期刊文献+

失血性休克大鼠PKCα mRNA表达变化规律及对血管低反应性的调节作用 被引量:3

Changes of PKCα mRNA expression and its role in vascular hyporeactivity during hemorrhagic shock in rats
下载PDF
导出
摘要 目的观察PKCα在大鼠失血性休克血管平滑肌中mRNA表达变化规律,及其对失血性休克血管反应性和钙敏感性的调控作用。方法采用PCR技术测定大鼠肠系膜上动脉不同休克时间点(休克即时、30min、1h、2h、4h)的PKCamRNA表达;用离体血管环张力测定技术观察不同休克时间点的肠系膜上动脉一级分支的血管环反应性和钙敏感性变化,以及PKCα激动剂和抑制剂对休克2h血管反应性、钙敏感性的影响。结果①失血性休克后大鼠血管反应性和钙敏感性早期增高、晚期降低,PKCαmRNA表达逐渐增高,于1h达到峰值(P〈0.01),4h时仍处于较高水平(P〈0.01)。②PKCα激动剂和抑制剂可分别增高和降低休克2h大鼠的血管反应性和钙敏感性。结论PKCα在失血性休克血管反应性和钙敏感性调控中起重要作用,可能是休克血管功能的重要保护性分子。 Objective To observe the changes of PKCα mRNA expression of superior mesenteric artery(SMA) tissue and its role in vascular hyporeactivity following hemorrhagic shock(HS) in rats. Methods The SMA from hemorrhagic shock rats of different time after shock( immediately, 30 min, 1 h, 2 h, 4 h) were adopted to determine the mRNA expression of PKCα using RT - PCR technique, and the first class arborization of SMA were adopted to determine the vascular reactivity and calcium sensitivity via observing the contraction initiated by norepinephrine(NE) and Ca^2+ with isolated organ perfusion system. The agonist and inhibitor of PKCot were used to observe the regulation of PKCα on vascular hyporeactivity following hemorrhagic shock. Results ①Vascular reactivity and calcium sensitivity of the first class arborization of SMA were increased at the early stage of HS, then decreased gradually. PKCα mRNA showed a time - dependent increase following HS, peaked at 1 h( P 〈0. 01 ) and maintained at a high level at 4 h( P 〈 0.01 ). It was low level - expressed in normal control group. ②The agonist of PKCα thymelea toxin increased the vascular reactivity and calcium sensitivity of SMA at 2 h shock, and Go - 6976,its inhibitor, decreased the vascular reactivity and calcium sensitivity. Conclusion PKCα plays an important role in the regulation of vascular reactivity and calcium sensitization following HS, it may be an important protective molecule to vascular function after shock.
出处 《中国急救医学》 CAS CSCD 北大核心 2009年第1期46-49,共4页 Chinese Journal of Critical Care Medicine
基金 国家重大基础研究计划项目973项目(No.2005CB522601) 国家杰出青年科学基金项目(No.30625037)
关键词 失血性休克 血管反应性 钙敏感性 蛋白激酶C Hemorrhagic shock Vascular reactivity Calcium sensitivity PKCα
  • 相关文献

