• Akihide Kurita, Takumi Taniguchi, and Ken Yamamoto.
• Department of Anesthesiology and Intensive Care Medicine, Graduate School of Medical Science, Kanazawa University, Kanazawa, Japan.
• Anesth. Analg. 2010 Nov 1; 111 (5): 1207-10.

BackgroundCarvedilol 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.MethodsTwenty-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.ResultsThe 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.ConclusionsThe 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.

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