犬心脏停搏复苏后脑氧供需变化及高血压性再灌流的影响

Changes of supply and demand in cerebral oxygen after resuscitation from cardiac arrest and the effect of hypertensive reperfusion in dogs

目的 观察犬心脏停搏 (cardiacarrest,CA)复苏后再灌流期间脑氧代谢情况变化及高血压性再灌流的影响。方法 建立犬电击引起室颤 (ventricularfibrillation ,VF)性CA 8min后开胸心肺复苏 (CPR)模型 ,动物随机分两组 :正常血压性再灌流 (NT)组 (n =6) ,高血压性再灌流 (HT)组 (n =6) ,在自主循环恢复 (ROSC)后 ,MAP在NT组维持于CA前基础值水平 ,而HT组维持于基础值的 110 %～ 115 %。取动脉血及脑矢状窦血行血气分析 ,观察CA前及CA再灌流后 3 0、60、12 0、2 40min的脑动脉 矢状窦氧含量差 (Ca ssDO2 )及矢状窦氧分压 (PssO2 )变化。结果 与基础值比较 ,CA后再灌流 3 0min ,NT组Ca ssDO2显著下降 (P <0 0 5 ) ,PssO2 显著升高 (P <0 0 1) ,直至再灌流 2 40min ,Ca ssDO2 升高显著 (P <0 0 1) ,PssO2 下降显著 (P <0 0 1)。两组间比较 ,再灌流 3 0min ,HT组Ca ssDO2 下降显著 (P <0 0 1) ,PssO2 升高显著 (P <0 .0 1) ,但此后 4h内两组脑氧代谢值差别不显著 (P >0 0 5 )。结论 CA复苏后脑氧供需关系失衡 。

Objective To observe the changes of cerebral oxygen metabolism during the process of reperfusion after resuscitation from cardiac arrest (CA) in dogs and the effects of hypertensive reperfusion. Methods Twelve dogs were subjected to 8 min of ventricular fibrillation resulted from electric shock followed by open chest cardiopulmonary resuscitation (CPR). Dogs were randomly assigned to group NT (normotensive reperfusion, i.e. MAP was at the baseline level before cardiac arrest, n =6) and group HT (hypertensive reperfusion, i.e. MAP was elevated by 10%-15% higher than the baseline, n =6). Cerebral arteriovenous (saggital) oxygen content difference (Ca ssDO 2) and venous (saggital sinus) PO 2 (PssO 2) were determined before cardiac arrest (CA) and at 30, 60, 120, and 240 min after CA. Results In group NT, the Ca ssDO 2 before CA was higher ( P <0.05) than that at 30 min after arrest and lower ( P <0.01) than that at 240 min after arrest. In group HT, the Ca ssDO 2 was not significantly different from that in group NT before arrest, but it was significantly higher ( P <0 01) than that in group NT at 30 min after CA. These values were not significantly different between group NT and HT thereafter( P >0.05). In two groups, PssO 2 was higher ( P <0.01) at 30 min after reperfusion and lower ( P <0.05) at 240 min after reperfusion than that before arrest. At 30 min after reperfusion, PssO 2 was higher ( P <0.01) in group HT than that in group NT. There was no significant difference ( P <0.01) between the two groups thereafter ( P >05). Conclusion There is an imbalance between cerebral oxygen supply and oxygen demand after cardiac arrest and resuscitation. Hypertensive reperfusion can improve early cerebral oxygen supply after cardiac arrest.