期刊文献+

内毒素休克大鼠心脏IP_3Ⅰ型及Ⅲ型受体表达的变化及意义 被引量:1

The expression of IP_3Ⅰreceptor and IP_3 Ⅲ receptor in the heart of rat with endotoxic shock
下载PDF
导出
摘要 目的:建立内毒素休克动物模型留取心脏检测1,4,5三磷酸肌醇(IP3)Ⅰ型及Ⅲ型受体表达的变化,探讨内毒素休克中心脏收缩性下降的可能机制。方法:股静脉注射脂多糖(LPS)建立内毒素休克动物模型,留取心脏标本用免疫组化方法检测大鼠心脏IP3Ⅰ型受体及Ⅲ型受体的表达。结果:IP3Ⅰ型受体的表达与对照组相比升高,早期的增强最为明显,早期与对照组及同剂量内毒素组后期之间差异有统计学意义(P<0.01)。除闰盘处表达增强外,还可见沿细胞膜异位表达。IP3Ⅲ型受体的表达较对照组也见增强(P<0.01),但未见异位表达,5mg/kg内毒素组的增强高于10mg/kg组,(P<0.01),处死组增强最明显,与对照组及10mg/kg组之间差异显著(P<0.01)。结论:IP3Ⅰ型和Ⅲ型受体表达的变化可能影响心肌收缩性,进而参与内毒素休克中平均动脉压的调节。 Objective:To probe for the possible mechanism of myocardial depression in endotoxic shock by establishing the animal model of endotoxic shock and detecting the change of the expression of IP3 receptor type Ⅰ and Ⅲ. Methods:The animal model of endotoxic shock was established by injecting lipopolysacchafide of different doses via femoral vein, heart sample was prepared and the expression of IP3 receptor type Ⅰ and Ⅲ was detected by immunohistochemistry. The change of IP3 receptor type Ⅰ and Ⅲ expression was observed with statistical analysis. Results:The expression of IP3 receptor type Ⅰ and Ⅲ was elevated after injecting lipopolysaccharide compared with the control group. The overexpression of them was the most in the early stage of endotoxic shock. The expression of IP3 receptor type Ⅰ was seen along the cell membrane of myocyte besides intercalated disc. The difference of IP3 receptor type Ⅲ expression between different dose groups of lipopolysaccharide was statistically significant,and the difference between control group and 10 mg/kg group was statistically significant,too. Conclusion:The change of IP3 receptor type Ⅰ and Ⅲ expression may affect the myocardial contractility, and may be involved in the regulation of mean arterial pressure in endotoxic shock.
出处 《中国医科大学学报》 CAS CSCD 北大核心 2007年第5期508-510,共3页 Journal of China Medical University
基金 国家自然科学基金资助项目(30170849)
关键词 内毒素休克 心脏 IP3Ⅰ型受体 IP3Ⅲ型受体 endotoxic shock heart IP3 receptor type Ⅰ IP3 receptor type Ⅲ
  • 相关文献

参考文献7

  • 1王雪莲,赵悦,马力,刘沛.内毒素诱导感染性休克动物模型的建立及血清TNF-α测定[J].中国医科大学学报,2004,33(5):390-391. 被引量:11
  • 2LIPP P,LAINE M,TOVEY SC,et al.Functional inositol 1,4,5- triphosphate receptors that may modulate excitation-contraction coupling in the heart [J]. Curr Biol,2000,10(5) :939-942.
  • 3GARCIA KD, SHAH T, GARCIA J. Immunolocalization of type 2 inositol 1,4,5-triphosphate receptors in cardiac myocytes from newborn mice[J]. Am J Physiol Cell Physiol,2004,287(4): C1048-1057.
  • 4HATTORI M, SUZUKI AZ, HIGO T,et al. Distinct roles of IP3R type land 3 in Ca^2+ signaling[J]. J Biol Chem,2004,279(12) : 11967-11975.
  • 5MACKENZIE L,BOOTMAN M,LAINE M,et al. The role of inositol 1,4,5-triphosphate receptors in Ca^2+ signaling and the generation of arrhythmia in rat atrial myocytes [J]. J Physiol,2002,541 (Pt2): 395 -409.
  • 6WOODCOCK EA, MATKOVICH SJ. Ins ( 1,4,5 )P3 receptors and inositol phosphates in the heart-evolutionary artifacts or active signal transducers? [J]. Pharmacol Ther, 2005,107(2) : 240-251.
  • 7TOVEY SC,DYER JL,GODFREY RE,et al. Subtype identification and functional properties of inositol 1,4,5-triphosphate receptors in heart and aorta [ J ]. Pharmacol Res, 2000,42(6) : 581-590.

二级参考文献7

  • 1[1]Schletter J, Heine H, Ulmer A J, et al. Molecular mechanisms of endotoxin activity[J]. Arch Microbiol,1995,164(6) :383 -389.
  • 2[2]Calandra T, Glarser MP. Cytokines and septic shock[J]. Diagn Microbiol Infect Dis,1990,113(2) :377 -378.
  • 3[3]Tracey K, Lowry S. The role of cytokine mediators in septic shock[J]. Adv Surg,1990,23(1) :21 -56.
  • 4[4]Parker SJ, Watkins PE. Experimental models of Gram-negative sepsis[ J ]. Br J Surg,2001 ,88( 1 ) :22 -30.
  • 5[5]Kumar A, Haery C , Parillo JE. Myocardial dysfunction in septic shock[J]. Crit Care Clin ,2000, 16(2) :251 -287.
  • 6[6]Turner A, Tsamitros M, Bellomo R. Myocardial dell injury in septic shock[J]. Crit Care Med, 1999, 27(9) :1775 -1781.
  • 7[7]Eichenholz PW , Eichacker PQ, Hoffman WD, et al. Tumor necrosis factor challenges in canines: patterns of cardiovascular dysfunction[J]. Am J Physiol, 1992, 263(2) :H668 -675.

共引文献10

同被引文献4

二级引证文献1

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