Biomedical subjects

Johnnie B Andersen

Publications and source records attributed to Johnnie B Andersen.

6 recordsLinked to original sources

PubMed2005

Postprandial increase of oleoylethanolamide mobilization in small intestine of the Burmese python (Python molurus).

Oleoylethanolamide (OEA) is an endogenous lipid mediator that inhibits feeding in rats and mice by activating the nuclear receptor peroxisome proliferator-activated receptor-alpha (PPAR-alpha). In rodents, intestinal OEA levels increase about threefold upon refeeding, a response that may contribute to the induction of between-meal satiety. Here, we examined whether feeding-induced OEA mobilization also occurs in Burmese pythons (Python molurus), a species of ambush-hunting snakes that consume huge meals after months of fasting and undergo massive feeding-dependent changes in gastrointestinal hormonal release and gut morphology. Using liquid chromatography/mass spectrometry (LC/MS), we measured OEA levels in the gastrointestinal tract of fasted (28 days) and fed (48 h after feeding) pythons. We observed a nearly 300-fold increase in OEA levels in the small intestine of fed compared with fasted animals (322 +/- 121 vs. 1 +/- 1 pmol/mg protein, n = 3-4). In situ OEA biosynthesis was suggested by the concomitant increase of N-acyl phosphatidylethanolamine species that serve as potential biosynthetic precursors for OEA. Furthermore, we observed a concomitant increase in saturated, mono- and diunsaturated, but not polyunsaturated fatty-acid ethanolamides (FAE) in the small intestine of fed pythons. The identification of OEA and other FAEs in the gastrointestinal tract of Python molurus suggests that this class of lipid messengers may be widespread among vertebrate groups and may represent an evolutionarily ancient means of regulating energy intake.

Animals↗

PubMed2005

Arterial acid-base status during digestion and following vascular infusion of NaHCO(3) and HCl in the South American rattlesnake, Crotalus durissus.

Digestion is associated with gastric secretion that leads to an alkalinisation of the blood, termed the "alkaline tide". Numerous studies on different reptiles and amphibians show that while plasma bicarbonate concentration ([HCO(3)(-)](pl)) increases substantially during digestion, arterial pH (pHa) remains virtually unchanged, due to a concurrent rise in arterial PCO(2) (PaCO(2)) caused by a relative hypoventilation. This has led to the suggestion that postprandial amphibians and reptiles regulate pHa rather than PaCO(2). Here we characterize blood gases in the South American rattlesnake (Crotalus durissus) during digestion and following systemic infusions of NaHCO(3) and HCl in fasting animals to induce a metabolic alkalosis or acidosis in fasting animals. The magnitude of these acid-base disturbances were similar in magnitude to that mediated by digestion and exercise. Plasma [HCO(3)(-)] increased from 18.4+/-1.5 to 23.7+/-1.0 mmol L(-1) during digestion and was accompanied by a respiratory compensation where PaCO(2) increased from 13.0+/-0.7 to 19.1+/-1.4 mm Hg at 24 h. As a result, pHa decreased slightly, but were significantly below fasting levels 36 h into digestion. Infusion of NaHCO(3) (7 mmol kg(-1)) resulted in a 10 mmol L(-1) increase in plasma [HCO(3)(-)] within 1 h and was accompanied by a rapid elevation of pHa (from 7.58+/-0.01 to 7.78+/-0.02). PaCO(2), however, did not change following HCO(3)(-) infusion, which indicates a lack of respiratory compensation. Following infusion of HCl (4 mmol kg(-1)), plasma pHa decreased by 0.07 units and [HCO(3)(-)](pl) was reduced by 4.6 mmol L(-1) within the first 3 h. PaCO(2), however, was not affected and there was no evidence for respiratory compensation. Our data show that digesting rattlesnakes exhibit respiratory compensations to the alkaline tide, whereas artificially induced metabolic acid-base disturbances of same magnitude remain uncompensated. It seems difficult to envision that the central and peripheral chemoreceptors would experience different stimuli during these conditions. One explanation for the different ventilatory responses could be that digestion induces a more relaxed state with low responsiveness to ventilatory stimuli.

Acidosis↗

PubMed2005

Physiology: postprandial cardiac hypertrophy in pythons.

Oxygen consumption by carnivorous reptiles increases enormously after they have eaten a large meal in order to meet metabolic demands, and this places an extra load on the cardiovascular system. Here we show that there is an extraordinarily rapid 40% increase in ventricular muscle mass in Burmese pythons (Python molurus) a mere 48 hours after feeding, which results from increased gene expression of muscle-contractile proteins. As this fully reversible hypertrophy occurs naturally, it could provide a useful model for investigating the mechanisms that lead to cardiac growth in other animals.

