| Background and objectiveCardiopulmonary resuscitation (CPR) is an effective treatment for the victims of cardiac arrest (CA). Administrating constrictive vasoactive substances during CPR can increase the restoration of spontaneous ciuculation (ROSC). Epinephrine treated during CPR increases ROSC. However, because the effect of (3 receptor increases myocardial oxygen consumption, aggravates post-resuscitation myocardial dysfunction, shortens survival time. Vasopressin, as one of non-adrenergic receptor agonist, admistrated during CPR, can increase ROSC as well. And since it has noβadrenergic effect, it may be beneficial to long survival. However, the outcomes of studies about vasopressin admistrated during CPR are controversial. There are not enough evidences to prove vasopressin can substitute epinephrine during CPR.Based on the above reasons, this study was to testify if epinephrine is superior to vasopressin during CPR in a mouse CA model and find the ideal dose of epinephrine in this mouse CA model. Furthermore, this study was to investigate the beneficial or side effect of epinephrine during a rat VF model and if hypothermia could counteract or alleviate the side effect of epinephrine during CPR and post-resuscitation.Methods:1. Transoesophageal cardiac pacing was performed so as to elicit cardiac arrest in Kunming male mice. The first, we compare the effect of epinephrine and vasopressin in a mouse CA model:30 mice were rancomized into three groups (n=10/group) and received saline (Sal-gro,0.2ml i.a.), vasopressin (Vas-gro,0.4U/kg i.a.) and epinephrine (Epi-gro,0.04mg/kg i.a.). The second, we compare the effect of different doses of epinephrine in this model:40 mice were randomized to 4 group (n=10/group):received saline (Sal-gro,0.2ml i.a.) or epinephrine 0.02mg/kg (low-dose, Lepi),0.04mg/kg (midium-dose, Mepi) and 0.2mg/kg (high-dose, Hepi) i.a respectively. The main measurements were the rate of ROSC, changes of respiration after resuscitation and survival time.2. Ventricular fibrillation (VF) was induced with increases in current delieved to right ventricular endocardium in rats. At the 8 min of VF, CPR was performed with ventilation for 8 min. Epinephrine (0.02mg/kg, Epi-gro, n=8) or saline (control group, Con-gro, n=8) were admistrated 3 min prior to defibrillation to investigate the benificial or side effect of epinephrine in a rat VF model. Measurements including CPP, PetCO2, and the number of defibrillations, the rate of ROSC, myocardial function and survival time were observed.3. VF was induced with increases in current delieved to right ventricular endocardium in 32 rats. At the 8 min of VF, animals were randomized to four groups:normothermic control control group (Con), normothermic epinephrine group (Epi), hypothermic control group (H+Con) and hypothermic epinephrine group (H+Epi). CPR then was started with ventilation for 8 min. Epinephrine or saline were admistreated 3 min prior to defibrillation. In normothermic group, temperature was maintain to 37.0±0.2℃with a heat lamp untile 4 hours after ROSC. While in hypothermic groups, hypothermia was induced with ice packs and a fan to 34±0.2℃when epinephrine was given and to 32±0.2℃when defibrillation was attempted. After 4 hours of ROSC, animals were rewarmed to 37.0±0.2℃with heat lamp for 2 hours. Animals were mornitored for 4 hours after ROSC to investigate the effect of ephnephrine during hypothermic CPR in a rat VF model. Measurements including the rate of ROSC, myocardial function, the changes of ECG and survival time were observed.Results:1. Rates of ROSC in Vas-gro and Epi-gro were significantly higher than in Sal-gro (9/10,10/10 vs 3/10, P<0.05,P<0.01 respectively). All resuscitated mice treated with 0.04mg/kg epinephrine restored spontaneous breathing while 4 of 9 animals with 0.4U/kg vasopressin (P<0.05). Survival time in Epi-gro was longer than that in Vas-gro or in Sal-gro (P<0.05, P<0.05 respectively).Rates of ROSC in different doses of Epi-gro were significantly higher than in Sal-gro (9/10,10/10,10/10 vs 3/10, P<0.05, P<0.01, P<0.01, respectively). With increasing dosage of epinephrine, the number of mice which could be withdrawn the ventilatior decreased. Survival time of 0.02mg/kg epinephrine group was longer than that of other groups (P<0.05).2. Epinephrine increased CPP (P<0.001), decreased PetCO2 (P<0.001). Number of defibrillation was less in Epi-gro during CPR than that of Con-gro (1±1 vs 4±2, P<0.05). All of Epi-gro animals were resuscitated while 5 of Con-gro animal did. Myocardial dysfunction was more severely in Epi-gro after 1h of ROSC than that of Con-gro (P<0.01). Survival time was shorter in Epi-gro than that of Con-gro (P<0.05).3. Epinephrine increased CPP either in normothermic group or in hypothermic group. Except for three animals in the control group, all the animals were successfully resuscitated. Heart rate was lower in hypothermic groups after ROSC than that in normothermic groups (P<0.01). Myocardial dysfunction including EF and CO, was improved after epinephrine was administrated in hypothermia than normothermia (72±2%and 109±15ml/min, vs 41±7% and 61±10ml/min, P<0.05 respectively). ST elevation was lower in hypothermic groups than that in normothermic groups (P<0.05). Animals in hypothermic groups survived more than 3 months while 1 of 8 in normothermic epinephrine group and none in normothermic control group survived for 3 months (P<0.01).Conclusion:1. Both vasopressin and epinephrine increased the rates of ROSC in mice. High dose of epinephrine had no facilitation of the restoration of respiration following ROSC and consequently shortened the survival time.2. Epinephrine increased the rate of ROSC in VF rats under the condition of normothermia, however, it resulted in venous admixture, decreased PetCO2, and aggravated myocardial dysfunction, shortened the survival time.3. Hypothermia partly alleviated the side effect of epinephrine during CPR and improved the myocardial and cerebral function and prolonged the survival time in the rat VF model.
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