4.3 Non-steroidal Anti-inflammatory Drugs
The use of NSAIDs, initially in the form of plant extracts (e.g. willow bark), for
reducing inflammation and treatment of pain in man has a long history. Similarly
there have been reports on the use of salicylates in dogs and horses for many years
(Abbitt et al. 1978 ). Their use in domestic animals was mainly associated with the
treatment of musculo-skeletal pain and the alleviation of arthritic pain and this use
is still significant today.
Before 1971 the mechanism of action of the NSAIDs was poorly understood
(Vane 1971 ); however, in the decades since, many of the molecular mechanisms
have been elucidated (Simmons et al. 2004 ). In contrast with most other analgesic
agents which act on neurotransmitter receptors involved in nociceptive pathways,
NSAIDs are enzyme inhibitors and have somewhat different pharmacological
properties. The NSAIDs available today range from acetylsalicylic acid to the
COX-2 selective coxibs. Moreover, the development of more potent agents that
inhibit both cyclo-oxygenase (COX)-1 and COX-2, and the increased focus on
COX-2 selective inhibitors, has led to their additional use prophylactically for the
prevention of peripheral pain sensitisation, as well as the provision of long-term
primary analgesia. There is also increasing evidence that NSAIDs can exert anal-
gesic effects in the central nervous system in addition to their peripheral effects
(Dolan et al. 2003 ). The factors associated with the generation of NSAID suscep-
tible pain have been widely investigated and described (Lees et al. 1991 ) and are
generally accepted as being attributable to the inhibition of prostaglandin produc-
tion and hence the prevention of neuronal sensitisation by these eicosanoids.
However, some NSAIDs additionally inhibit leukotriene production (Dawson
et al. 1982 ) and, although it is now thought that this mechanism does not apply to
the classical NSAIDs, drugs such as tepoxalin and licofelone inhibit COX,
5-lipoxygenase and cytokine synthesis (Ritchie et al. 1995 ). In addition, drugs
that augment the release of nitric oxide as well as inhibiting COX have been
developed as novel analgesic agents (Wallace et al. 1994 ).
Table 4Doses and intervals for opioids in farm animals
Drug Sheep Goat Pig Horse
Buprenorphine
6–12 h
0.005–0.01 0.005 0.005–0.05 0.004–0.006
Butorphanol
3–8 h
0.5 0.5 0.1–0.3 0.05–0.1
Meperidine
(Pethidine)
2–4 h
2–21–2
Morphine
2–4 h
0.2–0.5 0.2–0.5 0.2–1 0.1
All doses are in mg/kg for subcutaneous or intramuscular injection.
Data from Flecknell ( 1996 ); Thurman et al. ( 1996 ); Wolfensohn and
Lloyd ( 1998 ); Dobromylskyj et al. ( 2000 )
178 A. Livingston