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Volume 27, Issue 8, Pages 935-941 (October 2009)


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Dose-response of vasopressin in a rat model of asphyxial cardiac arrest

Meng-Hua Chen, MDaCorresponding Author Informationemail address, Feng-Qing Song, MDa, Lu Xie, DPharmb, Li-Ping Wang, MDb, Jun-Yu Lu, MMa, Xian-Wei Zhang, MMa, Xiao-Fen Tian, MMa

Received 7 June 2008; received in revised form 23 June 2008; accepted 24 July 2008.

Abstract 

The advantage of vasopressin over epinephrine in the treatment of cardiac arrest (CA) is still being debated, and it is not clear whether a high dose of vasopressin is beneficial or detrimental during or after cardiopulmonary resuscitation (CPR) in a rat model of CA. In this study, asphyxial CA was induced in 40 male Sprague-Dawley rats. After 10 minutes of asphyxia, CPR was initiated; and the effects of different doses of vasopressin (low dose, 0.4 U/kg; medium dose, 0.8 U/kg; and high dose, 2.4 U/kg; intravenous; n = 10 in each group) and a saline control (isotonic sodium chloride solution, 1 mL, intravenous) were compared. Outcome measures included the rate of restoration of spontaneous circulation (ROSC) and changes of hemodynamic and respiratory variables after ROSC. The rates of ROSC were 1 of 10 in the saline group and 8 of 10 in each of the 3 vasopressin groups. There were no differences in mean aortic pressure or changes of respiratory function after CPR among the vasopressin groups. However, the heart rate was lower in the high-dose vasopressin group than in the low- and medium-dose groups. These findings indicate that different doses of vasopressin result in a similar outcome of CPR, with no additional benefits afforded by a high dose of vasopressin during or after CPR, in a rat model of asphyxial CA. The mechanism and physiologic significance of the relative bradycardia that occurred in the high-dose vasopressin group are currently unknown and require further investigation.

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 grants from the Guangxi Natural Science Foundation (nos. 0640081 and 0718007B-41), PR China.

PII: S0735-6757(08)00556-1

doi:10.1016/j.ajem.2008.07.031


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