Adaptation, Physiological↗

PubMed2003

Effects of inhibition gastric acid secretion on arterial acid-base status during digestion in the toad Bufo marinus.

Digestion affects acid-base status, because the net transfer of HCl from the blood to the stomach lumen leads to an increase in HCO3(-) levels in both extra- and intracellular compartments. The increase in plasma [HCO3(-)], the alkaline tide, is particularly pronounced in amphibians and reptiles, but is not associated with an increased arterial pH, because of a concomitant rise in arterial PCO2 caused by a relative hypoventilation. In this study, we investigate whether the postprandial increase in PaCO2 of the toad Bufo marinus represents a compensatory response to the increased plasma [HCO3(-)] or a state-dependent change in the control of pulmonary ventilation. To this end, we successfully prevented the alkaline tide, by inhibiting gastric acid secretion with omeprazole, and compared the response to that of untreated toads determined in our laboratory during the same period. In addition, we used vascular infusions of bicarbonate to mimic the alkaline tide in fasting animals. Omeprazole did not affect blood gases, acid-base and haematological parameters in fasting toads, but abolished the postprandial increase in plasma [HCO3(-)] and the rise in arterial PCO2 that normally peaks 48 h into the digestive period. Vascular infusion of HCO3(-), that mimicked the postprandial rise in plasma [HCO3(-)], led to a progressive respiratory compensation of arterial pH through increased arterial PCO2. Thus, irrespective of whether the metabolic alkalosis is caused by gastric acid secretion in response to a meal or experimental infusion of bicarbonate, arterial pH is being maintained by an increased arterial PCO2. It seems, therefore, that the elevated PCO2, occuring during the postprandial period, constitutes of a regulated response to maintain pH rather than a state-dependent change in ventilatory control.

Acid-Base Equilibrium↗

PubMed2003

Cardiovascular responses to hypoxia and anaemia in the toad Bufo marinus.

Amphibians exhibit cardiorespiratory responses to hypoxia and, although several oxygen-sensitive chemoreceptor sites have been identified, the specific oxygen stimulus that triggers these responses remains controversial. This study investigates whether the cardiovascular response to oxygen shortage correlates with decreased oxygen partial pressure of arterial blood (Pa(O(2))) or reduced oxygen concentration ([O(2)]) in toads. Toads, equipped with blood flow probes and an arterial catheter, were exposed to graded hypoxia [fraction of oxygen in the inspired air (FI(O(2)))=0.21, 0.15, 0.10, 0.07 and 0.05] before and after reductions in arterial [O(2)] by isovolemic anaemia that reduced haematocrit by approximately 50%. Toads responded to hypoxia by increasing heart rate (fH) and pulmocutaneous blood flow (Q(pc)) and reducing the net cardiac right-to-left-shunt. When arterial [O(2)] was reduced by anaemia, the toads exhibited a similar cardiovascular response to that observed in hypoxia. While arterial CO(2) partial pressure (Pa(CO(2))) decreased significantly during hypoxia, indicative of increased alveolar ventilation, anaemia did not alter Pa(CO(2))). This suggests that reductions in [O(2)] mediate cardiovascular adjustments, while ventilatory responses are caused by reduced Pa(O(2)).

Anemia↗

PubMedDate not supplied

The effects of fasting duration on the metabolic response to feeding in Python molurus: an evaluation of the energetic costs associated with gastrointestinal growth and upregulation.

The oxygen uptake of Python molurus increases enormously following feeding, and the elevated metabolism coincides with rapid growth of the gastrointestinal organs. There are opposing views regarding the energetic costs of the gastrointestinal hypertrophy, and this study concerns the metabolic response to feeding after fasting periods of different duration. Since mass and function of the gastrointestinal organs remain elevated for several days after feeding, the metabolic increment following a second meal given soon after the first can reveal whether the metabolic costs relate to the upregulation of gastrointestinal organs or merely the metabolic cost of processing a meal. Eight juvenile pythons were kept on a regular feeding regime for 6 mo after hatching. At the beginning of the metabolic measurements, they were fed mice (20% of body mass), and the metabolic response to similarly sized meals was determined following 3, 5, 7, 14, 21, 30, and 60 d of fasting. Our data show that the metabolic response following feeding was large, ranging from 21% to 35% of ingested energy (mean=27%), but the metabolic response seems independent of fasting duration. Hence, the extraordinarily large cost of digestion in P. molurus does not appear to correlate with increased function and growth of gastrointestinal organs but must be associated with other physiological processes.

Animals↗