6-ketoprostaglandin-f1-alpha and Genital-Diseases--Female

The gynecologic and obstetric implications of the smooth muscle-relaxing, antiaggregatory prostacyclin and its endogenous antagonist, thromboxane A2, are reviewed. In addition to the vascular wall and circulating platelets, which are primary sources for prostacyclin and thromboxane A2, respectively, reproductive tissues produce great amounts of these prostanoids, evidently for the regulation of the vascular tone and/or vascular platelet interaction. Several gynecologic and obstetric disorders are characterized by abnormalities in prostacyclin and/or thromboxane A2. In primary menorrhagia the uterine release of prostacyclin is increased, and consequently menstrual blood loss can be reduced with various prostaglandin synthesis inhibitors. Prostacyclin relaxes the nonpregnant myometrium in vitro and may also do so in vivo, although intravenous infusion of prostacyclin has no effect upon the uterine contractility in nonpregnant or pregnant subjects. Patients with pelvic endometriosis may have increased levels of prostacyclin and thromboxane A2 metabolites in the peritoneal fluid. The prostacyclin/thromboxane A2 balance shifts to thromboxane A2 dominance in patients with gynecologic cancer. During pregnancy the production of prostacyclin and thromboxane A2 increases in the mother and fetoplacental tissue. Preeclampsia and other chronic placental insufficiency syndromes are accompanied by prostacyclin deficiency in the mother and in fetomaternal tissues and by an overproduction of thromboxane A2, at least in the placenta. These changes may account for the vasoconstriction and platelet hyperactivity, which are pathognomonic for hypertensive pregnancies. By directing the prostacyclin/thromboxane A2 balance to prostacyclin dominance (by dietary manipulation, administration of prostacyclin and/or its analogues, drugs with prostacyclin-stimulating and/or thromboxane A2-inhibiting action), it may be possible to prevent and/or treat hypertensive pregnancy complications in the future.

Topics: 6-Ketoprostaglandin F1 alpha; Animals; Ascitic Fluid; Endometriosis; Epoprostenol; Estrogens; Female; Genital Diseases, Female; Genital Neoplasms, Female; Humans; Hypertension; Menorrhagia; Platelet Aggregation; Pre-Eclampsia; Pregnancy; Pregnancy Complications; Pregnancy Complications, Cardiovascular; Progestins; Thromboxane A2; Thromboxane B2; Thromboxanes; Uterine Contraction; Vasoconstriction

In order to investigate whether prostanoids are involved in the pathophysiology of endometriosis, prostaglandin and leukotriene concentrations in peritoneal fluid were measured in adenomyosis, ovarian chocolate cyst and uterine leiomyoma. In the secretory phase, there was no significant difference in 6-keto PGF1 alpha concentration in peritoneal fluid between the adenomyosis group and the leiomyoma group. TXB2 concentration did not significantly differ in the three study groups. Leukotriene C4 level in the adenomyosis group was significantly higher than that of leiomyoma in the secretory phase. Leukotriene B4 could not be detected by our assay system. Our results suggest that leukotriene C4 is possibly involved in the pathophysiology of endometriosis.

Topics: 6-Ketoprostaglandin F1 alpha; Adult; Ascitic Fluid; Endometriosis; Female; Genital Diseases, Female; Humans; Leukotriene B4; Prostaglandins; SRS-A; Thromboxane B2; Uterine Neoplasms

Products of the cyclooxygenase and lipoxygenase pathways of arachidonic acid metabolism were estimated in the cul-de-sac fluid from patients with endometriosis, pelvic adhesions and normal laparoscopic examinations, with and without chronic pelvic pain. No correlation between the symptoms, underlying diagnoses, and the concentrations of eicosanoids were observed.

Topics: 6-Ketoprostaglandin F1 alpha; Abdominal Pain; Arachidonic Acid; Arachidonic Acids; Ascitic Fluid; Chronic Disease; Dinoprostone; Eicosanoids; Endometriosis; Female; Genital Diseases, Female; Humans; Laparoscopy; Leukotriene B4; Pelvis; Tissue Adhesions