We recently interviewed Dr. Dane Crossley, Professor of Physiology in the College of Biological Sciences at the University of North Texas about the research his laboratory presented at the recent APS Intersociety meeting, Comparative Physiology: From Organisms to Omics in an Uncertain World.
The title of his presentation was, “A large heart: How does developmental hypoxia affect individual cardiomyocyte performance in the American alligator, Alligator mississippiensis.”
Thank you for taking time to answer our questions Dr. Crossley. Your recent publication about cardiac function in American alligators was interesting because it showed how exposure to environmental challenges during development can persist long after hatching. How often do these alligators experience hypoxia (low oxygen) in their natural environment?
Dr. Crossley: Well, there are a limited number of studies from the field, however those studies that have been conducted report that crocodilians and turtles experience periods of hypoxia as embryos. As juveniles or adults, crocodilians can undertake prolonged dives which have been reported to be 340 min in length or longer subjecting the animal to hypoxemia.
Our readers may not be familiar with the cardiac physiology of an alligator. Would you please help us understand how blood flow and cardiac function in alligators compares to mammals?
Dr. Crossley: The crocodilian heart is very similar to the mammalian heart. It is composed of two atria and two distinct ventricles. The crocodilian cardiovascular anatomy is unique because they possess two aortae. Specifically, blood can exit the right ventricle via the pulmonary artery and/or the left aorta. Blood from the left ventricle can only exit the heart via the right aorta but can pass from the right aorta into the left aorta via a connection at the base of each aorta called the foramen of Panizza.
Findings from your most recent publication show that alligators exposed to hypoxia develop larger hearts and that blood appears to move from the left ventricle of the heart through the left aorta. Was that finding surprising and how might that impact the animals during exercise?
Dr. Crossley: We have consistently found that embryonic hypoxia results in embryonic cardiac enlargement that persists in juvenile animals. In our most recent study, we found an interesting anecdotal. By measuring intraventricular pressures in surgically recovered animals we were able to establish that during swimming and acute hypoxic exposures blood flow in the left aorta must originate from the left ventricle based on the pressure profiles. It is difficult to predict how these findings would impact activity in the wild. It does suggest that alligators maintain pulmonary perfusion when swimming at the surface which would support sustainable aerobic activity.
What are you working on now?
Dr. Crossley: We continue to work to understand how embryonic hypoxia programs the cardiovascular phenotype of the American alligator. Most recently we have taken a reductionistic approach and have begun investigating the functional phenotype of the juvenile American alligator cardiomyocytes. We are investigating the contractility of individual cells to determine the basis for the phenotypic effects we see at the level of the whole animal.
Good luck, Dr. Crossley! We look forward to seeing the next installment of your research at a future meeting.