ABSTRACT
Menstruation The most accepted theory regarding the cause of menstruation is that when the corpus luteum fails, because pregnancy has not occurred, there is an abrupt drop in estrogen and progesterone (sometimes referred to as estrogen-progesterone withdrawal). This withdrawal reduces hormone support to the endometrium, thus allowing rather sudden shrinking. Spiral arteries soon begin to kink upon themselves, thereby shutting off blood supply to the endometrium. Although the precise mechanism for vascular necrosis is uncertain, many believe it to be due in part to spasm of blood vessels caused by locally produced prostaglandins (e.g., PGF2). There have been large quantities of prostaglandins found in the secretory endometrium and in menstrual blood, and infusion of prostaglandins produces endometrial necrosis and bleeding. One credible theory holds that in necrotic endometrial cells, lysosomal membranes break down, causing activation of enzymes (e.g., phospholipase A2) that foster release of unsaturated fatty acids (e.g.. arachidonic acid) from the two position of membrane-bound phospholipids. These unsaturated fatty acids then become substrates for the formation of prostaglandins, which in turn produce vasospasm, vascular necrosis, and menstrual flow. This concept seems plausible, for without a blood supply endometrial tissues necrose, the epithelium is sloughed off, and several layers of endometrial tissue are lost by hemorrhage.
