摘要
在离休大鼠心脏缺血再灌损伤模型上，研究水杨酸钠（ＳＡ）对缺血再灌后心功能恢复及心肌组织Ｃａ２＋含量的影响。与缺血再灌组比较，ＳＡ（０．１－１．０ｍｍｏｌ·Ｌ－１）呈剂量依赖性显著抑制心脏再灌后心功能的恢复。心肌组织Ｃａ２＋含量显著增高。络合剂ＥＤＴＡ和小牛血清白蛋白均能显著对抗ＳＡ诱导的心功能损害，使心肌组织Ｃａ２＋含量显著降低。提示ＳＡ能加重离休大鼠心脏缺血再灌损伤。其机理可能与其促进Ｃａ２＋超负荷引起的心肌损伤有关。ＥＤＴＡ和小牛血清白蛋白具有对抗ＳＡ的心肌毒性作用。
This study was designed to examinethe effects of sodium salicylate(SA) on ischemiareperfusion injury in isolated perfused rat hearts.After30 min ischemia and 30 min reperfusion, myocardialfunction was impaired,as shown by 29%, 23% and46% decreases in the left ventricular pressure (LVP),the maximal rate of left ventricular pressure rise (LVdp/ dtmax)and coronary flow (CF),respectively,andCa2+ content of myocardial tissue was markedly ele-vated. However,pretreatment with SA significantly de-teriorated reperfusioninduced damages in a dose-dependent manner. Ca2+ content of myocardial tissuein the presence of SA was higher compared to control.The effect of SA was attenuated or abolished bvEDTA (0.1 mmol·L-1) and 3% BSA,respectively.These results suggest that SA detenoratesischemiareperfusion injury in isolated perfused rathearts and that the mechanism may be related tofacilitation of calcium overload on mvocardial tissue.
出处
《中国药理学与毒理学杂志》
CAS
CSCD
北大核心
1994年第3期187-190,共4页
Chinese Journal of Pharmacology and Toxicology
关键词
水杨酸钠
再灌损伤
心脏
钙
sodium salicylate,reperfusioninjuries,heart,calcium
