PubMed · 8907741
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D B Lott. 1996. Diazepam.. https://doi.org/10.1016/s0001-2092(06)63220-1
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The effects of intravenous administration of variable-dose midazolam (0, 0.05, 0.075, 0.1, 0.3 and 0.5 mg/kg) and ketamine (3 mg/kg) were studied in twenty-four healthy unmedicated cats from time of administration until full recovery. End-points were chosen to determine the optimal dose to allow a short period of restraint without noxious stimuli, a short period of restraint with noxious stimuli and endotracheal intubation. Recovery characteristics, as well as undesirable behaviours observed during recovery, were also recorded. The dose of midazolam to achieve lateral recumbency with head down was found to be 0.016 mg/kg in 50% of the population (ED50) and 0.054 mg/kg in 95% (ED95) of the population. A midazolam dose of 0.286 mg/kg was required to prevent conscious perception of a stimulus to the ulnar nerve in 50% of the population and 0.652 mg/kg in 95% of the population. The ED50 and ED95 of midazolam required to prevent swallowing in response to a laryngoscope placed on the back of the tongue were found to be 0.265 mg/kg and 0.583 mg/kg, respectively. The ED50 doses of 0.265 mg/kg for intubation and 0.286 mg/kg for restraint with noxious stimulation were close to the tested dose of 0.3 mg/kg. At that dose, the lack of responses lasted 3.67 +/- 2.27 min for laryngoscope and 2.50 +/- 2.20 min for ulnar nerve stimulation, with recovery to walking with ataxia taking 41.50 +/- 15.18 min and complete recovery taking 3.6 +/- 1.3 h. The predominant behavioural pattern during recovery was found to be normal, but some cats also exhibited abnormal behavioural patterns. Nine of the twelve cats exhibited an abnormal arousal state, with 4 being restless and 5 being sedated. Seven of the twelve cats exhibited an abnormal behaviour when approached, with three of the cats being more difficult to approach and four of the cats being easier to approach. Eight of the twelve cats exhibited an abnormal behavioural pattern when restrained, with the cats equally divided between more difficult and easier to restrain. Five of the twelve cats vocalized more during the recovery. The ED50 of 0.042 mg/kg to induce chemical restraint without a noxious stimulus is close to the tested dose of 0.05 mg/kg. At that dose, cats remained lateral with head down for 5.49 +/- 4.02 min, took 25.96 +/- 5.77 min to walk with ataxia and 1.7 +/- 0.4 h for complete recovery. The predominant behavioural patterns during recovery were normal, with several cats exhibiting some abnormal patterns. Two cats were sedated, one cat was more difficult to approach, one cat was easier to restrain and three cats were more vocal.
UNLABELLED: We studied the effect of preemptive intrathecal ketamine administration on the development of mechanical hyperalgesia in a rat model of mononeuropathy. Rats given intrathecal ketamine 1 mg/kg or normal saline were subsequently rendered neuropathic by placing four loose ligatures around the sciatic nerve. The onset of resultant hyperalgesia was evaluated using von Frey monofilaments. Preemptive ketamine significantly slowed the onset of mechanical hyperalgesia at both 2.35 g (P < 0.04) and 4.19 g (P < 0.05) thresholds through the third postoperative day but did not alter the ultimate degree of hyperalgesia in either severity or frequency in this model. We conclude that ketamine delayed the onset, but failed to prevent the development of, mechanical hyperalgesia in a rat model of peripheral mononeuropathy. IMPLICATIONS: Pain in response to light touch may follow nerve injury. Prevention of this complication would be clinically useful. Ketamine, an anesthetic, was administered spinally to rats before nerve injury in an attempt to prevent the development of chronic pain. Hypersensitivity to light touch was delayed by preemptive ketamine.
PURPOSE: Inhibition of the NMDA receptor likely contributes to ketamine's neurodepressive properties. Magnesium also inhibits the NMDA receptor by binding to a site associated with the ketamine-binding domain. Electrophysiological studies suggest that magnesium prevents ketamine from binding to the NMDA receptor and thereby prevents ketamine inhibition. We undertook an in vivo study to determine if magnesium deficiency was associated with an increased sensitivity to ketamine. METHODS: Weanling rats were maintained on a Mg(2+)-deficient or control diet for 14 days. In Study I, rats were anaesthetized then sacrificed and the Mg2+ concentrations in the brain and plasma were measured. In a second prospective study, experimental animals were rendered hypomagnesaemic and the potency of 125 mg.kg-1 ip ketamine was evaluated. Animals were then were fed a Mg(2+)-containing diet and ketamine sensitivity was re-examined 14 days later. RESULTS: The Mg(2+)-deficient diets rendered the rats hypomagnesaemic as indicated by the brain and plasma concentration of Mg2+. In Study 2, the time to loss of righting reflex was shorter; 1.9 +/- 0.3 min (n = 12) and 2.6 +/- 0.2 min (n = 16, P < 0.05), whereas the latency to toe pinch was prolonged: 25.0 +/- 5.8 min (n = 12) vs 3.1 +/- 2.1 min (n = 16, P < 0.05) in the Mg(2+)-deficient compared with age-matched control animals, respectively. The hypomagnesaemic animals had a higher death rate following ketamine injection. The increased sensitivity to ketamine was no longer apparent when the animals were re-tested following replenishment of Mg2+. CONCLUSION: Hypomagnesaemia is associated with an increased sensitivity to ketamine.