• 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.