sodium-ethylxanthate and Ischemia

This hypothesis proposes that carcinogens in the breast are generated by the action of superoxide free radicals released when acinal gland distension, under the influence of unopposed prolactin, causes microvessel ischaemia. Inadequate nipple care in the at-risk years leads to ductal obstruction preventing the elimination of carcinogens from the breast. The regular production of oxytocin (OT) from nipple stimulation would cause contraction of the myoepithelial cells, relieving acinal gland distension and aiding the active elimination of carcinogenic fluid from the breast. Mechanical breast pump stimulation causes an increase in plasma OT levels in the luteal but not in the follicular phase of the menstrual cycle. OT production upon nipple stimulation in the luteal phase of premenopausal, non-lactating women may be protective against the high rates of mitotic breast cell division noted at this time via the potential to block the effect of oestrogen. The epidemiology of breast cancer suggests that lengthy lactation time is beneficial. Sexual activity in nulliparous women also protects and OT levels have been shown to rise with orgasm in women and in men. OT systems in the brain are intricately linked to oestrogen and progesterone levels, and it is possible that these hormones may modify the OT secretory response both centrally and through an effect on the sensitivity of the breast. OT production with nipple care and in sex and lactation, and the reduction in cycling ovarian hormones that occurs with pregnancy, may all be important preventative factors in the development of breast cancer both pre- and post-menopausally.

Topics: Breast Neoplasms; Female; Humans; Ischemia; Lactation; Menstrual Cycle; Microcirculation; Models, Biological; Nipples; Oxytocin; Prolactin; Sex; Superoxides

From Wistar rats, data are presented which indicate that inbred females a) have a greater ability to clear particulate matter from the blood stream than do males of the same strain; b) are significantly more resistant to two different forms of lethal circulatory stress (e.g., intestinal ischemia and whole-body trauma) than are males; and c) exhibit a greater resistance to undergo reticuloendothelial system (RES) phagocytic depression after both forms of lethal trauma than do males. Estradiol treatment of males, using either acute, massive (1 or 10 mg/kg) or multiple, low dose (10 or 100 mug/kg) regimens, confers trauma resistance on such animals. Such estradiol treated male rats exhibit hyperactive RES's. These estradiol-treated males, when subjected to either lethal ischemia or trauma, fail to demonstrate the early RES phagocytic depression seen in untreated controls. Untreated female as well as estradiol-treated male rats exhibit significantly higher arterial blood pressures post-trauma than do untreated male rats. Direct microscopic observation of rat mesenteries indicr whole-b0dy trauma, the untreated females as well as the estradiol-treated males exhibit significantly less dilatation of microscopic capacitance vessels (i.e., venules) than do untreated male rats. The data reported herein could be used to suggest that estrogenic hormones may play pivotal roles in a) the amelioration of an organism's reaction to systemic stress; and b) control of macrophage and peripheral vascular functions.

Topics: Animals; Blood Pressure; Colon; Estradiol; Estradiol Congeners; Estrogens; Female; Ischemia; Male; Microcirculation; Phagocytosis; Rats; Rats, Inbred Strains; Rotation; Sex; Shock