Journal of Veterinary Anaesthesia最新文献

Glycopyrrolate (GLY) is a synthetic quaternary ammonium anticholinergic compound which offers a number of advantages over atropine, including less arrhythmogenic influence and lack of significant effect upon the central nervous system, eyes and foetus. Five healthy horses (7.4 ± 2.2 years, 462 ± 31.7 kg) were administered 2.5, 5 and 10 μg/kg doses of GLY iv in a randomised and blinded manner with at least 48 h between treatments. The electrocardiogram and heart rate were recorded on an oscilloscopic and chart recorder while gastrointestinal (GIT) motility was assessed by auscultation of 4 abdominal quadrants, assigning a subjective score from 0 (no motility) to 4 (normal motility). Heart rate, which was observed at baseline, 2, 5, 10, 15, 30 min, and 1, 2, 3, 4, 6, 9, 12, 18 and 24 h post GLY, revealed no change with the 2.5 μg/kg dose, and an increase with 5 μg/kg (59%) and 10 μg/kg (109%) for up to 1 h. The 2.5 and 5 μg/kg doses did not prevent the development of second degree atrioventricular block in some horses for up to 15 min, while the 10 μg/kg dose eliminated any pre-existing block within 5 min. There was a complete loss of GIT motility with the 5 and 10 μg/kg doses and partial loss with the 2.5 μg/kg dose. Subsequent return of motility was apparently dose-dependent with 50% of baseline motility score returning in 2.4, 6.4 and 11.5 h with 2.5, 5 and 10 μg/kg doses, respectively. Two horses receiving a 10 μg/kg dose developed abdominal discomfort. Passage of faeces and appetite were not significantly different with any dose. Glycopyrrolate did not induce any change in the pupillary response to a light source at any stage of observation. The results of this study indicate that 5 μg/kg induces a reasonable increase in heart rate without affecting GIT motility for an excessive length of time in awake, healthy, adult, unsedated horses.

Inhalational anaesthetics potentiate neuromuscular blocking drugs. The exact sites are not known, but may include the central nervous system, the neuromuscular junction or muscle. Anaesthetic action in the brain could potentiate neuromuscular block directly, or indirectly by altering plasma catecholamine concentrations.

In 5 goats anaesthetised with fentanyl and pentobarbitone, an experimental preparation was used in which isoflurane (end-tidal/exhaust 1.2–1.3%) was selectively delivered to either the torso (via the lungs) or brain (via an oxygenator/roller pump) during a stable ≅60% metocurine blockade (≅= 4–8 μg/min). Bilateral evoked gastrocnemius muscle twitch was accomplished with electrical stimulation (0.1 Hz) of the sciatic nerves, one of which was cut proximal to the stimulation site; output from the force transducer was digitised and stored on a computer. Blood samples were taken for metocurine, noradrenaline and adrenaline analysis.

When isoflurane was added to the brain, % depression of the muscle twitch was unchanged at 64 ± 13% on the uncut side; the cut side was also unchanged. When isoflurane was added to the torso, % depression increased from 68 ± 14% to 82 ± 12% (P < 0.05) on the uncut side and from 68 ± 8% to 81 ± 5% on the cut side (P < 0.05). Metocurine concentration in the torso decreased slightly when isoflurane was added to the torso (133 ± 19 ng/ml to 121 ± 18 ng/ml, P < 0.05) and increased slightly when isoflurane was added to the head (116 ± 31 ng/ml to 136 ± 31 ng/ml, P < 0.05). There were no significant changes in noradrenaline or adrenaline concentrations.

These data suggest that the periphery (neuromuscular junction or muscle) is the important site where isoflurane potentiates metocurine-induced neuromuscular blockade.