Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0344307 (analgesia)
 28,200 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Sarapin is a distillate of the pitcher plant that has long been used in human and veterinary medicine for 'regional analgesia'. The mechanism of the reported analgesic response is unknown; however, the agent is purported to provide more effective analgesia for slow, chronic pain than for sharp, acute pain. Reportedly, Sarapin is also widely used as an analgesic agent in the horse, generally in combination with corticosteroids and other agents. To determine its local anaesthetic efficacy in the horse, we tested Sarapin in a unilateral abaxial sesamoid block model at two dose levels, 2 mL and 10 mL per site, respectively. Cutaneous pain was induced with a light/heat lamp, and analgesia was assessed by measuring the hoof-withdrawal reflex latency period. Neither dose of Sarapin altered hoof-withdrawal reflex latency in this experimental model tested over a two-week period. Based on the demonstrated efficacy of this local anaesthetic model, it seems clear that Sarapin has no significant classical local anaesthetic actions in the horse, and probably not in other species either.
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PMID:Lack of local anaesthetic efficacy of Sarapin in the abaxial sesamoid block model. 918 90

The objective of this study was to determine the effects of the alkalinization on the local analgesic efficacy of 1% ketamine in the abaxial sesamoid nerve block in horses. Thirty-six mature healthy horses were randomly assigned to four groups for the following treatments; an abaxial sesamoid block with 5 mL of saline solution (control saline); an abaxial sesamoid block with 5 mL of a solution containing 1% ketamine (KETs 1%); an abaxial sesamoid block with 5 mL of a solution containing saline solution and 0.5 mEq of sodium bicarbonate (control bicarbonate); and an abaxial sesamoid block with 5 mL of a solution containing 1% ketamine and 0.5 mEq of sodium bicarbonate (KETb 1%). All blocks were performed in one randomly selected front leg. To determine analgesia, hoof withdrawal from thermal stimulus from radiant heat lamp was assessed. Before each block, the hoof withdrawal reflex latency (HWRL) (time between lamp illumination and withdrawal of the hoof) was determined; after the block, local analgesic effects were determined using the heat lamp at 2 and 5 min after the injection and then every 5 min for 1 h. In KETs 1% group, there were significant increases in HWRL between basal values and values from 2 to 10 min after an abaxial sesamoid block. In KETb 1% group, significant increases in HWRL was collected between the basal value and values from 2 to 25 min following an abaxial sesamoid block. In KETs 1% group, of the nine horses, four had an abaxial sesamoid block that was unsuccessful. However, in KETb 1% group, only one of the nine horses had an abaxial sesamoid nerve block that was unsuccessful. The alkalinization of a 1% ketamine solution produced a more consistent and persistent local analgesia in horses when compared with 1% ketamine solution alone.
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PMID:Effect of alkalinization on the local analgesic efficacy of ketamine in the abaxial sesamoid nerve block in horses. 1288 8

Acute nociceptive models which have been validated for large animal species are limited, yet nociceptive assessment in non-rodent species is important in analgesic drug development where larger animals may be necessary because of the technical requirements of the study. Here we report development and validation of a canine hind paw thermal escape model and the effect of analgesics on withdrawal latencies. Individual focused projection bulbs were used as left and right voltage-adjusted thermal stimuli placed below a glass plate in a specifically designed canine holding apparatus. After acclimation, dogs were lightly restrained in a fabric sling while standing on the glass plate. The anterior center of the metatarsal pad of the left and right hind paw was positioned on the glass over each light, and duration of stimulation tolerance timed. For every trial, the escape latency from lamp actuation to paw withdrawal was recorded twice for each hind paw. The mean population baseline withdrawal latency of 9.3+/-1.7s (mean+/-S.D., n=12 dogs) was shown to be repeatable between paws, within and between individual animals, and between test days. This latency corresponded to a glass surface temperature of 49.5 degrees C. A cut-off time of 20s (corresponding to a glass surface temperature of 56.5 degrees C) was set to prevent tissue damage. Intravenous administration (mg/kg) of morphine (1.0), hydromorphone (0.2), butorphanol (0.4), fentanyl (0.01), and dexmedetomidine (0.01) significantly (p<0.05) increased withdrawal latency from baseline within 15-30 min of administration while buprenorphine (0.03) produced a delayed, modest but significant latency increase. Rank order of opioid analgesic duration was morphine=hydromorphone>butorphanol>bupenorphine>fentanyl=saline. A dose-effect curve for hydromorphone was generated and corresponded to previously described dose-effect relationships in other species. The non-analgesic tranquilizer acepromazine (0.1mg/kg) produced mild sedation, but no significant increase in latency from that of saline. The model yielded a clear distinction between analgesia and sedation for all agents tested. These studies provide validation of a canine thermal escape model and have demonstrated the efficacy of clinically relevant doses of analgesics in elevating escape latencies. This model will facilitate quantification of the effects of parenterally and neuraxially administered analgesics in dogs.
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PMID:Development of a canine nociceptive thermal escape model. 1805 83

Venom ophthalmia caused by venoms of spitting elapid and other snakes: report of ten cases with review of epidemiology, clinical features, pathophysiology and management. Chu, ER, Weinstein, SA, White, J and Warrell, DA. Toxicon XX:xxx-xxx. We present ten cases of ocular injury following instillation into the eye of snake venoms or toxins by spitting elapids and other snakes. The natural history of spitting elapids and the toxinology of their venoms are reviewed together with the medical effects and management of venom ophthalmia in humans and domestic animals including both direct and allergic effects of venoms. Although the clinical features and management of envenoming following bites by spitting elapids (genera Naja and Hemachatus) are well documented, these snakes are also capable of "spraying" venom towards the eyes of predators, a defensive strategy that causes painful and potentially blinding ocular envenoming (venom ophthalmia). Little attention has been given to the detailed clinical description, clinical evolution and efficacy of treatment of venom ophthalmia and no clear management guidelines have been formulated. Knowledge of the pathophysiology of ocular envenoming is based largely on animal studies and a limited body of clinical information. A few cases of ocular exposure to venoms from crotaline viperids have also been described. Venom ophthalmia often presents with pain, hyperemia, blepharitis, blepharospasm and corneal erosions. Delay or lack of treatment may result in corneal opacity, hypopyon and/or blindness. When venom is "spat" into the eye, cranial nerve VII may be affected by local spread of venom but systemic envenoming has not been documented in human patients. Management of venom ophthalmia consists of: 1) urgent decontamination by copious irrigation 2) analgesia by vasoconstrictors with weak mydriatic activity (e.g. epinephrine) and limited topical administration of local anesthetics (e.g. tetracaine) 3) exclusion of corneal abrasions by fluorescein staining with a slit lamp examination and application of prophylactic topical antibiotics 4) prevention of posterior synechiae, ciliary spasm and discomfort with topical cycloplegics and 5) antihistamines in case of allergic kerato-conjunctivitis. Topical or intravenous antivenom and topical corticosteroids are contraindicated. Clinical outcome of venom ophthalmia is largely dependent on prompt treatment and appropriate follow-up.
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PMID:Venom ophthalmia caused by venoms of spitting elapid and other snakes: Report of ten cases with review of epidemiology, clinical features, pathophysiology and management. 2033 93