Long term effects of chronic prenatal exposure to hypercarbia on organ growth and cardiovascular responses to adrenaline and hypoxia in common 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 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 hypercarbia exposure would cause persistent effects on morphology and physiological responses in C. 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. Lungs and stomach exhibited higher growth rates in H3.5. Divergent cardiovascular responses between groups to adrenaline injection were observed for heart rate, pulmonary blood flow, pulmonary mean arterial pressure, blood shunt, systemic stroke volume, and stomach perfusion. 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 pulmonary flow and stroke volume, and stomach blood perfusion were reduced. These data support the hypothesis that exposure to hypercarbia during embryonic development has long term effects on organ morphology and cardiovascular responses of C. serpentina.
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