Arteriovenous Shunts in the Human Lung.

Abstract

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.

Detection of Intracardiac and Intrapulmonary Shunts at Rest and During Exercise Using Saline Contrast Echocardiography

“…Specifically, there are data suggesting that intrapulmonary arteriovenous anastomoses are patent in the supine position, but not in the upright position (Stickland et al, 2004;Elliott et al, 2011b). Also, Tobin & Zariquiey demonstrated that intrapulmonary arteriovenous anastomoses 20 to 500 m in functional diameter are located in the apex of the human lung (Tobin & Zariquiey, 1950). Together, these data support the idea that perfusion of the apices of the lung may open these vessels.…”

“…The studies that established the existence of these pathways used solid, large diameter microspheres to prove that there are large diameter pathways that bypass pulmonary capillaries (von Hayek, 1940;Tobin & Zariquiey, 1950;Tobin, 1966). More recent studies by our group have used microspheres to demonstrate the existence of large diameter (>25 to 50 m) intrapulmonary arteriovenous anastomoses in isolated, ventilated and perfused healthy human and baboon lungs under physiologic conditions (Lovering et al, 2007).…”

Hypoxemia in pulmonary embolism, a clinical study

“…The lack of correlation between the mean pulmonary artery pressure and the per cent of the cardiac output shunted weighs against the opening of potential anatomical pathways for shunting which, though normally present, are usually not patent; this is a mechanism proposed but not proven by animal experimentation (39)(40)(41)(42) and human autopsy studies (43,44). Furthermore, our data indicate that intracardiac shunts occasionally do occur but were relatively infrequent among our subjects.…”

Arterial air embolism of venous origin in dogs: effect of nitrous oxide in combination with halothane and pentobarbitone

“…Spillover of VAE through pulmonary shunts is likely 26'2v although any direct action of halothane on these vessels is not reported. Extra-alveolar pulmonary shunts were reported in three out of four dogs examined, zs ranging in size up to 240 microns diameter 27 and although rarely in man, they have been reported as large as 500 microns, 29 Niden and Aviado 27 suggested that pulmonary shunts may be pressure responsive and open with elevated PAP or hypoxia, allowing venous glass beads to spillover into the pulmonary veins.…”