Table –

Current tocolytic classes.

Tocolytic	Mechanism	Issues
Selective beta 2 (β2) agonists: Ritodrine Terbulatine	– Impairs intracellular cyclic AMP concentration and facilitate myometrial relaxation.	– Lack of long-term benefit – Maternal side effects include tachysystole, chest pain, cardiac arrhythmias, electrolyte disturbances, pulmonary edema, lower blood pressure, tremor.
Nitric oxide (NO): Nitroglycerine (NTG)	– Powerful vasodilator synthesized during an amino acid oxidation process catalyzed by NO synthase. It increases cGMP content by interaction with guanylyl cyclase.	– Intravenous use of NTG required to obtain the desired degree of uterine relaxation is extremely variable in an acute setting and may be accompanied by significant hypotension.
Prostaglandin-synthase or cyclooxygenase (COX) isoforms: Indomethacin	– Nonspecific COX inhibitor – COX-1 and −2 are essential enzymes for converting arachidonic acid to prostaglandins. – Prostaglandins are thought to promote uterine contraction by enhancing myometrial gap junction and increasing intracellular calcium concentration.	– Use should be restricted in duration and limited to pregnancies below 32 weeks because of fetal ductus arteriosus closure risk and decreased urine production responsible for oligohydramnios. – These treatments also have maternal side effects including gastric ulcer or asthma recurrence.
Oxytocin receptor (OTR) antagonists: Atosiban	– Oxytocin mediates its myometrial effects primarily through activation of oxytocin receptors (OTR) which classically Gq couple to activate phospholipase-C beta (PLCb) thereby triggering IP3 and DAG pro-contractile second messenger pathways, the main effect of which seems to involve enhancing intracellular calcium levels. – OTR antagonists block this pathway.	– Mixed affinity between both the OTR and vasopressin (V1a receptors), limited parenteral route of administration, and variable bioavailability. – Possible fetal concerns if used prior to 28 weeks. – Lack of long-term efficacy.
Voltage-Gated Calcium channel (VGCC) blockers: Nifedipine	– Interferes with calcium ion transfer through the myometrial cell membrane to decrease intracellular free calcium concentration and promote myometrial relaxation.	– As a peripheral vasodilator it may cause symptoms such as nausea, flushing, headache, dizziness, and palpitation, hypotension. – Lack of long-term efficacy.
Magnesium sulfate:	– Exact mechanism has not been completely delineated. – It likely competes with calcium at the level of the plasma membrane voltage-gated channels, hyperpolarizes the plasma membrane, inhibits myosin light-chain kinase activity by competing with intracellular calcium.	– Maternal side effects include diaphoresis, flushing, headache, magnesium toxicity. – Lack of long-term efficacy.