Background The optimal goal of naloxone infusion in intensive care units is to ameliorate opioid-induced side effects in therapy or eliminate the symptoms of opioid toxicity in overdoses. Accurately monitoring and regulating the doses is critical to prevent adverse effects related to naloxone administration. The present study aimed to compare treatment outcomes when using two methods of intravenous naloxone infusion: an infusion pump or the standard method. Methods: This study involved 80 patients with signs and symptoms of opioid overdose. The patients were randomly assigned into two groups with respect to intravenous infusion of naloxone by either an infusion pump or the standard method. Results: Comparison of study parameters between the two groups at 12 and 24 hours after intervention showed significantly more compensatory acid-base imbalance in the naloxone infusion pump group. In the group that received naloxone by pump, only one patient experienced withdrawal symptoms, but withdrawal symptoms appeared in 12 patients (30.0%) in the standard intravenous infusion group within 12 hours and in seven additional patients (17.5%) within 24 hours of intervention. In the group receiving pump-based naloxone infusion therapy, no another complications were reported; however in the standard infusion group, the 12-hour and 24-hour complication rates were 55.0% and 32.5%, respectively. The length of hospital stay was 2.85±1.05 and 4.22±0.92 days for the pump and standard infusion groups, respectively (P<0.001). Conclusions: Naloxone infusion using an infusion pump may be safer with regard to hemodynamic stability, resulting in shorter hospitalization periods, and fewer posttreatment complications.
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BACKGROUND Naloxone,an opioidant agonist, has been s hown t o have a c ar di ovascular pressor effect in states of hemorrhagic and endotoxic shock.We determined the direct inotropic effect of naloxone using guinea pig right ventricular papillary muscles. METHODS With institutional approval,isometric contractile force was measured in normal and 26mM K+ Tyrode's solution at various stimulation rates.Normal and slow action potentials (APs) were measured with conventional microelectrode technique.The effects of naloxone on sarcoplasmic recticulum function were evaluated by measuring rapid cooling contractures (RCCs)in normal Tyrode 's solution and rested-state (RS)contraction in low Na+ (25 mM)Tyrode's solution.Patch clamp study was performed to examine the direct effect on Ca2+ current in myocytes. RESULTS Naloxone (50,100,200 micro M)caused dose-dependent depression of peak force and maximal rate of peak force (dF/dt-max)by 30,50 and 70%,respectively.Modest depression was shown in RS contraction in low Na+ Tyrode's solution.In 26 mM K+ Tyrode's solution,100 micro M naloxone markedly depressed late force development.100 micro M naloxone depressed RCCs by 20%. While 100 micro M naloxone did not alter amplitude or dV/dt-max in normal and slow APs at 0.25 Hz, AP duration was prolonged significantly.In patch clamp study,50 micro M naloxone depressed Ca2+ current by 50%. CONCLUSIONS Naloxone depresses contractile force.Myocardial depressant effect partly seems to be caused by depressed Ca2+ influx through cardiac membrane.Rapid release of Ca2+ from the sarcoplasmic reticulum by depolarization and release by rapid cooling seems to be minimally affected.