THE ARRHYTHMOGENIC DOSE OF EPINEPHRINE IN HALOTHANE AND ISOFLURANE-ANESTHETIZED DOGS - AN ASSESSMENT OF REPEATABILITY

Citation
G. Pettifer et al., THE ARRHYTHMOGENIC DOSE OF EPINEPHRINE IN HALOTHANE AND ISOFLURANE-ANESTHETIZED DOGS - AN ASSESSMENT OF REPEATABILITY, Canadian journal of veterinary research, 61(3), 1997, pp. 221-226
Citations number
39
Categorie Soggetti
Veterinary Sciences
ISSN journal
08309000
Volume
61
Issue
3
Year of publication
1997
Pages
221 - 226
Database
ISI
SICI code
0830-9000(1997)61:3<221:TADOEI>2.0.ZU;2-6
Abstract
Repeat determinations of the arrhythmogenic dose of epinephrine (ADE) were made over two 6 h periods on 2 separate days during halothane and isoflurane anesthesia. Each of 6 dogs underwent 4 trials (2 halothane and 2 isoflurane). During each trial, the ADE was determined at basel ine, 3 and 6 h. Epinephrine was infused for 3.0 min at increasing dose rates (2.5, 5.0, 10.0 and 20.0 mg/kg/min) until the arrhythmia criter ion (4 or more intermittent or continuous premature ventricular contra ctions) was reached. The inter-infusion interval was 20 min. There wer e no significant differences in the measured cardiovascular parameters (SBP, DBP, MBP, and HR), arterial blood gases, or acid-base status pr ior to each determination during a single trial. The cardiovascular re sponses to epinephrine infusion were not significantly different betwe en inhalants or determinations. The range of the ADE determined over b oth trials during isoflurane anesthesia was 30.12 +/- 12.21 mu g/kg to 50.83 +/- 9.17 mu g/kg. The baseline ADE during Day 1 of halothane an esthesia (6.70 +/- 1.36 mu g/kg) was significantly greater than ADE de terminations at 3 (4.65 +/- 0.88 mu g/kg) and 6 h (4.61 +/- 0.87 mu g/ kg). The reduction in the ADE over time during day 2 of halothane anes thesia was not statistically significant (P = 0.0669). These results s uggest that during halothane anesthesia, the ADE is not repeatable ove r time, and they may influence our interpretation of the results of in vestigations that measure alterations in the ADE due to pharmacologica l manipulations without repeated control ADE determinations.