Peter R Chai1, Jason B Hack2. 1. Division of Medical Toxicology, Department of Emergency Medicine, University of Massachusetts Medical School, Worcester, MA 01655. 2. Department of Emergency Medicine, Alpert Medical School at Brown University/Rhode Island Hospital, Providence, RI 02903. Electronic address: Jason_hack@brown.edu.
Abstract
CONTEXT: Intravenous lipid emulsion (ILE) is a potential antidote for severe overdose of certain lipophilic drugs. Cocaine overdose is often fatal and has no antidote. The use of ILE after cocaine-induced cardiac arrest has been suggested but is not well characterized. OBJECTIVE: The objective of the study is to determine if ILE would reverse cocaine-induced cardiac arrest in a rat model. MATERIALS AND METHODS: Twelve Sprague-Dawley rats with intra-arterial and intravenous access were sedated with isoflurane and split into 2 cocaine dose groups, then given either ILE or normal saline (NS) intravenously (IV)-group A, 7 animals received cocaine (10 mg/kg IV) with 6 of 7 given ILE (15 mg/kg IV) and 1 of 7 given NS (equal volume); group B, 5 animals received cocaine (5 mg/kg IV) with 3 of 5 given ILE (15 mg/kg IV) and 2 of 5 given NS (equal volume). Closed chest compressions were initiated for asystole and continued for 15 minutes with rhythm checks every minute. RESULTS: All 12 rats experienced cardiac arrest after cocaine bolus. Resuscitation was successful in 1 of 7 rats in group A and 0 of 5 in group B. CONCLUSIONS: Intravenous lipid emulsion administration did not affect outcome of cocaine-induced cardiac arrest compared with control in this model.
CONTEXT: Intravenous lipid emulsion (ILE) is a potential antidote for severe overdose of certain lipophilic drugs. Cocaineoverdose is often fatal and has no antidote. The use of ILE after cocaine-induced cardiac arrest has been suggested but is not well characterized. OBJECTIVE: The objective of the study is to determine if ILE would reverse cocaine-induced cardiac arrest in a rat model. MATERIALS AND METHODS: Twelve Sprague-Dawley rats with intra-arterial and intravenous access were sedated with isoflurane and split into 2 cocaine dose groups, then given either ILE or normal saline (NS) intravenously (IV)-group A, 7 animals received cocaine (10 mg/kg IV) with 6 of 7 given ILE (15 mg/kg IV) and 1 of 7 given NS (equal volume); group B, 5 animals received cocaine (5 mg/kg IV) with 3 of 5 given ILE (15 mg/kg IV) and 2 of 5 given NS (equal volume). Closed chest compressions were initiated for asystole and continued for 15 minutes with rhythm checks every minute. RESULTS: All 12 rats experienced cardiac arrest after cocaine bolus. Resuscitation was successful in 1 of 7 rats in group A and 0 of 5 in group B. CONCLUSIONS: Intravenous lipid emulsion administration did not affect outcome of cocaine-induced cardiac arrest compared with control in this model.