Luminal CO2 Research Articles

Water and total CO2 reabsorption along the rat proximal convoluted tubule.

Micropuncture experiments were performed on rat kidney to evaluate the profile of water and total CO2 reabsorption along the proximal tubule. Three to eight samples were collected along the same nephron and the puncture-to-glomerulus distances were mea- sured for each site. In Munich rats with accessible glomeruli, the water reabsorption rate was found to be constant all along the first five millimeters of proximal tubule. In Sprague Dawley rats with no accessible glomerulus, the same observation was made for these five millimeters, and the water reabsorption rate per mm along this segment was found to be a function of the glomerular filtration rate. For the two last milli- meters of tubule accessible at the kidney surface, the water reabsorption rate was found to decrease in 5 out of the 21 tubules studied and ranged from 0.15- 3.5 nl. rain- 1. ram- 1. In Sprague Dawley rats the fall in the luminal total CO2 concentration (CO2)t along the tubular length was nearly constant (21mmole.1-1) between Bowman's capsule and the end proximal tubule, irrespective of the plasma (CO2)t value. The distance needed to reach half- maximum total COz reabsorption varied from 1.1- 1.9 mm from one tubule to another, as a function of the total CO2 filtered load. These data suggest that the tubular length involved in "avid" bicarbonate re- absorption increases as a function of the filtered load and that in the first millimeters of tubule, bicarbonate reabsorption depends on a rapidly saturable mech- anism. However, no close relationship was found between total CO2 movement or the calculated transepithelial chloride gradient on the one hand and water reabsorption along the convoluted proximal tubule on the other.

Absorption of Short-Chain Fatty Acids by the Colon

Short-chain fatty acids (SCFAs) constitute the major solute fraction of normal stool water and are responsible for the diarrhea associated with carbohydrate (CHO) malabsorption. Although SCFA absorption from the human small bowel has been reported previously, the fate of SCFAs in the colon--their major site of production--was investigated in the present study. The colon of normal volunteers was perfused with neutral, isotonic solutions containing SCFA, 0-90 mM. Propionate was studied in detail with limited observations on acetate and n-butyrate. SCFA absorption was concentration-dependent; back diffusion of metabolic products, ketone bodies, was quantitatively insignificant. The transport process was accompanied by increased Na, K, and water absorption, by luminal alkalinization due to bicarbonate accumulation, and by a fall in lumen PCO2. The results are consistent with the existence of two mechanisms for colonic SCFA absorption: first, nonionic diffusion of protonated SCFA involving consumption of luminal CO2; this process accounts for about 60% of total SCFA absorption; and second, cellular uptake by ionic diffusion of the Na or K salt of the SCFA.

Intestinal villus blood flow measured with carbon monoxide and microspheres.

The purpose of the present study was to compare the small intestinal blood flow that equilibrates with luminal CO (FLco) with simultaneous determinations of villus blood flow measured by a recent modification of the microsphere technique. These studies, carried out in rabbits, showed that FLco closely correlated (r = 0.83) with villus flow measured with microspheres over a three-fold range of flows, and the mean rate of flow to the villi by both techniques was about 0.08 ml/min X g of intestine. Thus, FLco appears to be a measure of villus blood flow. Based on previous studies of inert gas uptake from the rabbit small intestine, it appears that absorption of readily diffusible substances in the rabbit can be represented by a simple two-component model: a flow-limited component in which substances equilibrate with villus blood flow and are carried away without subsequent countercurrent exchange, and a diffusion-limited component which presumably represents uptake by the blood flow of the crypt region or submucosa.

Mechanisms of disposal of acid and alkali in rabbit duodenum.

Stripped duodenal mucosa of rabbits was mounted in Ussing chambers containing a Ringer solution gassed with 100% O2. The disappearance of acid or alkali from the mucosal solution of short-circuited tissue was measured with a pH stat while the serosal pH was kept at 7.4. The duodenum rapidly disposed of both acid and alkali; neither property was altered by gassing with N2 while iodoacetate was in the perfusing solutions. Prevention of release of CO2 from the mucosal chamber obliterated the early rapid phase of acid disposal by the mucosa while a similar maneuver in the serosal chamber increased the appearance of serosal acid without altering the rate of acid disposal. Gut sacs of rabbit duodenum in vitro and in vivo showed a positive correlation between acid disposal and the rate of luminal CO2 production. While acid disposal progressively decreased with time for the in vitro gut sacs, the in vivo gut sac showed no fatigue in this respect. Luminal acidification in the Ussing chamber was associated with a profound reduction in short-circuit current (Isc), partially reversible by elevation of the mucosal pH but not by luminal glucose. Our data suggest that acid disposal occurs in part by intraluminal neutralization and in part by diffusion into the mucosa.

Effect of luminal sodium concentration on bicarbonate absorption in rat jejunum.

An exchange of Na(+) for H(+) has been proposed to explain why jejunal Na(+) absorption is influenced by luminal concentrations of H(+) and HCO(3) (-). We studied the influence of luminal Na(+) concentration on net HCO(3) (-) absorption by perfusing rat jejunum in vivo. When Na(+) was omitted from the perfusion fluid, HCO(3) (-) absorption diminished by a fixed amount over a range of initial HCO(3) (-) concentrations of 15 to 80 mM. This change was not caused by alterations in transmural PD or direction of water movement. Because the rate of HCO(3) (-) absorption decreased as the luminal HCO(3) (-) concentration lessened, Na(+)-dependent HCO(3) (-) absorption accounted for an increasing percent of total absorption as the luminal concentration of HCO(3) (-) diminished. The effect of Na(+) on HCO(3) (-) absorption is mediated, at least in part, by H(+) secretion, because luminal CO(2) production (manifested by luminal P(CO2)) dimished as HCO(3) (-) absorption decreased. The changes in P(CO2) are caused by reaction of H(+) with HCO(3) (-) in the luminal fluid because luminal P(CO2) is augmented by the presence of HCO(3) (-) and is diminished by addition of phosphate or Tris buffer. Whether all H(+) secretion requires luminal Na(+) cannot be determined with these experimental techniques because mucosal permeability to Na(+) and the unstirred layer make it impossible to eliminate Na(+) ions from the luminal cell surface. The nature of the mechanism for HCO(3) (-) transport that is not sodium dependent remains to be determined.