Feng-Qing Song

Naloxone and epinephrine are equally effective for cardiopulmonary resuscitation in a rat asphyxia model

Background:  It is not known whether naloxone is as efficacious as epinephrine during cardiopulmonary resuscitation (CPR). The aim of the study was to compare the effects of naloxone and epinephrine on the outcomes of CPR following asphyxial cardiac arrest in rats.

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

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.

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

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.

Tea polyphenols alleviate oxidant injury following CPR in an asphyxia rat model

Background Cerebral ischemia/reperfusion injury following cardiac arrest and cardiopulmonary resuscitation (CPR) have been demonstrated. Oxidant injury plays a critical role in the process. We have reported that tea polyphenols from green tea improved the survival time and neurological deficit score of CPR in an asphyxia rat model. However, whether it acts via preventing the oxidising reaction by its phenolic hydroxyl group combined of oxygen free radicals and lipid peroxides in this model remains unknown. Therefore, we hypothesised that tea polyphenols would counteract the oxidant injury. Methods Male Sprague–Dawley rats, weighing 200–400 g, were induced cardiac arrest by clamping the trachyeal tubes. At the end of 8 min of clamping, mechanical chest compression at a rate of 180/min was performed. Ventilation was started with room air at 70 breaths per min and tidal volume adjusted to 6 ml. Epinephrine was administered at 1 min of CPR. Animals were randomly treated with either saline (n=52, Sal-gro) or 10mg/kg tea polyphenols (n=24, TP-gro) following ROSC. Animals in the sham control group (n=15, Con-gro) were only treated with anesthesia, and underwent surgical operation. Each group was divided into 3 groups according to the 12h, 24h, 48h points with five rats respectively. The changes of Superoxide Dismutase (SOD), Malondialdehyde (MDA) in serum were assayed. Results There were no significant differences in regard to hemodynamics among three groups before asphyxia. Time from the initiation of asphyxia to cardiac arrest and the duration of CPR were not significant among the groups. However, SOD of serum at 12h, 24h, 48 h following ROSC was significantly higher in TP-gro than in sal-group (p<0.05), the level of serum MDA at each point following ROSC was significantly lower in TP-gro than in that of sal-gro (p<0.05). Conclusion Tea ployphenols alleviated oxidant injury following CPR in an asphyxial rat model.