调节肽在休克发病中的作用

本文探讨了三种调节肽在休克发病中的作用。结果表明:(1)败血症休克大鼠血浆内皮素(ET)成倍增加,给健康大鼠持续滴注低剂量ET可致明显的休克表现,而给轻度失血休克大鼠静滴ET,则致休克不可逆,用特异的ET-抗血清治疗休克,具有明显疗效;(2)败血症休克大鼠血浆降钙素基因相关肽(CGRP)增加2.6倍,休克早期或晚期运用低剂量CGRP治疗都具有显著疗效;(3)休克大鼠心肌、主动脉组织血管紧张素Ⅱ明显增加,休克早期抑制其增加可加剧休克,晚期抑制其升高则具有显著疗效.结论认为,ET是参与休克发病的重要体液因素,CGRP参与休克时机体的代偿调节,组织血管紧张素Ⅱ在休克不同时期作用不同。     

Possibility of Targeting Treatment for Ischemic Heart Disease With Liposome(Ⅱ)

Studies on the isolated rat heart perfusion model have proved that perfusion with high Ca_(2+) (4.5 mmol/L), high K~+ (8.7 mmol/L) or tree radical generating system (FRGS) significantly increases myocardial uptake of liposomes. Intravenous injection of liposomes covalently combined with antibody of rat myocardial cells obviously elevates the target action of liposomes to myocardium. Liposome-carried SOD for treatment of rat myocardial ischemia-repertusion injury is much more effective than simple SOD. The results evidence that the liposome as drug carrier for treatment of ischemic heart diseases shows a broad prospect for its clinical use.