Abstract

To explore the therapeutic effects of atropine for hypoxic bradycardia during the occurrence of cardiac arrest. Sixty-four adult New Zealand rabbits were selected and allocated randomly into 2 groups: instant resuscitation group and 8-minute resuscitation group. Each animal was anesthetized by an intravenous injection of sodium pentobarbital and intubated through tracheostomy. The tracheostomy tube was then clamped off to induce acute hypoxia. At soon as heart rate (HR) decreased to a half of basic-heart-rate, either atropine 50 µg/kg or 0.9% normal saline as control was randomly administered intravenously. In instant resuscitation group (group T1), the tracheostomy tube was unclamped and cardiopulmonary resuscitation (CPR) initiated for the occurrence of cardiac arrest (MAP < 10 mm Hg). In 8-minute resuscitation group (group T2), the tracheostomy tube was clamped for 8 minutes and then CPR initiated. The statistical data were analyzed by SPSS 10.0. All data were reported as x(-) ± s. T test was used to compare the means of cardiac arrest time between two groups, one-way ANONA to compare HR & mean arterial pressure (MAP) and Fisher's exact probabilities test to compare the survival rates between two groups. A value of P < 0.05 was considered statistically significant. The heart rate of atropine treated group was higher than that of normal saline group for about 90 minutes post-dosing. In atropine group, the MAP decrease was significantly faster than that of normal saline group (P < 0.01). Most importantly, after the clamping of tracheostomy tube, the average time of cardiac arrest occurred at (335.43 ± 43.25) s in atropine group versus (371 ± 55) s in normal saline group (P = 0.006). Although atropine treatment of severe hypoxic bradycardia improves the decrease of HR for a short time, it decreases MAP and accelerates the occurrence of cardiac arrest result from acute hypoxia. But the mortality rate is not improved by the treatment of atropine.

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