摘要
目的 在犬急性心肌缺血模型上观察血浆 GMP1 4 0 水平及血流动力学变化 ,探讨左旋精氨酸对其影响 .方法 2 4只犬随机等分为 3组 :生理盐水组 (A组 ) ,灌注左旋精氨酸组(B组 )和灌注 NO合成酶阻断剂 L- MNNA组 (C组 ) .分别于狭窄前和狭窄后 5,1 5,30 ,60和 1 2 0 min检测远端冠状动脉压 (DCP)、冠脉每分血流量 (CBF)、血浆 NO2 -和血小板 α颗粒膜蛋白 GMP1 4 0 .结果 B组 DCP较 A组下降 ,CBF显著增加 (P<0 .0 1 ) ,GMP1 4 0 明显低于 A组 (P<0 .0 1 ) ,NO2 -明显高于 A组 (P<0 .0 1 ) ;C组较 A组 DCP升高 ,CBF下降 (P<0 .0 5) ,GMP1 4 0 高于 A组 (P<0 .0 5) ,血浆 NO2 -与 A组无明显差异 (P>0 .0 5) .结论 左旋精氨酸增加冠脉血流 ,降低血浆 GMP1 4 0 ;抑制 NO合成酶 ,防止血小板集聚 ,改善微循环 。
AIM The dog model under severe ischemic myocardium was established for investigating L Arginie's influence on GMP 140 levels and its mechanism. METHODS Dogswere randomly divided into three groups. A: Perfusing 0.9% NaCl group. B: Perfusing L Arg group. C: Perfusing NO synthase blocking L MNNA group. DCP, CBF, NO 2 and GMP 140 in plasma were measured before stenosis and after stenosis insertion. RESULTS DCP declined and CBF increased ( P <0.01) in group B. GMP 140 was much lower and NO 2 - higher in group B than in group A ( P <0.01). NO 2 and GMP 140 have remarkable difference between group C and group A. CONCLUSION L Arginie can decrease the production of GMP 140 to protect ischemic myocardium. It may be its mechanism that L arg facilitates NO synthesis and prevents platelet activation.
出处
《第四军医大学学报》
北大核心
2002年第16期1483-1485,共3页
Journal of the Fourth Military Medical University
