scholarly journals Inhibition of Gastric Secretion of Hydrochloric Acid in vivo by Carbonic Anhydrase Inhibition

Nature ◽  
1952 ◽  
Vol 170 (4325) ◽  
pp. 499-499 ◽  
Author(s):  
HENRY D. JANOWITZ ◽  
HENRY COLCHER ◽  
FRANKLIN HOLLANDER
Keyword(s):  
Hydrochloric Acid ◽  
Carbonic Anhydrase ◽  
Gastric Secretion ◽  
Carbonic Anhydrase Inhibition ◽  
Inhibition Of Gastric Secretion

scholarly journals Protective effects of carbonic anhydrase inhibition in brain ischaemia in vitro and in vivo models

2021 ◽  
Vol 36 (1) ◽  
pp. 964-976
Author(s):  
Ilaria Dettori ◽  
Irene Fusco ◽  
Irene Bulli ◽  
Lisa Gaviano ◽  
Elisabetta Coppi ◽  
...  
Keyword(s):  
Carbonic Anhydrase ◽  
Protective Effects ◽  
Brain Ischaemia ◽  
In Vivo Models ◽  
Carbonic Anhydrase Inhibition

CARBONIC ANHYDRASE INHIBITION AND GASTRIC SECRETION*

1952 ◽  
Vol 15 (2 Series II) ◽  
pp. 54-55 ◽  
Author(s):  
HENRY D. JANOWITZ ◽  
HENRY COLCHER ◽  
FRANKLIN HOLLANDER
Keyword(s):  
Carbonic Anhydrase ◽  
Gastric Secretion ◽  
Carbonic Anhydrase Inhibition

scholarly journals Carbonic anhydrase inhibition for the management of cerebral ischemia: in vivo evaluation of sulfonamide and coumarin inhibitors

2015 ◽  
Vol 31 (6) ◽  
pp. 894-899 ◽  
Author(s):  
Lorenzo Di Cesare Mannelli ◽  
Laura Micheli ◽  
Fabrizio Carta ◽  
Andrea Cozzi ◽  
Carla Ghelardini ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Carbonic Anhydrase ◽  
In Vivo Evaluation ◽  
Carbonic Anhydrase Inhibition

Postcapillary changes in blood pH in vivo during carbonic anhydrase inhibition

1977 ◽  
Vol 43 (4) ◽  
pp. 582-590 ◽  
Author(s):  
E. D. Crandall ◽  
A. Bidani ◽  
R. E. Forster
Keyword(s):  
Carbonic Anhydrase ◽  
Carbonic Anhydrase Activity ◽  
Stopped Flow ◽  
Arterial Blood ◽  
Blood Ph ◽  
Pulmonary Capillary ◽  
Carbonic Anhydrase Inhibition ◽  
Glass Ph Electrode ◽  
Electrode Chamber

A rapidly responding stopped-flow glass pH electrode apparatus was used to investigate pH changes in blood in vivo after it exits from an exchange capillary. Arterial blood was drawn from anesthetized animals through the apparatus. Temperature and pH of the blood in the electrode chamber were continuously recorded, both during withdrawal and after flow was stopped. Blood pH did not change after stopping flow in control experiments. When benzolamide (2 mg/kg) was given to inhibit carbonic anhydrase activity available to plasma (e.g., due to lysis) while having less effect on intracellular activity, pH increased 0.02–0.04 (t1/2 approximately 8 s) after stopping flow. Administration of acetazolamide (50 mg/kg) resulted in pH decreasing 0.07–0.10 (t1/2 approximately 15 s) after stopping flow. Ventilation for 1 min with N2 resulted in an increased rise in pH for the benzolamide-treated animals but a decreased fall in pH for the acetazolamide-treated animals. These shifts in arterial blood pH after gas exchange are largely due to disequilibrium of [H+] between red cells and plasma at the end of the pulmonary capillary.

