@article{cole_argenzio_eisemann_2004, title={Physiological responses in swine treated with water containing sodium bicarbonate as a prophylactic for gastric ulcers}, volume={82}, DOI={10.2527/2004.8292757x}, abstractNote={Maintenance of gastric pH above 4.0 aids the prevention of bile acid-mediated ulcerative damage to the pars esophageal tissue in pigs. One means of doing so is the addition of buffering compounds, such as sodium bicarbonate, to the water supply; however, any potential physiological effect of buffer consumption has yet to be determined. Experiment 1 tested the acute effects of buffer addition to the water supply on systemic acid-base and electrolyte balance in swine (BW 40.7 +/- 3.0 kg). Consumption of water calculated to a 200 mOsm solution with sodium bicarbonate for 24 h increased (P < 0.05) blood Na+, HCO3(-), and pCO2, although these effects were all within physiologically tolerable levels. Urine pH and Na+ excretion increased (P < 0.001) following the consumption of NaHCO3, with Na+ concentration almost threefold higher in treated pigs compared with controls. Experiment 2 determined the chronic systemic effects of buffer consumption by measuring blood and urine variables, with pigs consuming NaHCO3-treated water throughout. Water consumption increased (P < 0.001) during buffer consumption, although intake levels remained within normal ranges. Blood pH levels were not affected by long-term consumption of dietary buffer; however, blood HCO3(-) (P < 0.05), Na+, and pCO2 (P < 0.01) increased. Urine pH and urine Na+ concentration increased (P < 0.01) in buffer-treated compared with control animals. Results indicate that sodium bicarbonate can safely be added to the water supply for pigs, with no clinically relevant alterations in acid-base balance because the animals readily compensate for buffer intake.}, number={9}, journal={Journal of Animal Science}, author={Cole, J. T. and Argenzio, R. A. and Eisemann, J. H.}, year={2004}, pages={2757–2763} }
 @article{cole_blikslager_hunt_gookin_argenzio_2003, title={Cyclooxygenase blockade and exogenous glutamine  enhance sodium absorption in infected bovine ileum}, volume={284}, ISSN={0193-1857 1522-1547}, url={http://dx.doi.org/10.1152/ajpgi.00172.2002}, DOI={10.1152/ajpgi.00172.2002}, abstractNote={We have previously shown that prostanoids inhibit electroneutral sodium absorption in Cryptosporidium parvum-infected porcine ileum, whereas glutamine stimulates electroneutral sodium absorption. We postulated that glutamine would stimulate sodium absorption via a cyclooxygenase (COX)-dependent pathway. We tested this hypothesis in C. parvum-infected calves, which are the natural hosts of cryptosporidiosis. Tissues from healthy and infected calves were studied in Ussing chambers and analyzed via immunohistochemistry and Western blots. Treatment of infected tissue with selective COX inhibitors revealed that COX-1 and -2 must be blocked to restore electroneutral sodium absorption, although the transporter involved did not appear to be the expected Na+/H+exchanger 3 isoform. Glutamine addition also stimulated sodium absorption in calf tissue, but although this transport was electroneutral in healthy tissue, sodium absorption was electrogenic in infected tissue and was additive to sodium transport uncovered by COX inhibition. Blockade of both COX isoforms is necessary to release the prostaglandin-mediated inhibition of electroneutral sodium uptake in C. parvum-infected calf ileal tissue, whereas glutamine increases sodium uptake by an electrogenic mechanism in this same tissue.}, number={3}, journal={American Journal of Physiology-Gastrointestinal and Liver Physiology}, publisher={American Physiological Society}, author={Cole, Jeffrey and Blikslager, Anthony and Hunt, Elaine and Gookin, Jody and Argenzio, Robert}, year={2003}, month={Mar}, pages={G516–G524} }