• R M Bednarski, R A Sams, L J Majors, and S Ashcraft.
• Department of Surgical Science, School of Veterinary Medicine, University of Wisconsin-Madison.
• Am. J. Vet. Res. 1988 Mar 1;49(3):350-4.

AbstractThe effect of ketamine administration on the ventricular arrhythmogenic dose of epinephrine (VADE) was studied in 4 halothane-anesthetized cats. Each cat was anesthetized 4 times, 1 week apart, with halothane (end-tidal concentration, 1.5%) and with halothane (end-tidal concentration, 1.5%) combined with ketamine infusion (50, 100, and 200 micrograms/kg of body weight/min). Epinephrine was infused in progressively increasing doses. The VADE (micrograms/kg) was calculated as the product of infusion rate of epinephrine and time of infusion necessary to induce 4 or more ventricular premature depolarizations within 15 s. The mean (+/- SD) VADE during halothane anesthesia was 1.1 (+/- 0.30) micrograms/kg. Ketamine infusion significantly (P less than 0.01) lowered the VADE independently of dose. The dose of epinephrine (micrograms/kg) that induced an ECG change in P-wave configuration was calculated similarly. Less epinephrine was necessary to induce a change in P-wave configuration than was necessary to induce 4 or more ventricular premature depolarizations within 15 s. Blood samples were collected after 4 hours of ketamine infusion and again immediately after determination of the VADE for analysis of plasma ketamine and norketamine concentrations by use of gas chromatography. Plasma ketamine and norketamine concentrations after a 4-hour infusion and immediately after determination of the VADE were similar for any given ketamine infusion rate, indicating that steady-state plasma concentrations had been reached for each infusion rate. Blood pressure and heart rate were measured immediately before (base line) and immediately after infusion of the VADE. Ketamine infusion significantly (P less than 005) lowered base-line blood pressure, but not heart rate.(ABSTRACT TRUNCATED AT 250 WORDS)

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