Thirty-six female dogs undergoing ovariohysterectomy were randomly allocated into three groups in this assessor-blinded study. The control group received no ketamine, the preketamine group were given ketamine (2.5 mg kg(-1)i.m.) at anaesthetic induction (in addition to the induction agents), the post-ketamine group received ketamine (2.5 mg kg(-1)i.m.) at extubation. Mechanical nociceptive thresholds and visual analogue scale (VAS) scores were measured before premedication and post-operatively at 20 minutes, 1, 2, 4, 8 and 18 hours after extubation. Dogs in the control group required more rescue analgesics than those in the other two groups (significantly more than the preketamine group), they also had consistently higher VAS pain scores throughout the post-operative period. Administration of ketamine post-operatively delayed the onset of post-operative wound hyperalgesia; dogs in the control group had the greatest amount of post-operative wound hyperalgesia. A single subanaesthetic dose of ketamine provided effective but short acting analgesia and preoperative administration may confer some benefits over administration post-operatively.

Copyright 2000 Harcourt Publishers Ltd.
Publication Types: Clinical Tria, Randomized Controlled Trial
PMID: 11020366 [PubMed - indexed for MEDLINE]

In addition to its use for intravenous (I.V.) anesthesia, ketamine can provide pain relief in humans when administered spinally. To elucidate the mechanisms of intrathecal (I.T.) ketamine analgesia, we observed differences in the effects of I.V. and I.T. ketamine on intraspinal evoked potentials (ISEPs) in 28 dogs anesthetized with pentobarbital. Bipolar extradural electrodes were inserted at the cervical and lumbar regions of the spinal cord for recording descending ISEPs represented by the two negative deflections, Waves I and II. I.V. ketamine 2 and 10 mg/ kg did not affect the amplitude and latency of Wave I, whereas the large dose (10 mg/kg) significantly decreased the amplitude but not the latency of Wave II. I.T. ketamine 1 and 5 mg/kg caused significant dose-dependent decreases in both Wave I and II amplitudes and prolongations of both Wave I and II latencies. These I.T. effects on ISEPs are consistent with previous in vitro observations that ketamine blocks axonal conduction. We conclude that axonal conduction block may contribute to the analgesic mechanism of I.T. ketamine.

PMID: 9212131 [PubMed - indexed for MEDLINE]

BACKGROUND: Tissue damage may produce hyperalgesia, allodynia, and persistent
pain. The authors recently reported that fentanyl elicits analgesia but also activates N-methyl-D-aspartate-dependent pain facilitatory processes opposing analgesia. In nonsuffering rats, this leads to a long-lasting enhancement in pain sensitivity. The current study assessed whether fentanyl could amplify carrageenan-induced hyperalgesia.
METHODS: First, rats were injected once with carrageenan in a hind paw, with fentanyl (60 or 100 microg/kg each given four times at 15-min intervals [4 x 60 or 4 x100]) or saline. Second, rats were injected with carrageenan twice without fentanyl (7-day interval), with the
second injection either in the previously injected paw or in the other paw. Third, rats were injected twice with carrageenan in the same hind paw: the first ketamine injection was given (10 mg/kg each given three times at 5-h intervals) with or without fentanyl (4 x 60 microg/kg), and second injection was given without ketamine or fentanyl. The consequences of treatments on long-term hyperalgesia were examined by the paw-pressure vocalization test.
RESULTS: The long-lasting hyperalgesia induced by the first carrageenan injection was
dose-dependently enhanced in both duration and magnitude in 4 x 60 or 4 x 100 microg/kg fentanyl-treated rats: 5 or 10 days, respectively, as compared with 2 days in saline-treated rats. Hyperalgesia observed in the hind paw contralateral to the first carrageenan injection was enhanced in fentanyl-treated rats. The second carrageenan injection, performed in any hind paw, induced an exaggerated hyperalgesia, especially in fentanyl-treated rats. Pretreatment with ketamine totally prevented the carrageenan- and fentanyl-induced enhancement of the long-lasting hyperalgesia.
CONCLUSION: Central sensitization in inflammatory pain states is reinforced by an opiate treatment, which could be prevented by N-methyl-D-aspartate receptors blockade.


PMID: 11818772 [PubMed - indexed for MEDLINE]