VPT 321: Veterinary Neuropharmacology (2+1)

MECHANISM OF ACTION OF BARBITURATES

• Bind to GABA receptors – increase the duration of Cl­^- channel opening – exert facilitation of GABA binding.
• At high concentration  directly increase Cl^- conductance and inhibit     Ca ⁺⁺ dependent release of neurotransmitters
• Also depress glutamate-induced action potentials
• At very high concentration affect K⁺ and Na⁺ channels

Pharmacology

• CNS – Depression ranging from mild sedation to anaesthesia
• Depression of motor areas leads  to control convulsions
• Depression of sensory areas leads to anaesthesia
• Subtherapeutic doses – hyperalgesia observed
• Respiration – slight depression. On intravenous administration it produces more severe depression than oral
  • Death in barbiturate overdose is due to severe depression of respiration
• Cardiovascular System – myocardial depression. Normal rhythm. Large doses results in  hemodilution,
• CVS effects depend on other co-drugs, eg. Acepromazine, dose of barbiturate and condition of the animal
• GI tract – Initial depression followed by  increase of tone and motility
• Kidney and liver – not significant. But metabolism and excretion affected if there is any defect in these organs
• Uterus – At anaesthetic doses – depress uterine contraction. Cross placenta and depress fetal respiration. Not preferred for caesarean sections. If it is to be done, surgery completed very quickly and respiration of young one stimulated to overcome depression
• Skeletal muscles – poor relaxation. Additional relaxants are needed