Histamine exerts both direct H2-mediated and indirect catecholaminergic effects on heart rate in pythons.

The vertebrate heart is regulated by excitatory adrenergic and inhibitory cholinergic innervations, as well as non-adrenergic non-cholinergic (NANC) factors that may be circulating in the blood or released from the autonomic nerves. As an example of NANC signaling, an increased histaminergic tone, acting through stimulation of H2 receptors, contributes markedly to the rise in heart rate during digestion in pythons. In addition to the direct effects of histamine, it is also known that histamine can reinforce the cholinergic and adrenergic signaling. Thus, to further our understanding of the histaminergic regulation of the cardiovascular response in pythons, we designed a series of in vivo experiments complemented by in vitro experiments on sinoatrial and vascular ring preparations. We demonstrate the tachycardic mechanism of histamine works partly through a direct binding of cardiac H2 receptors and in part through a myocardial histamine-induced catecholamine release, which strengthens the sympathetic adrenergic signaling pathway.

Low cost of gastric acid secretion during digestion in ball pythons.

Due to their large metabolic responses to digestion (specific dynamic action, SDA), snakes represent an interesting animal group to identify the underlying mechanisms for the postprandial rise in metabolism. The SDA response results from the energetic costs of many different processes ranging over prey handling, secretions by the digestive system, synthesis of enzymes, plasticity of most visceral organs, as well as protein synthesis and nitrogen excretion. The contribution of the individual mechanisms, however, remains elusive. Gastric acid secretion has been proposed to account for more than half of the SDA response, while other studies report much lower contributions of the gastric processes. To investigate the energetic cost of gastric acid secretion, ball pythons (Python regius) were fed meals with added amounts of bone meal (up to 25 g bone meal kg(-1) snake) to achieve a five-fold rise in the buffer capacity of the meals. Direct measurements within the stomach lumen showed similar reduction in gastric pH when buffer capacity was increased, but we found no effects on the rise in oxygen consumption over the first three days of digestion. There was, however, a slower return of oxygen consumption to resting baseline. We conclude that gastric acid secretion only contributes modestly to the SDA response and propose that post-absorptive processes, such as increased protein synthesis, are likely to underlie the SDA response.

Closed system respirometry may underestimate tissue gas exchange and bias the respiratory exchange ratio (RER).

Closed respirometry is a commonly used method to measure gas exchange in animals due to its apparent simplicity. Typically, the rates of O2 uptake and CO2 excretion (VO2 and VCO2, respectively) are assumed to be in steady state, such that the measured rates of gas exchange equal those at tissue level. In other words, the respiratory gas exchange ratio (RER) is assumed to equal the respiratory quotient (RQ). However, because the gas concentrations change progressively during closure, the animal inspires air with a progressively increasing CO2 concentration and decreasing O2 concentration. These changes will eventually affect gas exchange causing the O2 and CO2 stores within the animal to change. Because of the higher solubility/capacitance of CO2 in the tissues of the body, VCO2 will be more affected than VO2, and we hypothesize therefore that RER will become progressively underestimated as closure time is prolonged. This hypothesis was addressed by a combination of experimental studies involving closed respirometry on ball pythons (Python regius) as well as mathematical models of gas exchange. We show that increased closed duration of the respirometer reduces RER by up to 13%, and these findings may explain previous reports of RER values being below 0.7. Our model reveals that the maximally possible reduction in RER is determined by the storage capacity of the body for CO2 (product of size and specific capacitance) relative to the respirometer storage capacity. Furthermore, modeling also shows that pronounced ventilatory and circulatory response to hypercapnia can alleviate the reduction in RER.