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Biomedical subjects

L C Garg

Publications and source records attributed to L C Garg.

At least 91 records · Page 5Linked to original sources
PubMed1978

The effect of acid--base changes on skeletal muscle twitch tension.

The effects of acid--base alterations produced by changing bicarbonate (metabolic type), carbon dioxide tension (respiratory type), or both bicarbonate and carbon dioxide tension (compensated type) on skeletal muscle twitch tension, intracellular pH, and intracellular potassium were studied in vitro. Hemidiaphragm muscles from normal rats and rats fed a potassium-deficient diet were used. Decreasing the extracellular pH by decreasing bicarbonate or increasing CO2 in the bathing fluid produced a decrease in intracellular pH, intracellular K+, and muscle twitch tension. However, at a constant extracellular pH, an increase in CO2 (compensated by an increase in bicarbonate) produced an increase in intracellular K+ and twitch tension in spite of a decrease in intracellular pH. The effect on twitch tension of the hemidiaphragms showed a rapid onset, was reversible, persisted until the buffer composition was changed, and was independent of synaptic transmission. It is concluded that the twitch tension of the skeletal muscle decrease with a decrease in intracellular K+. The muscle tension also decreases with an increase in the ratio of intracellular and extracellular H+ concentration. However, there is no consistent relationship between muscle tension and extracellular or intracellular pH. The muscle tension of the diaphragms taken from K+-deficient rats is more sensitive to variations in CO2, PH, and bicarbonate concentration of the medium than that of the control rat diaphragms.

Acid-Base Equilibrium↗
PubMed1978

Severe hyperchloremic acidosis complicating jejunoileal bypass.

In summary, severe hyperchloremic acidosis developed in two patients as a late complication after jejunoileal bypass for morbid obesity. This acidosis was associated with episodes of dizziness, ataxia, headache, weakness, confusion and transient loss of consciousness. Recognition of this symptom complex in the patient with a jejunoileal bypass should suggest metabolic acidosis as a complication of this surgical procedure. Bicarbonate replacement provided prompt, but temporary, improvement in the symptoms and the acidosis. Revision of the intestinal bypass was required for correction. Special studies to rule out renal tubular acidosis were performed and definitely excluded the kidney as a source of the acidosis.

Acidosis↗
PubMed1977

Inhibition of carbonic anhydrases of rat liver by halides.

The hepatic carbonic anhydrases from male rat are known to differ from those of female rat in being resistant to inhibition by sulfonamides. In the present work the inhibition of carbonic anhydrases from livers of male and female rats by chloride and iodide was studied in the CO2 hydration reaction. The hepatic carbonic anhydrases from male rats were found to be more susceptible to inhibition by halides (I50 and Cl- = 7-15 mM, and I- = 0.7-1.5 mM). On the other hand, the hepatic carbonic anhydrases from female rats were less susceptible to inhibition by halides (I50 for Cl- = 150-250 mM and for I- = 3-10 mM). The presence of bicarbonate increased I50 of both Cl- and I- for liver isoenzymes of both male and female rats by about 2- to 20-fold. The differential susceptibility of carbonic anhydrases from livers of male and female rats to inhibition by halides was in contrast to their susceptibility to inhibition by sulfonamides.

Animals↗
PubMed1976

Failure of parathyroid hormone and cyclic AMP to inhibit renal carbonic anhydrase.

It has been suggested that the parathyroid hormone and cyclic AMP produce their bicarbonaturic effects through inhibition of renal carbonic anhydrase. In the present study, the incubation of renal carbonic anhydrase with parathyroid hormone or cyclic AMP in presence of ATP, Mg++ and K+ ions, did not produce any inhibition of the enzyme when the pH of the solution was maintained above 7. It is concluded, that parathyroid hormone and cyclic AMP produce urinary bicarbonate excretion by a mechanism independent of carbonic anhydrase inhibition.

Animals↗
PubMed1976

The effect of acetazolamide on the movements of anions into the posterior chamber of the dog eye.

The rate of entry of bicarbonate and chloride ions the posterior chamber of the dog, a species that has both HCO3- and Cl- concentrations in excess of plasma in this chamber, was measured in order to clarify the mechanisms involved in the produciton of aqueous humor. Four animals were given H14CO3- and 36Cl- intravenously first in a control series and then after pretreatment with acetazolamide, (50 mg/kg), a carbonci anhydrase inhibitor. Samples were taken from arterial blood and the posterior chamber. Acetazolamide did not affect chloride entry into the posterior chamber but bicarbonate entry was decreased about 50%. It is concluded that in this species, bicarbonate is the key anion for the decrease of aqueous humor production caused by the administration of acetazolamide.