参考文献9

  • 1Li T, Liu LM, Liu JC, et al. Mechanisms of rho kinase regulation of vascular reactivity following hemorrhagic shock in rats [ J ]. Shock, 2008, 29 (5) : 65 - 70.
  • 2Liu LM, Dubick MA. Hemorrhagic shock - induced vascular hyporeactivity in the rat: relationship to gene expression of nitric oxide, endothline - 1, and select cytokines in corresponding organs [ J ]. J Surg Res, 2005,125 (12) : 128 - 136.
  • 3刘良明,胡德耀,陈惠孙.循环休克肾上腺素能受体失敏研究进展[J].中国病理生理杂志,1998,14(1):100-103. 被引量:12
  • 4刘杰,赵克森.重症休克大鼠细动脉平滑肌膜电位变化在血管反应性降低中的作用[J].中国病理生理杂志,1998,14(1):39-42. 被引量:11
  • 5Jing Xu, Liangmin Liu. The role of calcium desensitization in vascular hyporeactivity and its regulation following hemorrhagic shock [ J ]. Shock, 2005, 23(6) : 576 -581.
  • 6Hempel A, Lindschau C, Maasch C, et al. Calcium antagonists ameliorate ischemia - induced endothelial cell permeability by inhibiting protein kinase C[ J]. Circulation, 1999, 99(19) : 2523 -2529.
  • 7MeKenna TM, Fan SX, Li S. Lipopolysaccharide - responsive protein kinase C isotypes in the adult rat aorta[J]. Shock, 1997, 7 (4) : 269 - 273.
  • 8刘宏雁,谢湘林,吕国蔚,王维忠.PKCα、β_1、ε、ζ表达在缺氧预适应中的变化[J].中国老年学杂志,2001,21(3):213-214. 被引量:2
  • 9Kitazawa T, Eto M, Woodsome TP, et al. Agonists trigger G protein - mediated activation of the CPI - 17 inhibitor phosphopmtein of myosin light chain phosphatase to enhance vascular smooth muscle contractility[J]. J Biol Chem, 2000, 275(14) : 9897 -9900.

二级参考文献16

共引文献21

同被引文献22

  • 1朱水波,殷桂林,孙宗全,胡健才,王荣平,张晓明,刘勇,董永强.腺苷A1受体激动剂预处理对保存心脏效果的影响[J].中华实验外科杂志,2005,22(9):1087-1088. 被引量:5
  • 2朱学慧,焦建杰,唐铖,董伟林,张才丽,娄建石.高效液相色谱法测定家兔血浆中腺苷浓度[J].中国医院药学杂志,2006,26(4):437-439. 被引量:4
  • 3Rohilla A, Singh G, Singh M, et al. Possible involvement of PKC-delta in the abrogated cardioprotective potential of ischemic preconditioning in hyperhomocysteinemic rat hearts [ J ]. Biomed Phannacother, 2010, 64(3) : 195 -202.
  • 4Lochner A, Marais E, Genade S, et al, Protection of the ischaemic heart: investigations into the phenomenon of ischaemic preconditioning [ J ]. Cardiovasc J Afr, 2009, 20 ( 1 ) : 43 - 51.
  • 5Zhao H. Ischemic postconditioning as a novel avenue to protect against brain injury after stroke [J].J Cereb Blood Flow Metab, 2009, 29 (5): 873-885.
  • 6Kuzner J, Drevensek G, Gersak B, et al. Hypoxic and pharmacological preconditioning preserves vasomotor response of porcine coronary artery[J]. Pol J Pharmacol, 2004, 56(6) : 789 -797.
  • 7Ohnuma Y, Miura T, Miki T, et al. Opening of mitochondrial K (ATP) channel occurs downstream of PKC-epsilon activation in the mechanism of preconditioning[ J ]. Am J Physiol Heart Circ Physiol,2002, 283 ( 1 ) : H440 - H447.
  • 8Garg V, Hu K. Protein kinase C isoform-dependent modulation of ATP-sensitive K^+ channels in mitochondrial inner membrane[ J]. Am J Physiol Heart Circ Physiol, 2007, 293 ( 1 ) : H322 - H332.
  • 9Costa A D, Garlid K D, West I C, et al. Protein kinase G transmits the cardioprotective signal from cytosol to mitochondria[J]. Circ Res, 2005, 97(4) : 329 -336.
  • 10Baines C P, Zhang J, Wang G W, et al. Mitochondrial PKCepsilon and MAPK form signaling modules in the murine heart: enhanced mitochondrial PKCepsilon-MAPK interactions and differential MAPK activation in PKCepsilon-induced cardioproteetion[ J]. Circ Res, 2002, 90(4) : 390 -397.

引证文献3

二级引证文献8

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