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作 者:杨建民[1] 杨宗城[2] 陈发明[2] 何保斌[2] 齐顺贞[1] 孙志刚[1] 张晓华[1]
机构地区:[1]白求恩国际和平医院烧伤整形科,石家庄050082 [2]第三军医大学附属西南医院烧伤研究所
出 处:《中华创伤杂志》1999年第2期136-138,共3页Chinese Journal of Trauma
摘 要:目的观察心肌局部肾素-血管紧张素系统(RAS)在烧伤早期心肌损害及心功能障碍中的作用。方法测定烧伤前(对照组)及烧伤后3,8,24小时左心功能变化、血浆心肌球蛋白轻链1(CMLC1)含量、心肌血管紧张素转换酶(ACE)活性、血管紧张素Ⅱ(An)及钙离子(Ca2+)含量,测定心肌肌浆网(SR)Ca2+-ATPase活性及SRCa2+转运功能。结果烧伤大鼠左心室收缩功能明显降低,CMLC1显著升高,心肌ACE活性、An及Ca2+含量增加,SRCa2+-ATPase活性降低,SR Ca2+摄取减少。预防性给予ACE抑制剂可显著降低烧伤后心肌ACE活性,减少A。产生,使血浆CMLC1下降、Ca2+含量降低,增加SRCa2+-ATPase活性、SRCa2+摄取,明显改善左心室功能。结论心肌局部RAS激活参与烧伤后心肌损伤,抑制SRCa2+转运可能是其促进心功能障碍的机制之一。Objective To invedgnte the mechanism of myocardial ghufy and cardiacdysfunction in early postburn stage,and changes of cardiac renin and its effect onsarcoplasmic reticulum (SR) calCium transport function. Methods Eighty-eight ratS wererandomly diVided into 3 groups:the control group (n=8, without burns), the burn group (n=40,30% TBSA full thicknes bums), and the tractment group (n=40, gavage Lisinopril for 3 daysbefore 30% TBSA burns). The left ventricular (LV) contractile function was measured st 3, 8,and 24 hours postburn. Cardiac myosin light chain Ⅰ (CMLC1) levels in seam, aodotensinconverting enzyme (AcE) activities and aodotensin Ⅱ (A ) as well as calcium contents inmyocardium were also measured. At the same time, Ca2+-ATPase activities and calCiumtransprot function in SR were measured, too. Results The maximal rates of LV pressure rise(+dp/dtmax) and fall (-dp/dtmax) in the burn group were significantly lower than that of thecontrol group. Myocardial ACE activities, An and calcium contents,and serum CMLC1 levelswere markedly higher than that in the control group. Ca2+-ATPase activities and Ca2+ uptakefUnction in SR decreased siedcantiy in the burn group. After treatment with ACE inhibitor-Lisinopril, however, ACE activities, An and calcium contents, and CMLC1 levels significantlydecreased compared with that of the burn group. Meanwhile, Ca2+-ATPase activities, calciumuptake function and LV contractile function decreased markedly. Conclusions The cardiacrenin-angiotedsin System is activated rapidly after severe burn, which may play an importantrole in myocardial ischend and hypoxia injury.On the other hand, the cardiac RAS inhibitingthe calcium transport function of SR may be one of the mechanisms in cardiac dysfunctionfollowing burn.
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