Ventilatory compensation of the alkaline tide during digestion in the snakeBoa constrictor

Abstract

SUMMARYThe increased metabolic rate during digestion is associated with changes in arterial acid–base parameters that are caused by gastric acid secretion(the `alkaline tide'). Net transfer of HCl to the stomach lumen causes an increase in plasma HCO3– levels, but arterial pH does not change because of a ventilatory compensation that counters the metabolic alkalosis. It seems, therefore, that ventilation is controlled to preserve pH and not PCO2 during the postprandial period. To investigate this possibility, we determined arterial acid–base parameters and the metabolic response to digestion in the snake Boa constrictor, where gastric acid secretion was inhibited pharmacologically by oral administration of omeprazole.The increase in oxygen consumption of omeprazole-treated snakes after ingestion of 30% of their own body mass was quantitatively similar to the response in untreated snakes, although the peak of the metabolic response occurred later (36 h versus 24 h). Untreated control animals exhibited a large increase in arterial plasma HCO3– concentration of approximately 12 mmol l–1, but arterial pH only increased by 0.12 pH units because of a simultaneous increase in arterial PCO2 by about 10 mmHg. Omeprazole virtually abolished the changes in arterial pH and plasma HCO3– concentration during digestion and there was no increase in arterial PCO2. The increased arterial PCO2 during digestion is not caused, therefore, by the increased metabolism during digestion or a lower ventilatory responsiveness to ventilatory stimuli during a presumably relaxed state in digestion. Furthermore, the constant arterial PCO2, in the absence of an alkaline tide, of omeprazole-treated snakes strongly suggests that pH rather than PCO2 normally affects chemoreceptor activity and ventilatory drive.

Digesting pythons quickly oxidize the proteins in their meals and save the lipids for later

“…For over a century researchers have worked to quantify the relative energetic components of mechanical, physiological and biochemical processes associated with the costs of SDA (reviewed in Jobling, 1983;McCue, 2006;Secor, 2009). We now know that the costs of gastric digestion (Secor, 2003;Andrade et al, 2004) and protein synthesis (McCue et al, 2005;Enok et al, 2013) account for most of the SDA in pythons. Unfortunately, the source of this energy (i.e.…”

Alkaline tide and nitrogen conservation after feeding in an elasmobranch(Squalus acanthias)

“…The first was to develop a stomach tube feeding model because dogfish will not eat naturally when confined in small boxes, as required for the chronic blood sampling of acid-base studies. The second was to establish whether an alkaline tide occurs after dogfish are fed a realistic ration by this method and, if it does, whether it is modulated by 'respiratory compensation' (P CO ∑ retention to limit pH increases), as in many higher vertebrate carnivores (reviewed by Andrade et al, 2004). The third was to determine the effects of this feeding regimen on nitrogen metabolism, with particular emphasis on ammonia-N and urea-N excretion rates and corresponding blood levels of these two end products.…”

Fisiologia De Extremos: Digestão Em Répteis De Alimentação Esporádica

“…Dessa forma observa-se que o aumento do pH do plasma promove uma compensação respiratória via elevação da PCO 2 durante todo o período pós-prandial. Isso parece ocorrer devido a um papel inibitó-rio do pH sanguíneo sobre os quimiorreceptores periféricos (WANG; BURGGREN; NOBREGA, 1995;OVERGAARD et al, 1999a;BUSK et al, 2000;ANDRADE et al, 2004). Para a píton, há um aumento na concentração plasmática de HCO 3 -de 19,3 em jejum para 25,8 mmol.L -1 no estado alimentado, porém devido ao aumento da PCO 2 arterial de 21,1 para 27,9 mmHg, não há mudanças significantes no pH arterial do valor em jejum, 7,52.…”

“…Em comparação, na jiboia, serpente de hábito alimentar infrequente, o pH arterial em jejum é de 7,52 e aumenta significativamente a um valor má-ximo de 7,64 24 horas após a ingestão. O aumento na pressão parcial arterial do CO 2 é de 16,3 para 26,4 mmHg 12 horas após a alimentação (ANDRADE et al, 2004).…”

“…A queda na PO 2 pulmonar durante a hipoventilação pós-prandial não é suficiente para comprometer o transporte de O 2 na circulação pulmonar. Em crocodilos, os níveis de PO 2 arterial se mantêm inalterados após a alimentação; na verdade, estima-se que a saturação de O 2 da hemoglobina arterial aumenta ligeiramente de 86% para 90% em um período de 24-48h após a refeição (BUSK et al, 2000;ANDRADE et al, 2004) …”