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  • Uncomplicated premature labour
  • IM
  • IV
  • Oral
  • By intravenous infusion
    • initially 50 micrograms/minute
    • increased gradually according to response by 50 micrograms/minute every 10 minutes until contractions stop or maternal heart rate reaches 140 beats per minute
    • continue for 12–48 hours after contractions cease (usual rate 150–350 micrograms/minute)
    • max. rate 350 micrograms/minute
  • By intramuscular injection
    • 10 mg every 3–8 hours continued for 12–48 hours after contractions have ceased
    • then by mouth, 10 mg 30 minutes before termination of intravenous infusion, repeated every 2 hours for 24 hours, followed by 10–20 mg every 4–6 hours
    • max. oral dose 120 mg daily

  • Tocolytic
  • Uterine smooth muscle (myometrium) has beta-receptors on its membrane.
    • As with airway smooth muscle, treatment with beta-agonists relaxes its tone and inhibits its contractions.
    • Stimulation of beta-receptors activates the enzyme adenyl cyclase which converts ATP to cyclic-AMP.
    • Cyclic AMP, in turn, activates another enzyme, protein kinase A, that phosphorlyates K+ channels in the myometrial membrane and so opens them
    • Increased K+ permeability stabilises the membrane potential, thereby preventing action potentials and uterine contraction.
  • Selectivity
    • Has a bulky N-substituent => high β2-selectivity
    • Also, the 4'-hydroxy on the benzene ring is important for activity as it is needed to form hydrogen bonds
      • However, the 4'-hydroxy makes it susceptible to metabolism by catechol-O-methyl transferase (COMT)
    • Since it is β2-selective it is used for premature labor

Side effects
  • Concurrent beta-1 activity
    • => increase in heart rate, rise in systolic pressure, decrease in diastolic pressure, chest pain secondary to MI, and arrhythmia.
  • May also cause fluid retention secondary to decrease in water clearance
    • when added to the tachycardia and increased myocardial work may result in cardiac failure
  • In addition, they increase gluconeogenesis in the liver and muscle resulting in hyperglycemia, which increases insulin requirements in diabetic patients
  • The passage of beta-agonists through the placenta does occur and may be responsible for fetal tachycardia, as well as hypoglycemia or hyperglycemia at birth.