![](/wp-content/uploads/2021/03/abstractheadergraphic2009.gif)
Meeting Abstract
S5.10 Monday, Jan. 5 Evolution of the vertebrate cardiopulmonary system under varying atmospheric oxygen supply OWERKOWICZ, T.*; HICKS, J.W.; UC Irvine; UC Irvine towerkow@uci.edu
Evolutionary history of the vertebrates has been subject to the vagaries of oxygen flux in Earths atmosphere. Cell-cell signalling in embryonic heart and lungs is highly sensitive to local oxygen tension. Changes in the atmospheric oxygen supply can alter tissue pO2, and thus directly interfere with normal regulatory mechanisms (e.g., hypoxia-inducible factor, superoxides). Atmospheric oxygen can also affect cardiopulmonary development indirectly, as expression of mechanoreceptor proteins responds to a new mechanical milieu (stretch of lung parenchyma, shear in blood vessel walls). Altogether, this can produce viable novel morphologic and physiologic phenotypes, some of which may be adaptive to the changing environmental conditions. In order to better understand how the current diversity of cardiopulmonary Bauple arose, we argue it is necessary to study heart/lung development under appropriate atmospheric oxygen levels. We incubated eggs and raised hatchlings of the American alligator under chronic hyperoxia (30% O2) and hypoxia (12% O2) to resemble the atmospheric composition endured by early archosaurs in the oxygen-rich Permian and oxygen-poor Late Triassic. While hyperoxia does not appear to affect cardiopulmonary growth in alligators, hypoxia exerts a potent effect. Hypoxic alligators show persistent heart hypertrophy, driven mainly by right ventricular enlargement. Alligator lungs appear under-developed at hatching but exhibit strong compensatory growth after hatching. Unlike newborn mammals, hatchling alligators do not show a hypometabolic response to chronic hypoxia, but elevate their metabolism under hyperoxia. We discuss the potential cellular mechanisms, which may be responsible for the observed phenotypic plasticity. Funded by NSF IOB 04445680 to JWH.