EXPERIMENTAL POLYHYDRAMNIOS

该项目的目的是评估生理机制 导致羊水过多和胎儿水肿， 注射血管紧张素I在全身麻醉的情况下， 在脐静脉、颈静脉、 静脉、足动脉和静脉以及羊水和尿囊液。 将母体导管置于股动脉和子宫静脉中。 在一些动物中，可充气的封堵器将被放置在胎儿或胎儿上。 胎盘的母体静脉引流和胎儿或 母体终末主动脉 有待检验的假设是， 羊水过多的发展取决于胎盘的变化， Na和Cl的渗透率和反射系数， 中间步骤是从血管紧张素I转化为血管紧张素II， 没有第二个系统的水过滤渠道， 胎盘屏障，即血管紧张素I的高血压作用不是一个 水病的直接原因，即相同的胎盘变化，导致 完整胎儿的羊水过多引起肾切除胎儿水肿 胎儿和胎盘外转移的溶质是不是一个显着的 导致水污染的过程。 阐明 这些常见妊娠疾病的病理生理学将有助于 理性治疗

The purpose of the project is to evaluate the physiological mechanisms that cause polyhydramnios and hydrops fetalis when fetal sheep are infused with angiotensin I. Under general anesthesia, fetal sheep will be instrumented with indwelling catheters in the umbilical vein, the jugular vein, a pedal artery and vein and the amniotic and allantoic fluids. Maternal catheters will be placed in a femoral artery and uterine vein. In some animals inflatable occluders will be placed on the fetal or maternal venous drainages of the placenta and flow meters on the fetal or maternal terminal aorta. Hypotheses to be tested are that the development of polyhydramnios depends on a change in the placental permeabilities and reflection coefficients for Na and Cl, that an intermediate step is the conversion from angiotensin I to angiotensin II, that there is no second system of water filtration channels across the placental barrier, that the hypertensive effect of angiotensin I is not a direct cause of water disease, that the same placental changes that cause polyhydramnios in intact fetuses cause hydrops fetalis in nephrectomized fetuses and that extraplacental transfer of solutes is not a significant contributor to the process that produces water disease. Elucidation of the pathophysiology of these common diseases of pregnancy will help lead to rational therapy.