Exposure to high CO2 concentrations during embryonic development affects cardiovascular responses in juvenile snapping turtles

Reptilian embryos often face challenging environmental gas compositions during incubation, which may inflict long lasting effects in the individuals’ physiological responses. These conditions can have a lasting effect on the animal into juvenile life as chronic prenatal exposure to high CO2 concentrations (i.e. hypercarbia) results in enlarged hatchling organ size, higher growth rate and resting metabolic rate, although relatively smaller increment in metabolic scope during digestion. Therefore, we wanted to verify whether prenatal exposure to hypercarbia would cause persistent effects on morphology and physiological responses in the common snapping turtle, Chelydra serpentina. We measured organ masses and cardiovascular parameters in five years old turtles incubated either under 3.5% hypercarbia (H3.5) or normoxia (N21). We expected that: i) organ masses of H3.5 would be bigger than N21; ii) acute exposure to hypoxia should decrease blood flows in H3.5, since metabolic scope is presumably reduced in this group. As hypoxia exposure elicits catecholamine release, we also tested cardiovascular responses to adrenaline injection. Organ masses were similar between groups. Divergent cardiovascular responses to adrenaline were observed as systemic stroke volume decreased and pulmonary stroke volume increased in N21, but was unchanged in H3.5. Hypoxia caused decreased systemic blood flow and cardiac output, systemic and total stroke volume, and systemic vascular conductance in H3.5. These variables were unaffected in N21, but stomach blood perfusion reduced. These data support the hypothesis that exposure to hypercarbia during embryonic development has long term effects on cardiovascular responses of C. serpentina.