The principles of haemostasis in Obstetrics and Gynaecology are similar to those in other surgical specialties. The uterus and the endometrium, however, have some unique properties, especially in terms of menstruation, pregnancy, and delivery.
The myometrial smooth muscle cells are not homogenous. They are embedded in extracellular material composed mainly of collagen fibres, which facilitates the transmission of contractile forces generated by individual muscle cells.1 The muscle cells communicate with each other through gap junctions. These junctions are believed to synchronise myometrial function by conduction of electrophysiological stimuli during labour. In both human and animal myometria in late pregnancy, the gap junctions increase in number until onset of labour. The formation of gap junctions has been studied in vitro, and the regulatory roles for oestrogen, progesterone, and prostaglandins have been established. The relationship between the electrical activity, the conductivity properties of the myometrium and the density of gap junctions has been shown. This indicates that the various related components of myometrial cellular regulation including the formation of gapjunctions, enhancement of electrical activity, and response to oestrogen, oxytocin, and prostaglandins are simultaneous events. These collectively contribute to the increased myometrial activity of labour and postpartum.
The effect of oxytocin is mediated through myometrial oxytocin receptors that are modulated by various factors. Following administration of oestrogens the number of uterine receptors sensitive to oxytocin and «-adrenergic agonists increases. This can be prevented by concurrent administration of progesterone. In binding to the receptor, oxytocin has been shown to inhibit the Ca++ ATPase of the myometrial cell membrane. This pumps Ca++ from the inside to the extracellular milieu and promotes the influx of Ca++ both from the sarcoplasmic reticulum and the extracellular area. The increase in concentration of cytoplasmic Ca++ activates the contractile process. Oxytocin may also have a central regulatory function. At term, the deciduas parietalis shows a high concentration of oxytocin receptors. This may be a stimulus for prostaglandin synthesis as prostaglandins are found in high concentrations in decidual tissue obtained from women in labour.
Progesterone effects on the myometrium are characterised by a relative quiescence and uncoupling of the excitation-contraction mechanisms.
Oestrogens stimulate or increase sensibility to «-adrenergic receptors, leading to increased production of Prostaglandin F2A. In contrast, progesterone stimulates ^-adrenergic receptors, leading to preponderance of prostacyclin (PGI2) and, via C AMP, to the relaxation of smooth muscle. Mifepristone, a steroid acting as anti-progesterone at the receptor level, results in increased uterine activity and increased sensitivity to prostaglandins.
Prostaglandins are components of the eicosanoid system. They are acidic lipids arising from the principal precursor, arachidonic acid, via three different pathways. This is catalysed by cyclooxygenase leading to prostaglandins, prostacyclin, and thromboxane and by lipoxygenase leading to leucotrienes. Human amnion and chorion mainly produce PGE2 and PGF2A. It is suggested that the synthesis of PGE2 is the key event in the onset of regular contractions. Prostaglandins also cause increased myometrial contractility, and there appears to be a regional sensitivity of the uterus to various prostaglandins.
In contrast to other hormones, prostaglandins are synthesised at the site of action. PGE2 and PGF2A are known to stimulate uterine contractility, most likely acting as Ca++ ionophores.
The action of prostaglandins appears to be mediated by specific receptors located on the plasma membranes of target cells. The increase in myometrial activity is directly related to the rise in PGE2 and PGF2A. Prostaglandins produced in the placenta probably play a major role in the mechanism of placental separation and expulsion.
The rapid metabolism of natural prostaglandins is the reason why a number of analogues have been developed, that are not substrates for the initial step of the enzymatic degradation by 15-OH-dehydrogenase. These derivatives are more potent than the parent compound and action is more prolonged and more specific on uterine rather than other smooth muscle tissue.
The subcellular structure of smooth muscle is different from striated muscle. In smooth muscle cells, the thick myosin and the thin actin filaments occur in long random bundles throughout the smooth muscle cells and the continuity of the filaments is not interrupted by Z lines. Instead, intermediate filaments form a network that links protein structures known as dense bodies. They link the individual fibrils, composed of actin and myosin, into integrated mechanical units. Smooth muscle can exert pulling forces in any direction due to its organisation. This enables the uterus to generate forces in any axis necessary and assume any shape to accommodate foetuses of various sizes, during labour.
The endometrium is composed of two layers, the upper functional layer that is shed at the time of menstruation and an underlying basal layer from which the endometrium regenerates after each menstrual shedding. The endometrium shows the presence of oestrogen, progesterone, and androgen receptors in the stroma.2
Haemostatic mechanisms have two functions:
(a) To confine the circulatory blood to the vascular system.
(b) To arrest bleeding from injured vessels.
These mechanisms depend on:
(i) Normal vasculature.
(ii) Platelets — number and function.
(iii) Coagulation factors.
(iv) Healthy fibrinolysis.3
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