Acetazolamide↗
PubMed1976

The effect of acetazolamide on the movement of sodium into the posterior chamber of the dog eye.

The rate of appearance (entry) of 22Na into the posterior chamber of the eye was determined in eight dogs under control conditions and again after pretreatment with acetazolamide, 50 mg/kg i.v. In comparison with the paired controls, pretreatment with acetazolamide decreased the average rate of entry of 22Na by 29% during the first 3 minutes after the intravenous administration of a tracer dose of the isotope. In separate experiments, the volumes of the chambers of the dog eye and the rate of aqueous humor formation were determined for the purpose of calculating nascent fluid ion concentrations. Comparisons of sodium data with the previously reported anion data are made. Results support the suggestion that reduction of intraocular pressure caused by acetazolamide is partially, if not wholly, the result of the action of the drug to reduce the secretion of aqueous humor.

Acetazolamide↗
PubMed1975

The effect of acetazolamide and carbonic anhydrase inhibition on erythrocyte 2,3-diphosphoglycerate content and metabolism.

Experiments were designed to test the hypothesis that the change in erythrocyte 2,3-diphosphoglycerate (2,3-DPG) content which occurs when metabolic acidosis is induced by prolonged inhibition of carbonic anhydrase in vivo is the same as that which occurs with the induction of other types of metabolic acidosis states. 1) Thirteen-hour infusions of nondiuretic doses of a potent carbonic anhydrase inhibitor, acetazolamide (Diamox) did not alter erythrocyte 2,3-DPG levels in rats. 2) In vitro incubation of whole blood from rats for 10 days with high concentrations of two carbonic anhydrase inhibitors failed to alter the red cell content of 2,3-DPG. 3) Purified human carbonic anhydrase B had no phosphatase activity on 2,3-DPG and it appears unlikely that the enzyme hydrolyzes other phosphate esters of the erythrocyte which could indirectly alter 2,3-DPG content. 4) Acetazolamide administered in diuretic doses for 8 days to rats induced a metabolic acidosis which was accompanied by a decrease in erythrocyte 2,3-DPG. The change in 2,3-DPG content was similar to that produced by other methods of producing metabolic acidosis, namely NH4Cl treatment and nephrectomy. It appears that changes in 2,3-DPG content associated with effects of carbonic anhydrase inhibition can be ascribed to the metabolic acidosis resulting from the action of these drugs on the kidney.

Acetazolamide↗
PubMed1975

Effect of ouabain on cerebrospinal fluid formation after carbonic anhydrase inhibition.

The effect of ventriculo-cisternal perfusion of ouabain was determined on CSF production after inhibition of carbonic anhydrase by benzolamide in cats. An additional decrease in CSF formation was observed by combination of i.v. benzolamide and intraventricular ouabain. However, the effect of the combined drugs was less than the sum of the effects of the drugs given individually. It is concluded that the reduction of the CSF production by ouabain is probably partly due to its effect on Na-K exchange (through inhibition of Na-K-activated ATPase) and partly due to its effects on Na+ transport coupled to anion transport mediated by carbonic anhydrase.

Animals↗
PubMed1975

The absence of renal bicarbonate reabsorption maxima during carbonic anhydrase inhibition.

Present studies were performed to examine the effect of carbonic anhydrase inhibition on bicarbonate reabsorption under experimental conditions where extracellular fluid volume expansion was minimized. The data showed no tubular maximum for bicarbonate reabsorption in the normal state or after carbonic anhydrase inhibition. The data support a model which assumes that the bicarbonate reabsorption is accomplished by two processes. One process is independent of protonation from H+ secretion into the tubule and probably involves reabsorption of bicarbonate ion as such. This process has an unlimited capacity for reabsorption of bicarbonate. The contribution of this process increases with an increase in plasma bicarbonate. The second process is dependent on protonation, through the intracellular hydration of carbon dioxide. The relative contribution, through the intracellular hydration of carbon dioxide. The relative contribution of this process is normally about 33% and decreases with increased plasma bicarbonate.

Absorption↗
PubMed1975

Induction of hepatic carbonic anhydrase by estrogen.

Carbonic anhydrase activity was determined in livers of rats treated with estrogen and/or progesterone. When mature female rats were treated with beta-estradiol (100 mug daily) for 3 days followed by progesterone (25 mg daily) for 2 days, there was a 2-fold increase in hepatic carbonic anhydrase activity. