Digestive tracts of pig, dog, pony, and sheep. Arrows indicate termination of ascending colon. Major portion of colon of ruminants and pigs is arranged in 2 spirals. Centripetal spiral reverses direction to form centrifugal spiral, as indicated by slight upward bend near center of colon. Large (ascending) colon of pony is arranged in right and left ventral colons and left and right dorsal colons, which terminate at origin of small colon (transverse colon).

Volatile fatty acid (VFA) content, net VFA production, volume of water, and net transmural flux of water determined for individual segments of pony large intestine as a function of time. Negative values designate net absorption of VFA or water. Rates of flow determined by marker techniques 6 allowed volume and total VFA changes to be analyzed in terms of inflow and outflow to a segment and by difference, the rate of net addition or removal of VFA or water.

Digesta osmolality and ion concentrations along gastrointestinal tract of pony. Data represent mean values (n = 24, where n is the number of ponies) obtained over 12‐h period between meals for ponies fed either conventional diet or high‐fiber diet 12. Concentration of PO₄³⁻ was calculated under assumption that pK_a of NaH₂PO₄ was 6.8 and utilizing mean pH of contents in each segment. At pH of large intestinal contents, NH₃⁺ and organic acids (OA) exist primarily in their ionized forms. Concentration of HCO₃⁻ calculated as difference in concentration of measured cations and anions. S, stomach; SI₁, SI₂, SI₃, 3 equal segments of small intestine; C, cecum; VC, ventral colon; DC, dorsal colon; SC, small colon.

Mean concentrations (n = 9, where n is the number of dogs) of cations and anions along digestive tract of dog. Animals were killed 4–6 h after meat meal. S, stomach; J, jejunum; I, ileum; C, colon.

Possible mechanisms to account for results obtained from Ringer's and theophylline Ringer's solutions in proximal colon of pig. For simplicity, the models assume a single barrier to transport from lumen (L) to blood (B). In all likelihood, H ions and HCO₃ ions are produced by intracellular hydration of CO₂ 36, so barrier shown probably represents mucosal membrane. All values expressed in μeq · cm⁻² · h⁻¹. Values for short‐circuit current (I_sc) obtained from parallel in vitro experiments are included and are in reasonably good agreement with current flows calculated from in vivo experiments. Arrows between barriers represent net passive ion flows traversing tissue in response to transmural potential difference shown at bottom.

Net water movement in intestine of diarrhetic (shaded bars) and control (open bars) calves. Points examined were 15%, 40%, 65%, and 90% of distance from duodenum (D) to ileocecal valve (I). C, proximal spiral colon. Data are means ± SE of 10 animals in each group.

Partial pressure of CO₂ initially present in luminal solution and after perfusion through proximal colon of pig. Initial was set to approximate that of plasma. Solutions consisted of isotonic NaCl, mannitol, or sodium acetate buffered with HCO₃⁻. The final of mannitol solution was not significantly different from plasma, whereas final of NaCl and NaAc solutions were, respectively, greater and less than plasma concentration (P < 0.001). [Modified from Argenzio and Whipp 13.]

Relationship of net solute transport to net water transport in experiments with sodium acetate solution. Regression lines are shown over range of values encountered in these in vivo perfusion experiments of pig proximal colon. The 95% confidence limits are shown. Intercepts for HCO₃⁻, Na⁺, and acetate were −0.96 ± 0.06, 0.25 ± 0.06, and 1.4 ± 0.09 meq/min, respectively, at zero net water movement.

Possible mechanism to explain absorption of undissociated acid (HAc) and its partial dependence on Na⁺ absorption. A Na⁺‐H⁺ exchange mechanism on mucosal membrane provides additional source of luminal H ions to those resulting from consumption of luminal CO₂, as originally postulated by Ash and Dobson 16. Thus these 2 sources of H ions, in an unstirred layer adjacent to mucosal membranes, could continuously regenerate HAc for absorption into cell, despite alkalinization of contents in main lumen. Driving force for overall process would be rapid removal of HAc from cell by metabolism or transport across serosal membranes 10. Increased steady‐state production of intracellular H ion due to HAc absorption and dissociation inside cell could result in increased uptake of Na⁺ observed in presence of acetate. When net acetate absorption exceeds net Na⁺ absorption, a net increase in luminal HCO₃⁻ and a decrease in would be observed. In this case excess of intracellular H ions would have to leave cell via serosal membranes (not shown). For equal rates of HAc absorption and Na⁺‐H⁺ exchange, net alkalinization of lumen would not occur and a net consumption of luminal CO₂ would not be present.