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

Abstract

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% oxygen preconditions cardiac function, decreasing the reduction in cardiac contractility associated with acute 5% oxygen 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% O2 with the 10% O2 group responding with a greater rate of ventricular relaxation and greater left ventricle output compared the 21% O2 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 to juvenile alligators that did not experience embryonic hypoxia. When juveniles were exposed to 5% oxygen for 20 minutes, 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.