Hypoxic incubation at 50% of atmospheric levels shifts the cardiovascular response to acute hypoxia in American alligators, Alligator mississippiensis.

We designed a series of studies to investigate whether hypoxia (10% O2) from 20% of incubation to hatching, or from 20 to 50% of incubation, affects cardiovascular function when juvenile American alligators reached an age of 4-5 years compared to juveniles that were incubated in 21% O2. At this age, we measured blood flows in all the major arteries as well as heart rate, blood pressure, and blood gases in animals in normoxia and acute hypoxia (10% O2 and 5% O2). In all three groups, exposure to acute hypoxia of 10% O2 caused a decrease in blood O2 concentration and an increase in heart rate in 4-5-year-old animals, with limited effects on blood flow in the major outflow vessels of the heart. In response to more acute hypoxia (5% O2), where blood O2 concentration decreased even further, we measured increased heart rate and blood flow in the right aorta, subclavian artery, carotid artery, and pulmonary artery; however, blood flow in the left aorta either decreased or did not change. Embryonic exposure to hypoxia increased the threshold for eliciting an increase in heart rate indicative of a decrease in sensitivity. Alligators that had been incubated in hypoxia also had higher arterial PCO2 values in normoxia, suggesting a reduction in ventilation relative to metabolism.

Developmental oxygen preadapts ventricular function of juvenile American alligators, Alligator mississippiensis.

Developmental oxygen is a powerful stressor that can induce morphological and functional changes in the cardiovascular systems of embryonic and juvenile vertebrates. This plasticity has been ascribed, at least in part, to the unique status of the developing cardiovascular system, which undergoes organogenesis while meeting the tissue oxygen demands of the embryo. We have previously reported an array of functional and morphological changes in embryonic American alligators that persist into juvenile life. Most notably, cardiac enlargement as well as functional parameters of anesthetized juvenile alligators remains after embryonic hypoxic exposure. Because the effects of developmental oxygen in crocodilians have only been investigated in anesthetized animals, we explored the pressure dynamics of both ventricles as well as systemic pressure in response to stressors of acute hypoxia and swimming. Our current findings demonstrate that developmental programming of cardiac function (intraventricular pressure and heart rate) does persist into juvenile life, but it is chamber-specific and depends on the experimental manipulation. Acute hypoxic exposure revealed that juvenile alligators that had experienced 10% O2 as embryos maintain right ventricle function and increase left ventricle function during exposure. Finally, the data indicate blood flow in the left aorta must originate from the left ventricle during acute hypoxia and swimming.