6-ketoprostaglandin-f1-alpha and Esophageal-and-Gastric-Varices

Platelet aggregability and the coagulative and fibrinolytic systems were examined in 45 patients who underwent endoscopic injection sclerotherapy for oesophageal varices. Five per cent ethanolamine oleate, the sclerosant used, was injected into the oesophageal varices. There were significant increases in the concentrations of fibrinopeptide A, fibrinopeptide B-beta-15-42 and fibrin degradation products-E after the sclero-therapy. At 1 h after the sclerotherapy the mean(s.e.m.) platelet aggregation was significantly suppressed to 71.9(4.2) per cent of that before the treatment (P less than 0.01). There was a gradual recovery within 1 week to the same level seen before the sclerotherapy. Thromboxane B2 and 6-keto-prostaglandin F1 alpha, both stable products of thromboxane A2 and prostacyclin respectively, showed significant temporary increases after the sclerotherapy (P less than 0.01). The peak increase in the level of thromboxane B2 was noted within 1 h after the sclerotherapy and earlier than that for 6-keto-prostaglandin F1 alpha. This increased ratio of prostacyclin and thromboxane A2 may be related to the marked limitation in platelet aggregation.

Topics: 6-Ketoprostaglandin F1 alpha; Adult; Aged; Antithrombin III; Blood Coagulation Tests; Esophageal and Gastric Varices; Female; Fibrinogen; Humans; Male; Middle Aged; Oleic Acids; Platelet Aggregation; Platelet Aggregation Inhibitors; Platelet Count; Sclerosing Solutions; Thromboxane B2

The object of this study was to investigate clinical conditions in which increased production of prostacyclin (PGI2) has been reported. 6-Oxo-prostaglandin F1 alpha (6-oxo-PGF1 alpha) is the stable hydrolysis product of PGI2 and was measured in plasma from patients undergoing hepatic or cardiac surgery and in unoperated patients with vascular and hepatic disease, using gas chromatography/mass spectrometry. Blood obtained simultaneously from portal and peripheral veins, during emergency surgery for bleeding oesophageal varices in six patients with cirrhosis of the liver, contained very high concentrations of 6-oxo-PGF1 alpha (range 99-11,485 pg/ml of plasma). 6-Oxo-PGF1 alpha was higher in portal than in peripheral blood in five out of six patients. Six unoperated patients with cirrhosis and oesophageal varices which were not bleeding all had normal peripheral plasma concentrations of 6-oxo-PGF1 alpha less than 2 pg/ml (normal up to 5 pg/ml). Seventeen patients with severe vascular disease had normal basal plasma 6-oxo-PGF1 alpha concentrations (less than 2 pg/ml). Eighteen subjects with atheromatous coronary artery disease underwent aorta-coronary artery grafting, and plasma concentrations of 6-oxo-PGF1 alpha were markedly elevated during surgery (range 55-1207 pg/ml). We conclude that surgery stimulates PGI2 production substantially, and argue that the function of PGI2 may be to limit intravascular extension of thrombus from sites of haemostasis. Inappropriate PGI2 synthesis may contribute to the massive haemorrhage characteristic of oesophageal variceal bleeding.

Topics: 6-Ketoprostaglandin F1 alpha; Adult; Aged; Cardiopulmonary Bypass; Coronary Disease; Epoprostenol; Esophageal and Gastric Varices; Humans; Hypertension, Portal; Middle Aged; Vascular Diseases