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Oxytocin is a mammalian neurohypophysial hormone and is produced in the supraoptic and paraventricular nuclei of the hypothalamus. It is a neuropeptide that physiologically is a potent uterotonic, stimulating the smooth muscles of the uterus. It also causes contraction of the myoepithelial cells surrounding the mammary alveoli, leading to milk ejection during lactation.
The physiological effects of oxytocin are modified not only by circulating oxytocin, but also by the presence of oxytocinase and by the number and capacity of oxytocin receptors. Oxytocinase is a glycoprotein aminopeptidase produced during pregnancy that degrades oxytocin. Enzyme activity in the placenta increases as pregnancy progresses and rises steeply at term. After delivery it declines.
Around the onset of labour, uterine sensitivity markedly increases. This is explained by both an upregulation of oxytocin receptor mRNA levels and by a strong increase in the density of myometrial oxytocin receptors, reaching a peak during early labour. Before labour, oxytocin receptors increase not only in the myometrium but also in the decidua. During the course of labour, oxytocin receptor gene expression has been found to increase five-fold in human choriodecidual tissue. Also, in the decidua, oxytocin itself has a separate action in releasing the prostaglandin F2 alpha.
In a low-dose intravenous infusion, oxytocin elicits rhythmic uterine contractions. High doses of oxytocin, particularly if given by rapid intravenous injection, have a transient direct relaxing effect on vascular smooth muscle, resulting in brief hypotension, flushing and reflex tachycardia. Discontinuation or a significant reduction in the rate of oxytocin infusion usually leads to rapid decline of its effect on muscular activity. Oxytocin distributes throughout the extracellular fluid and plasma binding is very low. One of the advantages of intravenous infusion of oxytocin is its short half-life which, depending on the clinical circumstances and the assay used, is of the order of 3–20 minutes. When administered at the appropriate intravenous infusion rate, the uterine response starts gradually and usually reaches a steady state within 20–40 minutes.
Syntocinon is a synthetic nonapeptide identical to oxytocin. It does not contain vasopressin and has a constant and reliable effect. The solution for injection is clear and colourless and is available in ampoules containing 5 IU in 1 mL and 10 IU in 1 mL.
The recommended licensed regimen is that the initial infusion rate should be set at 1–4 mU/minute initially and increased at intervals no less than 20 minutes and increments of not more than 1–2 mU/minute until a contraction pattern similar to normal labour is established (3–4 contractions every 10 minutes). The recommended maximum dose is 20 mU/min and there is no mention of difference between nulliparous and multiparous women.
A low-dose regimen would be regarded as starting from 1 mU/minute increased every 30 minutes to a maximum dose of 12 mU/minute. Again little mention is made to differentiate between nulliparous and multiparous women.
A high-dose regimen would be regarded as 5 mU/minute increased every 15 minutes to a maximum dose of 30 mU/minute and maybe even higher.
The concentration, starting dose, incremental dose, rate of increase and maximum dose of oxytocin is not the main issue.
The main issue is the effect on the fetus and the uterus.
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