Department of Anesthesiology and Intensive Care Medicine, Graduate School of Medical Science, Kanazawa University, Kanazawa, Japan.
Anesth Analg. 2010 Nov;111(5):1207-10. doi: 10.1213/ANE.0b013e3181f1bd55. Epub 2010 Aug 12.
Carvedilol is a nonselective β-adrenoceptor and selective α(1)-adrenoceptor blocker and is widely used in the treatment of patients with hypertensive and/or chronic heart failure because, unlike classic β-blockers, this drug has additional endothelium-dependent vasodilatory effects. We evaluated the effects of oral administration of carvedilol on cardiopulmonary resuscitation (CPR) in a rat model of cardiac arrest (CA) induced by airway obstruction.
Twenty-four rats were randomly assigned to 2 groups: control group (no medication) and treatment group (oral administration of carvedilol [10 mg/kg/d] for 5 days) (n = 12 per group). All the animals were anesthetized, and CA was induced by obstructing the airway. Three minutes after CA, the animals were revived by administering CPR. The rate of chest compressions (CCs) was 240 to 260 CCs/min and the depth of CCs was adjusted to maintain the diastolic arterial blood pressure between 25 to 30 mm Hg in both groups. Epinephrine (0.02 mg/kg) was administered after 5 minutes of CPR. No other therapy was administered before, during, or after CA.
The time interval between airway obstruction and CA in the treatment group was significantly longer than in the control group (230 ± 27 vs 203 ± 24 seconds; P < 0.05). The rate of return of spontaneous circulation in the treatment group was significantly higher than in the control group (92% vs 50%; P < 0.05). Acidosis and increased glucose and tumor necrosis factor-α concentrations in the treatment group were significantly lower than in the control group.
The results of our study showed that rats that had been administered oral carvedilol for several days were more resistant to CA induced by airway obstruction, and when CA did occur, were more likely to be resuscitated. These findings suggest that carvedilol may prolong the safe ischemic time induced by respiratory failure.
卡维地洛是一种非选择性β肾上腺素受体和选择性α(1)-肾上腺素受体阻滞剂,广泛用于治疗高血压和/或慢性心力衰竭患者,因为与经典的β受体阻滞剂不同,这种药物具有额外的内皮依赖性血管扩张作用。我们评估了口服卡维地洛对气道阻塞引起的心脏骤停(CA)大鼠模型心肺复苏(CPR)的影响。
24 只大鼠随机分为 2 组:对照组(无药物)和治疗组(口服卡维地洛[10mg/kg/d],共 5 天)(每组 12 只)。所有动物均麻醉,并通过阻塞气道诱导 CA。CA 后 3 分钟,通过给予 CPR 使动物复苏。两组的按压频率(CCs)均为 240-260CCs/min,按压深度调整为维持舒张期动脉血压在 25-30mmHg 之间。在 CPR 后 5 分钟给予肾上腺素(0.02mg/kg)。在 CA 前后,未给予其他治疗。
治疗组气道阻塞与 CA 之间的时间间隔明显长于对照组(230±27 秒与 203±24 秒;P<0.05)。治疗组自主循环恢复率明显高于对照组(92%比 50%;P<0.05)。治疗组酸中毒和葡萄糖及肿瘤坏死因子-α浓度升高明显低于对照组。
我们的研究结果表明,口服卡维地洛数天的大鼠对气道阻塞引起的 CA 更具抵抗力,并且当 CA 确实发生时,更有可能复苏。这些发现表明,卡维地洛可能延长由呼吸衰竭引起的安全缺血时间。