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Biomedical subjects

K A Hubel

Publications and source records attributed to K A Hubel.

At least 37 records · Page 2Linked to original sources

Intestinal ion transport: effect of norepinephrine, pilocarpine, and atropine.

The effects of parenteral pilocarpine, atropine, and norepinephrine on salt and water transport were studied in jejunum and ileum of anesthetized rats. Pilocarpine increased jejunal transmural PD, reduced absorption of Na, K, HCO3, and H2O, and increased secretion of Cl; in ileum, it caused secretion of Na and H2O, elicited secretion of K, and reduced the absorption of Cl. In both segments, perfusate became more akaline, and there was less of a rise in PCO2. Atropine prevented all changes caused by pilocarpine. Atropine alone increased jejunal absorption of Na and HCO3 and acidity of perfusate, implying that cholinergic nerves influence transport. Norepinephrine augmented jejunal absorption of Na, Cl, and H2O but caused no change in PD. In ileum, norepinephrine increased absorption of Na and Cl, reduced the rise in pH, increased the rise in PCO2 of perfusate, but did not affect net HCO3 movement. With all agents, when Na absorption increased, perfusate became more acidic in jejunum and less alkaline in ileum, evidence of an association between Na and H transport.

Animals↗

The mechanism of bicarbonate secretion in rabbit ileum exposed to choleragen.

BICARBONATE MAY BE SECRETED INTO THE INTESTINAL LUMEN IN CHOLERA BECAUSE: HCO(3) (-) ions are transported, or because OH(-) ions accumulate and react with dissolved CO(2) to form HCO(3) (-). If HCO(3) (-) ions are transported into the lumen from the interstitial fluid, lumenal P(CO2) should increase (HCO(3) (-) right harpoon over left harpoon OH(-) + CO(2)); if OH(-) accumulates, P(CO2) should diminish. Net movement of H(2)O, and HCO(3) (-), and changes in pH and P(CO2) in lumenal fluid were studied in adjacent segments of rabbit ileum in vivo, one of which was exposed to choleragen. 4 h after exposure, segments were drained and infused with gassed Krebs-Henseleit solution whose P(CO2) exceeded arterial P(CO2). After 45 min, fluid was collected anaerobically from control and cholera segments. Among 13 cholera segments, lumenal P(CO2) diminished by a mean of 8.4 torr and was less than femoral arterial blood in six instances. In the paired control segments, mean P(CO2) increased by 4.4 torr, and was always greater than arterial P(CO2). Dilution could not account for the low P(CO2) in cholera segments because in hypertonic solutions that caused water to move into the lumen, the P(CO2) did not differ from control values obtained with isotonic solutions. The results suggest that OH(-) accumulation (by addition of OH(-) or removal of H(+)) causes HCO(3) (-) secretion in cholera. This does not result from secretion of some other base (e.g., HPO(4) (-)), because HCO(3) (-) accounts for most of the base in the lumenal fluid. The P(CO2) changes suggest that OH(-) reacts with CO(2) at the cell-lumen interface, but reaction at the cell-interstitial fluid interface cannot be excluded.

Animals↗

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.

Bicarbonates↗