缺血预调对体外循环NO释放和血管内皮功能的影响

目的：本文探讨了缺血预调对低温体外循环心脏NO释放和血管内皮功能的保护作用及机制。方法：16只健康杂种狗随机分成对照组C（n=8) 和预调组P（n=8)，常规建立体外循环。预调组于心脏停跳前钳闭主动脉3min、开放3min，重复两次，分别于转流前、主动脉阻断前、主动脉开放即刻、再灌注30min、60min测心输量（CO）、射血分数（EF），同时经冠状静脉窦抽血检测血清NO、Ca^2 ，于再灌注60min取冠脉血管内皮标本用作电镜观察。结果：预调组CO、EF于再灌注期间明显高于对照组（P＜0．01），同期两组NO水平均明显增加，但预调组低于对照组（P＜0．01）。电镜下预调组空泡明显减少，少有细胞破碎和变型。结论：缺血预调增加体外循环心脏停跳前NO释放,保持再灌注期间适当的NO水平，可防止缺血再灌注内皮损伤，增强心脏功能的恢复，过量NO释放－Ca^2 －氧自由基在缺血再灌注损伤中有协同作用。

Influence of Ischemic Preconditioning on Cardiac Release of NO and Vascular Endothelial Function during Cardiopulmonary Bypass

Objective To evaluate the influence of ischemic preconditioning(IP) on cardiac release of NO and vascular endothelial function during cardiopulmonary bypass(CPB).Methods Sixteen healthy mongrel dogs were divided randomly into two groups,C ( n =8,control group) and P ( n =8,preconditioning group). CPB was carried out routinely. The preconditioning regimen consisted of two 3-minute cycles of aortic cross-clamping followed by 3-minute of reperfusion before the onset of hypothermal cardioplegic arrest in group P. CO and EF were measured and blood samples were taken from coronary sinus for the determinations of NO,Ca 2+,before CPB,before aortic cross-clamping,immediately after reperfusion and 30 minutes,60 minutes after reperfusion. Coronary vascular endothelial specimens were taken just 60 minutes after reperfusion for electro-microscopic examination.Results CO and EF were found significantly increased in group P than in group C during reperfusion period ( P <0.01). NO was also increased in both two groups,but lower in group P during reperfusion period ( P <0.01). NO was higher before aortic cross-clamping in group P than in the group C ( P <0.01). Group P was found electro-microscopicaly with far less vacuoles and nearly no cell membrane disruption and deformation as compared with group C.Conclusion IPC increases the release of NO before cardiac arrest and preserve appropriate level of No during reperfusion; and prevents endothelium from ischemia and reperfusion injury,facilitating the recovery of cardiac function. Redundantly release of NO-Ca 2+-Oxygen free radicals plays an important role in reperfusion injury.