Embryonic developmental oxygen preconditions cardiovascular function response to acute hypoxic exposure and maximal β-adrenergic stimulation of anesthetized juvenile American alligators ( Alligator mississippiensis ).

The effects of the embryonic environment on juvenile phenotypes are widely recognized. We investigated the effect of embryonic hypoxia on the cardiovascular phenotype of 4-year-old American alligators (Alligator mississippiensis). We hypothesized that embryonic 10% O-2 preconditions cardiac function, decreasing the reduction in cardiac contractility associated with acute 5% O-2 exposure in juvenile alligators. Our findings indicate that dobutamine injections caused a 90% increase in systolic pressure in juveniles that were incubated in 21% and 10% O-2, with the 10% O-2 group responding with a greater rate of ventricular relaxation and greater left ventricle output compared with the 21% O-2 group. Further, our findings indicate that juvenile alligators that experienced embryonic hypoxia have a faster rate of ventricular relaxation, greater left ventricle stroke volume and greater cardiac power following beta-adrenergic stimulation, compared with juvenile alligators that did not experience embryonic hypoxia. When juveniles were exposed to 5% O-2 for 20 min, normoxic-incubated juveniles had a 50% decline in left ventricle maximal rate of pressure development and maximal pressure; however, these parameters were unaffected and decreased less in the hypoxic-incubated juveniles. These data indicate that embryonic hypoxia in crocodilians alters the cardiovascular phenotype, changing the juvenile response to acute hypoxia and beta-adrenergic stimulation.