7terone ( 2 5 ) will prolong the life of certain adrenalectomized mammals including the ferret and the cat. Regardless of what prolongs the life of adrenalectomized pregnant females, it has been shown that adrenalectomizing the mother results in hypertrophy of the adrenals of fetuses(5,6). I t has also been found that the injection of adrenal cortical extracts into the mother will prevent these effects(6). These observations raise a question as to whether the same factors responsible for hypertrophy of fetal adrenals after adrenalectomizing the mother play a part in the compensatory hypertrophy noted in the unilaterally adrenalectomized fetuses of this present series. It is reasonable to assume that one factor in both these instances is the action of an adrenocorticotrophin. A number of recent observations point to the view that adrenocorticotrophin is produced by the hypophysis of the mammalian fetus( 7-12). Against this view is a recent report that in 24. Emery, F. E., and Schwabe, E. L., Endocrin-2.5. Gaunt, R., and Hayes, H. W., Am. 1. Physiol., ology, 1936Physiol., ology, , v2G, 550. 1938 immature rats subjected to injections of epinephrine or to cold the hypophysis does not release ACTH until the 8th day and 16th day, respectively, after birth(26). This report poses a question as to whether the eff ective adrenocorticotrophin might have come from the maternal hypophysis, the fetal hypophysis or, conceivably, the placenta. Also one has to consider the possibility of the direct effect of reduced quantities of adrenal cortical hormones upon the fetal adrenal. From the observations noted in this series, it is not possible to settle the matter, Conclusion. Subjection of the fetal rat to unilateral adrenalectomy causes a compensatory hypertrophy of the intact adrenal. Manifestations of this include an increased volume of the gland and an increased size of cells of all cortical zones, Those cells at both borders of the intermediate zone show an increased vacuolation, suggesting that the zone had been widened by the metamorphosis of cells at these borders.The presence of arteriovenous (A-V) shunts bypassing the capillary circulation in the human lung has been suspected from studies on blood gas analyses( l ) , the passage of certain parasites through the lung(2), and the formation of telangectasis( 2 ) and arteriovenous aneurysms (3-6) within the lung.