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Volume 28, Issue 3, Pages 284-290 (March 2010)


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What is the optimal dose of epinephrine during cardiopulmonary resuscitation in a rat model?

Meng-Hua Chen, MDaCorresponding Author Informationemail address, Jun-Yu Lu, MOMa, Lu Xie, PharmDb, Jun-Hui Zheng, MOMa, Feng-Qing Song, MDa

Received 12 September 2008; received in revised form 24 November 2008; accepted 25 November 2008. published online 25 January 2010.

Abstract 

Objective

Because different species may require different doses of drug to produce the same physiologic response, we were provoked to evaluate the dose-response of epinephrine during cardiopulmonary resuscitation (CPR) and identify what is the optimal dose of epinephrine in a rat cardiac arrest model.

Methods

Rat cardiac arrest was induced via asphyxia, and then the effects of different doses of epinephrine (0.04, 0.2, and 0.4 mg/kg IV, respectively) and saline on the outcome of CPR were compared (n = 10/each group). The primary outcome measure was restoration of spontaneous circulation (ROSC), and the secondary was the change of spontaneous respiration and hemodynamics after ROSC.

Results

Rates of ROSC were 9 of 10, 8 of 10, 7 of 10, and 1 of 10 in the low-dose, medium-dose, and high-dose epinephrine groups and saline group, respectively. The rates of withdrawal from the ventilator within 60 minutes in the low-dose (7 of 9) and medium-dose epinephrine groups (7 of 8) were higher than in the high-dose epinephrine group (1 of 7, P < .05). Mean arterial pressures were comparable, but the heart rate in the high-dose epinephrine group was the lowest among epinephrine groups after ROSC. These differences in part of time points reached statistical significance (P < .05).

Conclusion

Different doses of epinephrine produced the similar rate of ROSC, but high-dose epinephrine inhibited the recovery of spontaneous ventilation and caused relative bradycardia after CPR in an asphyxial rat model. Therefore, low and medium doses of epinephrine were more optimal for CPR in a rat asphyxial cardiac arrest model.

a Institute of Cardiovascular Diseases, the First Affiliated Hospital of Guangxi Medical University, Nanning 530021, PR China

b Department of Physiology, School of Pre-Clinical Sciences, Guangxi Medical University, Nanning 530021, PR China

Corresponding Author InformationCorresponding author. Tel.: +86 771 5356536; fax: +86 771 5350031.

 This study was supported by Guangxi Natural Science Foundation of China (no. 0640081 and no. 0718007B-41).

PII: S0735-6757(08)00817-6

doi:10.1016/j.ajem.2008.11.023


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