| Abstrakt: |
Using an in vitro placental lobule perfusion technique, the human fetal placental vasculature has been found to respond vigorously with high sensitivity to various vasoconstrictor substances, including angiotensin II, endothelins 1 and 3, prostaglandins F2 alpha, E2 and D2 and the thromboxane A2 agonist U46619. Thromboxane A2 receptors mediating vasoconstriction have been characterized in fetal placental vessels and appear to be identical to those on human platelets and pulmonary blood vessels. Although the isolated fetal placental vessels are largely unresponsive to exogenous vasodilatory stimuli, when preconstricted they respond by vasodilatation to several vasodilator substances, including arachidonate, prostacyclin, prostaglandin E1, theophylline and nitroglycerine. The resistance offered to flow in vitro by the villous vasculature is therefore low, as it is in vivo. Both intrinsic and extrinsic mechanisms probably operate to cause relaxation of the vascular smooth muscle with the vasodilatory effects of locally released autacoids dominating the effects of those having vasoconstrictor actions. |
