Keith J C
Circ Shock. 1986;19(3):283-92.
The hemodynamic and ultrastructural effects of lidocaine HCl pretreatment were assessed on anesthetized rats subjected to acute hemorrhagic shock. After 40 minutes of acute hemorrhagic shock (mean arterial pressure = 40 mmHg), significantly less fluid infusion was needed to return mean arterial pressure to 120 mmHg in lidocaine HCl treated animals as compared to the hemorrhagic shock-untreated group (p less than 0.05). Heart rate was significantly lower in lidocaine treated animals in the immediate post-shock period (p less than 0.05). Twenty minutes after resuscitation from shock, arterial pressures, and heart rate were not significantly different from baseline values in the lidocaine HCl group. However, in the hemorrhagic shock-untreated group all arterial pressures were still significantly lower than their baseline values (p less than 0.05). Ultrastructural myocardial ischemic changes appeared to be less severe in the lidocaine HCl treated animals. Lidocaine HCl pretreatment improved the response to hemorrhagic shock and reinfusion in this model of hemorrhagic shock.
在急性失血性休克的麻醉大鼠身上评估了盐酸利多卡因预处理的血流动力学和超微结构效应。在急性失血性休克40分钟后(平均动脉压 = 40 mmHg),与未接受失血性休克治疗的组相比,盐酸利多卡因治疗的动物将平均动脉压恢复到120 mmHg所需的补液量显著更少(p < 0.05)。休克后即刻,利多卡因治疗的动物心率显著更低(p < 0.05)。休克复苏20分钟后,盐酸利多卡因组的动脉压和心率与基线值无显著差异。然而,在未接受失血性休克治疗的组中,所有动脉压仍显著低于其基线值(p < 0.05)。盐酸利多卡因治疗的动物超微结构心肌缺血改变似乎没那么严重。在这个失血性休克模型中,盐酸利多卡因预处理改善了对失血性休克和再灌注的反应。