Page 566 - WSAVA2018
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  Extinguish Wind
 GV-14
  Extinguishes interior Wind
 GV-16
   Extinguishes both interior and exterior Wind
   GB-20
  Extinguishes Wind and subdues Yang
   BL-17
 Influential point for Blood; activates Blood to dispel Wind
 SP-10
  Sea of Blood; activates Blood to dispel Wind
 Da-feng-men
   Classical point for Wind pattern
  Calm the Shen
  GV-20
 Calms Mind, extinguishes interior Wind, subdues Liver Yang
 HT-7
   Calms Mind and opens the Mind’s orifices
   An-shen
 Classical point for calming the Mind
 Nao-shu
   Brain association point for calming the brain
  Transform Phlegm
  ST-40
 Resolves Phlegm and opens the Mind’s orifices
 Special point
  GV-1
   Opens Mind’s orifices and extinguishes interior Wind
  During seizure
   GV-26
  Opens Mind’s orifices, extinguishes interior Wind, promotes consciousness
   Notes: Additional acupoints based on pattern diagnoses as follows:
1. Wind-Phlegm: BL-20, BL-21, ST-36
2. Phlegm-Fire: LIV-2, ST-36, Wei-jian
3. Blood Stagnation: LI-4, GB-41
4. Yin-Blood Deficiency: BL-23, LIV-8, SP-6, KID-3
     564
25-28 September, 2018 | Singapore
WSV18-0292
WSAVA GLOBAL PAIN
INJECTABLE AND ORAL TRAMADOL FOR PAIN CONTROL
L.N. Warne1
1College of Veterinary Medicine, Murdoch University, Western Australia
Tramadol, a synthetic racemic mixture of the 4-phenyl- piperidine analogue of codeine, has received widespread acceptance in human medicine since it was first introduced in 1977 in Germany. Its efficacy
is attributed to a dual mechanism of action, namely,
the interaction with μ opioid receptors and the monoaminergic effect on spinal pain modulation
through inhibition of the reuptake of norepinephrine
and serotonin. Tramadol does not have δ or κ opioid receptor affinity but its affinity for μ receptors is approximately 10 times less than codeine and 6000 times less than morphine. The (+) enantiomer of tramadol has a low affinity for μ receptors, inhibits the cellular reuptake of serotonin (5-hydroxytryptamine, 5-HT) and increases its extracellular release. The (-) enantiomer more effectively inhibits norepinephrine reuptake and increases its cellular release. Inhibition of norepinephrine reuptake leads to activation of the descending pain inhibitory system, causing inhibition of the transmission of painful stimuli through the dorsal horn of the spinal cord via endogenous opioids. The opioid receptor- associated analgesic efficacy of tramadol depends on the ability of the individual to convert the drug by P450 enzymes in the liver to the main active M1 metabolite, O-desmethyltramadol (ODM), with 86% to 100% of the drug and its derivatives being excreted through the
renal system. In humans, some individuals are unable
to convert tramadol to its metabolites efficiently due
to a P450 enzyme deficiency. The inability to produce tramadol metabolites results in decreased serum levels concentrations of ODM and consequently a significantly reduced analgesic effect of the medication. Dogs have
a low capacity to produce this active metabolite, which might be breed or individual dependent.(1-3) Therefore dogs are not expected to have substantial opioid
effects after tramadol administration. Repeated doses of tramadol either decreased drug absorption or enhanced presystemic metabolism of tramadol in dogs, in which a 60% to 70% decrease in tramadol plasma concentrations resulted after just eight days of treatment (20 mg/kg
by mouth).(4) The effects of multiple-day administration on the tramadol metabolites has not been reported. In contrast with dogs, cats produce high concentrations of ODM after tramadol administration and as a result have prominent opioid effects.(5) The concentrations
of ODM after 5.2 mg/kg tramadol by mouth were 10 times higher than ODM concentrations in humans after 100 mg by mouth. The terminal half-life of ODM after
43RD WORLD SMALL ANIMAL VETERINARY ASSOCIATION CONGRESS AND 9TH FASAVA CONGRESS











































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