This is an essential part of the interacting dynamic mechanism and is dependent on plasminogen activator in the blood. Fibrin is digested by plasmin, a proenzyme derived from an inactive plasma precursor, plasminogen. Activator levels are increased after surgical operations, trauma, and strenuous exercise.
Tissue activator is especially rich in the uterus and the ovaries, but cannot be extracted from the placenta. Activity around veins is greater than around arteries.
There are two inhibitors of fibrinolytic activity, anti-activators (anti-plasminogens) and anti-plasmins.
Anti-plasminogens include e-aminocaproic acid (EACA) and tranexamic acid. Tranexamic acid in a dose of 500 mg to 1 g gds is used in the control of menorrhagia, often as a first line treatment.4
Fibrin degradation products are formed when fibrinogen or fibrin is broken down by plasmin. Plasma fibrinolytic activity is decreased during pregnancy and returns to normal within one hour after pla-cental delivery. The fact that fibrinolytic activity resumes rapidly following delivery of the placenta and the placenta has been shown to contain inhibitors of fibrinolysis suggests that inhibition of fibrinoly-sis during pregnancy is mediated through the placenta.
Overall, the changes in the coagulation system during normal pregnancy are consistent with a continuous, low-grade level of coagulant activity. Fibrin deposition can be demonstrated in the intervil-lous space of the placenta and in all the walls of the spiral arteries supplying the placenta. The elastic lamina and the smooth muscle of these spiral arteries are replaced by a matrix containing fibrin, as pregnancy progresses. This allows expansion of the lumen to accommodate increasing blood flow and reduces arterial blood pressure flowing to the placenta.
Normal pregnancy is associated with an increase in cardiac output from 4.5 L to 6L. After placental separation (third stage of labour), blood supply ranging between 500 and 800ml/min to the uterus, has to be arrested within seconds to prevent a serious haemorrhage. Myometrial contraction plays a vital role in securing haemostasis, by reducing the blood flow to the placental site. Rapid closure of the terminal part of the spiral arteries will be further facilitated by the structural changes in their walls. The placental site is rapidly covered by a fibrin mesh following delivery. The increased levels of fibrino-gen and other coagulation factors will meet the sudden demand for haemostatic components, following placental separation.
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