Effects of feeding on arterial blood gases in the American alligator Alligator mississippiensis

Abstract

Reptiles habitually ingest large meals at infrequent intervals, leading to changes in acid-base status as the net secretion of acid to the stomach causes a metabolic alkalosis (the alkaline tide). In chronically cannulated and undisturbed amphibians and reptiles, the pH changes in arterial blood are, nevertheless, reduced by a concomitant respiratory acidosis (increased P(CO2) caused by a relative hypoventilation). Alligators (Alligator mississippiensis) have been reported to exhibit exceptionally large increases in plasma [HCO3(−)] following feeding, but these studies were based on blood samples obtained by cardiac puncture, so stress and disturbance may have affected the blood gas levels. Furthermore, crocodilian haemoglobin is characterised by a unique binding of HCO3(−) that act to reduce blood oxygen-affinity, and it has been proposed that this feature safeguards oxygen offloading by counteracting pH effects on blood oxygen-affinity. Therefore, to study acid-base regulation and the interaction between the alkaline tide and oxygen transport in more detail, we describe the arterial blood gas composition of chronically cannulated and undisturbed alligators before and after voluntary feeding (meal size 7.5+/−1% of body mass). Digestion was associated with an approximately fourfold increase in metabolic rate (from 0.63+/−0.04 to 2.32+/−0.24 ml O(2) min(−1)kg(−1)) and was accompanied by a small increase in the respiratory gas exchange ratio. The arterial P(O2) of fasting alligators was 60.3+/−6.8 mmHg (1 mmHg = 0.133 kPa) and reached a maximum of 81.3+/−2.7 mmHg at 96 h following feeding; there was only a small increase in lactate levels, so the increased metabolic rate seems to be entirely aerobic. Plasma [HCO3(−)] increased from 24.4+/−1.1 to 36.9+/−1.7 mmol l(−1) (at 24 h), but since arterial P(CO2) increased from 29.0+/−1.1 to 36.8+/−1.3 mmHg, arterial pH remained virtually unaffected (changing from 7.51+/−0.01 to 7.58+/−0.01 at 24 h). The changes in plasma [HCO3(−)] were mirrored by equimolar reductions in plasma [Cl(−)]. The in vitro blood oxygen-affinity was reduced during the post-prandial period, whereas the estimated in vivo blood oxygen-affinity remained virtually constant. This supports the view that the specific HCO3(−) effect prevents an increased blood oxygen-affinity during digestion in alligators.