Objective To study fibrinolysis in the endometrium in women with normal menstruation and dysfunctional uterine bleeding (DUB). Design Tissue plasminogen activator activity (t‐PA) and antigen (t‐PAAg) and plasminogen activator inhibitor Type 1 antigen (PAI‐1) were measured in homogenates of endometrium sampled between 24 and 36 h after the onset of menstruation. Subjects Women complaining of menorrhagia who had negative findings at clinical examination and curettage had their menstrual blood loss (MBL) measured from the third cycle after D&C. Those with MBL greater than 80 ml per cycle formed the DUB group. Measurements Fibrinolytic enzyme antigen levels were measured with ELISAs. Tissue plasminogen activator activity was assayed by measuring the rate of conversion of Glu‐plasminogen to plasmin, using a chromogenic plasmin substrate. Conclusions There is a strong positive correlation between endometrial t‐PA activity on the second day of menstruation and measured menstrual loss (P<0.05). Concentrations of endometrial t‐PAAg and PAI‐1 antigen are higher in women with DUB compared with normal women during menstruation.

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Summary. Menstrual fluid was obtained from the uterine cavity and vagina in 20 women within the first 48 h of menstruation. Ten of the women had normal menstrual cycles and blood loss and ten were patients with dysfunctional uterine bleeding. The menstrual samples were examined by electron microscopy for the presence of fibrin and platelets and nearly all were found to contain both fibrin and aggregating platelets. By a simple quantitative system no differences in fibrin and platelet content were found between samples collected from the uterine cavity or the vagina. Likewise no difference was found in the morphology of fibrin and platelets between women with normal menstrual loss and patients with dysfunctional uterine bleeding.

The initial reactions of the blood components and the intima of the rabbit abdominal aorta have been observed following mechanical trauma. The endothelium was removed by the insertion of a roughened metal probe into the lumen of the vessel, thus exposing the sub-endothelial fibres and the internal elastio lamina. On restoration of the blood flow, platelets and later leucocytes adhered to the injured surface. Only small clumps of platelets or single cells adhered to the surface. Under these conditions it was possible to study the morphology of the cells and vessel surface by scanning electron microscopy, as no large mass of thrombus material was present to obscure the picture. The platelets developed long branched projections on adhering to the injured surface. Platelets were found in larger numbers in areas where much collagen was present, such as the fenestrations of the internal elastic lamina, but were sometimes seen at sites where these fibres were absent. It was possible to observe that platelets were sometimes attached to endothelial basement membrane, but often they adhered to sites where neither basement membrane nor collagen could be seen. It would seem therefore that some other component from the damaged intima may be necessary for platelets to adhere to the injured surface. The presence of a subendothelial mucopolysaccharide layer was demonstrated with the dye ruthenium red. At no time was it possible to observe a complete covering of platelets over the whole injured area.