OBJECTIVE: Our purpose was to study the effects of inhibition of nitric oxide synthesis on perfusion pressure and flow rate-perfusion pressure relationships in the rat uterine circulation in situ. STUDY DESIGN: Nonpregnant, midpregnant (day 14), and late pregnant (day 21) Sprague-Dawley rats were studied. The vascular bed of the intact uterus and its contents were isolated and perfused with Krebs buffer (37 degrees C, pH approximately 7.4, 2% dextran and indomethacin, 10(-5) mol/L) through a cannula inserted into the abdominal aorta close to the iliac artery bifurcation, and perfusion pressure was monitored. After equilibration, the flow rate was increased from 1 mL/min to 8 or 16 mL/min, in the absence and presence of N(omega)-nitro-L-arginine methyl ester (L-NAME), phenylephrine, or both. RESULTS: The flow rate-perfusion pressure relationship in midpregnant rats (n = 9) was not significantly different from that in late pregnant rats (n = 12), but the latter was significantly greater than the relationship in nonpregnant animals (n = 5). L-NAME did not influence perfusion pressure and flow rate-perfusion pressure relationships in any of the groups. However, L-NAME enhanced the phenylephrine-induced and flow rate-induced increase in perfusion pressure in the vascular beds from nonpregnant and midpregnant animals, and to a lesser extent in late pregnant rats. L-arginine did not influence perfusion pressure or the flow rate-perfusion pressure relationship in any group. CONCLUSIONS: Vasoconstriction produced by phenylephrine uncovers basal release of endothelium derived nitric oxide. Vasoconstriction increases perfusion pressure responses to increases in flow rate in the uterine vascular beds of nonpregnant, midpregnant, and late pregnant rats. The release of endothelial nitric oxide in the uterine vascular beds depends on the basal contractile state of the vasculature.
ASJC Scopus subject areas
- Obstetrics and Gynecology