Serotonin release by hydrochloric acid: possibility of a feed-back mechanism

1961 ◽  
Vol 201 (6) ◽  
pp. 1017-1019 ◽  
Author(s):  
Robert H. Resnick ◽  
Seymour J. Gray
Keyword(s):  
Hydrochloric Acid ◽  
Gastric Secretion ◽  
Portal Vein ◽  
Serotonin Release ◽  
Secretory Function ◽  
Drug Induced ◽  
Rat Portal Vein ◽  
Inhibition Of Gastric Secretion ◽  
Intestinal Serotonin ◽  
Partial Depletion

This investigation was carried out to determine whether the release of upper intestinal serotonin produced by hydrochloric acid perfusion was responsible for a subsequent inhibition of gastric secretion. To explore this possibility, gastric secretion in the pyloric-ligated rat was studied after the administration of varying quantities of serotonin through the rat portal vein. In another series of tests, the capacity of intestinally perfused hydrochloric acid to inhibit gastric secretion was studied in animals partially depleted of serotonin by reserpine or subjected to drug-induced chemical blockade of serotonin effect. Results indicate that serotonin infused through the portal vein does not alter gastric pH or secretory volume and that partial depletion of tissue serotonin or the use of serotonin antagonists does not prevent the intestinal suppression of gastric secretory function. It is therefore concluded that the intestinal release of serotonin is not a factor in the reduction of gastric acidity after HCl perfusion of the small intestine.

Inhibition of NaCl absorption from perfused rat ileum by furosemide

1976 ◽  
Vol 230 (6) ◽  
pp. 1517-1523 ◽  
Author(s):  
MH Humphreys
Keyword(s):  
Carbonic Anhydrase ◽  
Electrolyte Solution ◽  
Perfusion Fluid ◽  
Nacl Transport ◽  
Rat Ileum ◽  
Carbonic Anhydrase Inhibition ◽  
Neutral Process ◽  
Net Flux ◽  
Unidirectional Fluxes

The effect of furosemide on intestinal absorption of water and electrolytes was studied using segments of rat ileum perfused in vivo. Furosemide (1 mM) in the perfusion fluid reduced absorption of Na, Cl, and water by 50% from a balanced electrolyte solution without changing the transepithelial potential difference (PD). This effect was also observed in the absence of luminal glucose and was largely reversible. Substitution of all Na in perfusion fluid with choline produced secretion of Na and water and abolished Cl absorption; substitution of all Cl with SO4 reduced Na absorption to 20% of control values. Under both these conditions, furosemide had only trivial effects on electrolyte absorption and exerted no effect on PD. Measurements of unidirectional fluxes of Na and Cl showed that furosemide decreased net flux by reducing lumen-to-blood flux of these ions rather than increasing blood-to lumen flux. These results resemble those obtained in this tissue following exposure to acetazolamide, and suggest that furosemide inhibits a coupled, neutral process of NaCl transport from lumen to blood. Although this effect could be a result of carbonic anhydrase inhibition it more likely occurs from a separate action of furosemide on ileal transport.

Gastric HCO3- secretion: relationship with Na+ secretion and effect of acetazolamide in humans

1991 ◽  
Vol 261 (2) ◽  
pp. G320-G326
Author(s):  
M. Feldman ◽  
M. Goldschmiedt
Keyword(s):  
Gastric Mucosa ◽  
Carbonic Anhydrase ◽  
Gastric Secretion ◽  
Intravenous Dose ◽  
Carbonic Anhydrase Inhibitor ◽  
Healthy Men ◽  
Carbonic Anhydrase Inhibition ◽  
K Secretion ◽  
The Relationship ◽  
Secretion Rates

We examined the relationship between gastric HCO3- and Na+ secretion under fasting and sham-fed conditions in nine healthy men and also evaluated the effect of the carbonic anhydrase inhibitor acetazolamide on gastric secretion of HCO3- and Na+. Secretion of H+, K+, and Cl- were also measured. Gastric HCO3- secretion rates under fasting and sham-fed conditions closely paralleled Na+ secretion rates. A maximally tolerated intravenous dose (10 mg/kg) of acetazolamide significantly inhibited H+, Cl- and K+ secretion but did not significantly affect Na+ or HCO3- secretion. Thus the gastric mucosa secretes HCO3- and Na+ in parallel in humans both under fasting and sham-fed conditions. Relative to parietal secretion of HCl, nonparietal secretion of HCO3- and Na+ is resistant to carbonic anhydrase inhibition.

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