| SubjectiveAs a local anesthetic of amide derivatives commonly used in the clinical pratice, Bupivacaine impressed people with its cardiovascular toxicity,but not with its long-acting effects.It's well known that bupivacaine-induced cardiac arrest is hard to resuscitate. so it is very important to known how to prevent and treat bupivacaine-induced cardiovascular toxicity.Epinephrine(Epi) is commonly used in the clinical emergency and cardiopulmonary resuscitation(CPR),now it is still the first choice for CPR. However,the use of epinephrine to treat bupivacaine-induced cardiovascular toxicity remains controversial. As a representative of Phosphodiesterase inhibitors(PDEIs), Milrinone is a non-catecholamine, non-glycoside,cardiotonic agent.It is reported that Milrinone owns the effects of reversing bupivacaine-induced cardiovascular toxicity. But how about the effecacy of Milrinone in reversing bupivacaine-induced cardiovascular toxicity when compared to that of Epinephrine? is it better? There exists no comparison study of the two until now.Therefore, the purpose of the study is to compare the efficacy of milrinone with that of epinephrine for the treatment of bupivacaine -induced cardiovascular toxicity in anesthesized canines, which will provide some helpful information for treating bupivacaine-induced cardiovascular toxicity in clinical practice.MethodsThe canines is divided into 3 groups randomly---milrinone group (Group M,n=9), epinephrine group(Group E,n=9) and control group (Group C,n=9).After anesthesized with pentobarbital,0.5% bupivacaine was infused at a rate of 0.5mg·kg-1·min-1 intravenously until mean arterial pressure (MAP) decreased to 40mmHg , which makes the bupivacaine cardiovascular toxicity model.In the Group M, a bolus dose of milrinone,50μg·kg-1 ( 50μg/ml),was given intravenously immediately after cardiovascular depression,followed by intravenously infusion at a rate of 0.5ug·kg-1·min-1(5μg/ml). In the Group E, a bolus dose of epinephrine,10μg·kg-1(10μg/ml),was given intravenously immediately after cardiovascular depression,followed by intravenously infusion at a rate of 0.03ug·kg-1·min-1 ( 0.3μg/ml).While in the Group C, isovolumetric saline was given at corresponding way. Watch closely and write down the hemodynamic parameters,HR,MAP,CVP and CO at the moment 1min,5min,10min,15min and 30min after the bolus dose of milrinone or epinephrine or saline.If the MAP≥65mmHg and maintains longer than 10 minutes after the administration of drug, we define as resuscitation success. During the 30 minutes'resuscitation,if the cardiac asystole remains or the MAP does not meet to the criteria of MAP≥65mmHg and maintains longer than 10 minutes,we define as resuscitation failure.At last, we compare the resuscitation efficacy of milrinone with that of epinephrine based on the survival rate,dysrhythmia and hemodynamic parameters,such as HR, MAP, CVP,CO,SV and SVR.ResultsAll nine dogs in Group C happened cardiac asystole, 7.5±2.1min after the infusion of bupivacaine stopped,and then died. All nine dogs in the Group M survived, none underwent dysrhythmia. In the Group E, five dogs suffered from severe ventricular dysrhythmia(one suffered ventricular fibrillation, four suffered tachycardia ), only one transverted to sinus rhythm 2 minutes later automatically, the other four happened cardiac asystole 12.3±3.8min after the infusion of bupivacaine stopped and died at the end. The differences in survival rate between the three groups are statistically significant(Group M vs Group C, P﹤0.0001;Group E vs Group C, P=0.019;Group M vs Group E, P=0.041,Fisher's exact test). the difference in dysrhythmia between Group M and Group E is also statistically significant (P=0.0147, Fisher's exact test).Moreover, HR, MAP, CO and SV increased steadily in Group M during the resuscitation, CVP and SVR decreased smoothly. while in Group E, there exists obvious fluctuation in MAP,CO and SV. ConclusionsMilrinone owns the effects of reversing bupivacaine-induced cardiovascular toxicity and is superior to epinephrine.
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