摘要
目的 探讨缺血缺氧在烧伤后“休克心”中的作用及其机制。 方法 健康成年Wistar大鼠 15 0只 ,分为对照组 (2 5只 )和 30 %TBSAⅢ度烧伤组 (12 5只 ) ,其中烧伤组又分为 1,3,6 ,12和 2 4h组 ,每组 2 5只。检测心肌收缩功能、心肌微血管通透性分值、心肌局部血流量、血浆中心肌肌球蛋白轻链 1(CMLC1)、心肌组织核转录因子 (NF -κB)活性、髓过氧化物酶 (MPO)、TNFαmRNA表达和心肌组织TNFα含量。 结果 伤后 1h ,心肌微血管通透性分值即开始增高 ,2 4h达对照值的 2 .1倍 ;心肌局部血流量显著降低 ,伤后 2 4h仍显著低于对照水平 ;CMLC1增高达对照组的 18.6倍。心肌组织NF -κB活性和TNFαmRNA表达明显增强 ,心肌组织TNFα含量增高。心肌组织MPO活性升高。左心室收缩峰压 (LVSP)、最大左心室等容收缩期中心室内压上升 下降的最大速率 (±dp dtmax)均显著降低 ,而左心室舒张末压 (LVEDP)上升 ,表明心肌收缩功能和舒张功能均减退。 结论 缺血缺氧造成了心肌严重损害 ,心肌组织NF -κB活性明显增强 ,心肌细胞TNFα等促炎因子表达上调是烧伤后“休克心”的重要因素。
Objective To evaluate the role of ischemia and hypoxia in the postburn “shock rat heart” and its pathogenesis. Methods A total of 150 healthy adult Wistar rats were divided into control group and burn group which was inflicted with 30% of total body surface area of third degree burn. The burn group was further divided into 1, 3, 6, 12 and 24 hours groups. Myocardial contraction function, myocardial microvascular permeability, volume of regional myocardial blood flow, levels of myocardial myosin light chain 1(CMLC1), myocardial NF-κB activity, mygloperoxidase (MPO), TNFα mRNA expression and levels of myocardial TNFα were observed. Results The myocardial microvascular permeability was increased at the postburn 1 hour and peaked at the 24th hour (2.1 times as much as the control group). The volume of the regional myocardial blood flow decreased significantly and remained at a level markedly lower than that in the control group 24 hours after burn. CM-LC1 also increased significantly and reached 18.6 times as much as that in the control group. Myocardial NF-κB activity and TNFα mRNA expression were significantly increased. Elevations of the levels of the myocardial TNFα and the MPO activity were found. The left ventricular systolic pressure (LVSP) and the ±dp/dt max were significantly decreased,while the left ventricular end-diastolic pressure (LVEDP) was increased, which indicated the decrease of both myocardial diastolic and systolic functions. Conclusions The ischemia and hypoxia cause severe myocardial damage following burns. Promotions of the myocardial NF-κB activity and the TNFα mRNA expression in the myocardium is an important factor resulting in the postburn “shock heart”.
出处
《中华创伤杂志》
CAS
CSCD
北大核心
2002年第4期205-209,共5页
Chinese Journal of Trauma
基金
国家重点基础研究发展规划资助项目(G19990 5 42 0 2 )
国家杰出青年科学基金资助项目 (3 0 12 5 0 40 )
关键词
烧伤
心肌缺血
细胞缺氧
NF-кB
心肌收缩
Burns
Myocardial ischemia
Cell hypoxia
NF-kappa B
Myocardial contraction
