The sedative and some physiological effects of iv romifídine at 120 μg/kg bwt were compared with the same dose administered subcutaneously (sc) and an iv placebo in 12 clinically normal adult beagle dogs in a blinded randomised change-over study. Following iv romifídine, the dogs became recumbent and there was an increase in a subjective score awarded to the degree of sedation. Heart rate and respiratory rate decreased and minor bradyarrhythmias were noted. When romifídine was given sc the onset of sedation was slower, and the magnitude of the sedative effect was less until 30 min after administration, after which time sedation was no different between the 2 routes of administration. Recovery from sedation was similar following either route. Heart rate and respiratory rate changes were similar with either route although respiratory rate decreased more quickly following iv romifídine. It appears therefore that, in dogs, romifídine is equally efficacious by either iv or sc routes.
To assess the effects of medetomidine, an α2-adrenoceptor agonist, on cardiac function, radionuclide ventriculograms (RNV) were performed in 7 normal anesthetised cats before and after im administration of the drug. Ejection fraction (EF), peak ventricular ejection rate (PVER), peak ventricular filling rate (PVFR), time to peak ejection (TPE) and time to peak filling (TPF) were determined. Medetomidine caused significant reductions in EF (baseline 55.0 ± 10.8%, post medetomidine 43.3 ± 10.7%), PVER (baseline 4.38 ± 0.83 EDV/s, post medetomidine 3.28 ± 0.73 EDV/s) and PVFR (baseline 4.46 ± 1.42 EDV/s, post medetomidine 3.05 ± 1.27 EDV/s). There was also a significant decrease in heart rate following medetomidine administration (baseline 115 ± 27.2 bpm, post medetomidine 100 ± 21.2 bpm). The TPE and TPF did not change significantly following medetomidine. The observed decrease in cardiac function may have been caused by a drug-induced increase in systemic vascular resistance, and the bradycardia due to central nervous system depression.
Haemodynamic variables, with emphasis on right ventricular (RV) contractility, were measured in horses prior to, during and following anaesthesia with xylazine/ketamine. In an attempt to elicit mechanisms of anaesthetic-induced alteration of myocardial function, serum ionised and total calcium concentrations were also measured. Xylazine caused decreased cardiac function, including RV contractility, that was not reversed immediately by ketamine but was insignificant from pre-anaesthetic baseline by recovery (45 min following induction). Serum ionised and total calcium concentrations did not change.
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