SYSTEMIC AND UTERINE BLOOD-FLOW DISTRIBUTION DURING PROLONGED INFUSION OF 17-BETA-ESTRADIOL

Prolonged 17 beta-estradiol (E(2)beta) infusion decreases mean arteria l pressure (MAP) and systemic vascular resistance (SVR) while increasi ng heart rate (HR) and cardiac output (CO). It is unclear, however, wh ich systemic vascular beds show increases in perfusion. The purpose of this study was to determine which reproductive and nonreproductive va scular beds exhibit alterations in vascular resistance and blood flow during prolonged E(2)beta infusion. Nonpregnant, ovariectomized sheep received either vehicle (n = 6) or E(2)beta (5 mu g/kg iv bolus follow ed by 6 mu g/kg over 24 h for 10 days; n = 9), and blood flow distribu tion was evaluated using radiolabeled microspheres at control and 120 min and 3, 6, 8, and 10 days of infusion. During E(2)beta infusion MAP (87 +/- 5 mmHg; mean +/- SE) decreased 3-9% and HR (83 +/- 5 beats/mi n) increased 4-31%. The combined baseline (control) perfusion to the u terus, broad ligament, oviducts, cenix, vagina, and mammary gland (rep roductive blood flows) was 49 +/- 9 ml/min; at 120 min, E(2)beta incre ased flow (P < 0.001) to 605 +/- 74 ml/min (1,263%) and it remained el evated, but at a reduced rate, on day 3 (218 +/- 44 ml/min; 399%), day 6 (144 +/- 23; 217%), day 8 (181 +/- 19; 321%), and day 10 (204 +/- 4 8; 454%), accounting for only 3-17% of the E(2)beta-induced increase i n CO. During this E(2)beta treatment, there also were significant decr eases in vascular resistances leading to increases (P < 0.05) in blood flows to several nonreproductive (systemic) vascular beds including s kin (32-113%), coronary (32-190%), skeletal muscle (25-133%), brain (2 1-292%), bladder (128-524%), spleen (87-180%), and pancreas (35-137%) vascular beds. Responses of these combined nonreproductive blood flows represent the major percentage (21-67%) of the E(2)beta-induced incre ase in CO. Vehicle infusion was without effect. We conclude that prolo nged E(2)beta infusion increases reproductive and nonreproductive tiss ue blood flows. The latter appears to principally be responsible for t he observed rise in CO and decrease in SVR.