Effect of changing lung liquid volume on the pulmonary circulation of fetal lambs

During fetal life the lung develops as a liquid-filled structure with low blood flow compared with postnatal life. We studied the effects of liquid expansion of the fetal lung by measuring vascular conductance in perfused lungs in situ and arterial diameters in excised lungs of fetal lambs. Pulmonary vascular conductance invariably rose as the lung was deflated from its initial volume; maximal deflation to residual volume increased conductance 122%. With reexpansion, conductance fell progressively, culminating in cessation of flow at lung volumes of twice the initial volume. These changes persisted after vagotomy and thoracic sympathectomy and therefore were mechanical in character. Lung expansion from residual volume initially expanded 300- to 500-micron arteries but compressed arteries greater than 1,500 micron. Further expansion reduced the caliber of all arteries. Thus increasing lung liquid volume progressively constricts the pulmonary circulation in the fetus. Because the fetal pulmonary vascular resistance-lung volume relationship differs from that of the U-shaped form found in adult lungs, concepts based on the adult pulmonary circulation are not appropriate for liquid-filled fetal lungs.     

Effects of sedation on the controlled pulmonary circulation

The pulmonary circulatory effects of sedatives and groups of sedatives in dosages commonly employed as pre cardiac catheterization sedatives were evaluated. The sedatives included: meperidine, thiamylal, hydroxyzine, promethazine, meperidine + chlorpromazine + promethazine and meperidine + hydroxyzine. An animal preparation with constant pulmonary blood flow and left atrial pressure was employed. This preparation has the unique advantage of permitting measurement of the active pulmonary vascular resistance change since passive effects are controlled. In order to establish the significance of a given change in active PVR, a dose response relationship for serotonin was established and the effect of the sedatives was calibrated against it. PVR increased following infusion of all sedatives tested except hydroxyzine and chlorpromazine.A technique was detailed to permit subtraction of passive PVR change from total PVR change in intact, unsedated animals. Results of active change in PVR of previous investigations in intact, unsedated animals were compared to the active change observed in this experiment and were found to be similar in direction and magnitude. This investigation stresses the need to consider possible effects of sedatives on the pulmonary circulation.