Cellular and molecular bases for dystocia.
In this review I have briefly outlined some of the cellular and molecular reasons for dystocia. I have described the myogenic, that may control the normal progression of labor and explain inadequate uterine contractility associated with dystocia. I have placed particular emphasis on our studies of gap junctions and their regulation. These studies show that there are specific physiologic mechanisms for regulating structural and functional coupling between myometrial cells during labor. The integration of these control mechanisms probably operates to ensure appropriate activation and maintenance of synchronous contractility of the myometrium and effective delivery.
D000818:Animals; D000242:Cyclic AMP / Q000378:metabolism; D004420:Dystocia / Q000209:etiology / Q000473:pathology* / Q000503:physiopathology; D004963:Estrenes / Q000502:physiology; D004967:Estrogens / Q000494:pharmacology / Q000502:physiology; D005260:Female; D005938:Glucocorticoids / Q000037:antagonists & inhibitors; D006801:Humans; D015735:Mifepristone; D009215:Myometrium / Q000294:innervation / Q000473:pathology / Q000502:physiology; D011247:Pregnancy; D011374:Progesterone / Q000494:pharmacology / Q000502:physiology; D013569:Synapses / Q000187:drug effects; D014590:Uterine Contraction
D004963:Estrenes; D004967:Estrogens; D005938:Glucocorticoids; D015735:Mifepristone; D011374:Progesterone; D000242:Cyclic AMP