Prostacyclin and thromboxane in gynecology and obstetrics.
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.
D015121:6-Ketoprostaglandin F1 alpha / Q000032:analysis; D000818:Animals; D001202:Ascitic Fluid / Q000378:metabolism; D004715:Endometriosis / Q000378:metabolism; D011464:Epoprostenol / Q000378:metabolism / Q000494:pharmacology / Q000502:physiology; D004967:Estrogens / Q000494:pharmacology; D005260:Female; D005831:Genital Diseases, Female / Q000378:metabolism; D005833:Genital Neoplasms, Female / Q000032:analysis; D006801:Humans; D006973:Hypertension / Q000188:drug therapy / Q000378:metabolism; D008595:Menorrhagia / Q000209:etiology / Q000378:metabolism; D010974:Platelet Aggregation; D011225:Pre-Eclampsia / Q000378:metabolism; D011247:Pregnancy; D011248:Pregnancy Complications / Q000378:metabolism; D011249:Pregnancy Complications, Cardiovascular / Q000188:drug therapy / Q000378:metabolism; D011372:Progestins / Q000494:pharmacology; D013928:Thromboxane A2 / Q000378:metabolism / Q000494:pharmacology / Q000502:physiology; D013929:Thromboxane B2 / Q000032:analysis; D013931:Thromboxanes / Q000378:metabolism / Q000494:pharmacology / Q000502:physiology; D014590:Uterine Contraction / Q000187:drug effects; D014661:Vasoconstriction
D004967:Estrogens; D011372:Progestins; D013931:Thromboxanes; D013929:Thromboxane B2; D013928:Thromboxane A2; D015121:6-Ketoprostaglandin F1 alpha; D011464:Epoprostenol