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)