidine 60mg/kg body weight during resuscitation. The changes of Plasma levels of AM and NO in every group of rats were observed before and after shock. Results The plasma level of both AM and NO in the rats of traumatic shock was higher than that in the rats of control group, and reached the highest 30min after resuscitation. The level changes of plasma AM and NO in the rats of aminoguanidine group were not significant. The level change of plasma AM was positive correlation with the level change of plasma NO. Conclusions AM and NO may play an important role in the pathological process of traumatic shock. AM develops its role probably by NO.
出处 《中国医师杂志》 CAS 2004年第5期613-615,共3页 Journal of Chinese Physician
基金 广东省自然科学基金资助项目 (0 0 1 0 4 8)
关键词 创伤性休克 大鼠 血浆AM 血浆NO 血管平滑肌细胞 Traumatic shock Adrenomedullin(AM) Nitric oxide(NO) Correlation
  • 相关文献

参考文献12

  • 1苏加林,汪丽蕙,李亮,周兰,杨军,高莲茹,唐朝枢,刘乃奎.败血症休克大鼠血浆肾上腺髓质素的变化[J].北京医科大学学报,1998,30(2):134-136. 被引量:6
  • 2冯浩淼,黄宗海,黄绪亮,宋慧娟,孙英刚,林洪武.大鼠创伤性休克后血清一氧化氮的动态变化及其机制[J].第一军医大学学报,2002,22(10):891-894. 被引量:17
  • 3孙高斌,黄宗海,孙英刚,杨文宇.一氧化氮合酶抑制剂对大鼠创伤性休克的干预作用[J].第一军医大学学报,2003,23(4):306-309. 被引量:5
  • 4Lepore DA,Kozlov AV,Stewart AG,et al.Nitric oxide synthase-independent generation of nitric oxide in rat skeletal muscle ischemia-reperfusion injury[J].Nitric Oxide,1999,3(1):75-84
  • 5Isumi Y,Shoji H,Sugo S,et al.Regulation of adrenomedullin production in rat endothelial cells[J].Endocrinology,1998,139(3):838-842
  • 6Mazzocchi G,Albertin G,Nussdorfer GG.Adrenomedullin (ADM),acting through ADM(22-52)-sensitive receptors,is involved in the endotoxin-induced hypotension in rats[J].Life Sci,2000,66(15):1445-1450
  • 7Minamino N,Kangawa K,Matsuo H.Adrenomedullin: a new peptidergic regulator of the vascular function[J].Clin Hemorheol Microcirc,2000,23(2 ):95-98
  • 8Saito T,Itoh H,Chun TH,et al.,Coordinate regulation of endothelin and adrenomedullin secretion by oxidative stress in endothelial cells[J].Am J Physiol Heart Circ Physiol,2001,281(3):H1364
  • 9Booke MF,Hinder F,McGuire R,et al.Selecitve inhibition of inducible nitric oxide synthase: effects of hemodynamics and regional blood flow in healthy and septic sheep[J].Crit Care Med,1999,27:157-162
  • 10Ogawa T,Nussler AK,Tuzuner E,et al.Inhibition of nitric oxide synthase dose not influence urinary nitrite plus nitrate excretion after renal ischemic injury[J].Langenbecks Arch Surg,2002,386(7):518-524

二级参考文献21

  • 1[1]Kirkeboen KA, Strand OA. The role of nitric oxide in sepsis an overview[J]. Acta Anaesthesiol Scand, 1999, 43(3): 275-88.
  • 2[2]Szabo C, Thiemermann C. Invited opinion: role of nitric oxide in hemorrhagic, traumatic, and anaphylactic shock and thermal injury [J]. Shock, 1994, 2(2): 145-55.
  • 3[3]Yao YM, Bahrami S, Leichtfried G, et al. Significance of NO in hemorrhage-induced hemodynamic alterations, organ injury, and mortality in rats[J]. Am J Physiol, 1996, 270(5 Pt 2): 1616-23.
  • 4[4]Goris RJ. Pathophysiology of shock in trauma[J]. Eur J Surg, 2000,166(1): 100-11.
  • 5[5]Schlag G, Redl H. Shock, sepsis and organ failure-nitric oxide[M].Germany: Springer-Verlag Berlin Heidelberg, 1995.84-96.
  • 6[6]Smail N, Catanla R A, Wang P, et al. Gut and liver: the organs responsible for increased nitric oxide production after trauma-hemor-rhage and resuscitation[J]. Arch Surg, 1998, 133(4): 399-405.
  • 7[7]Gebhard F, Nussler AK, Rosch M, et al. Early posttraumatic increase in production of nitric oxide in humans[J]. Shock, 1998, 10(4):237-42.
  • 8[8]Hansen PR. Inflammatory alterations in the myocardial microcirculation[J ]. J Mol Cell Cardiol, 1998, 30(12): 2555-9.
  • 9[9]Delonca J, Balteaux V, Giraud T, et al. EDRF/NO and endothelial functions[J]. Arch Mal Coeur Vaiss, 1993, 86(11): 1617-24.
  • 10[10]Carden DL, Granger DN. Pathophysiology of ischaemia-reperfusion injury[J]. J Pathol, 2000,190(3): 255-66.

共引文献25

同被引文献38

引证文献5

二级引证文献2

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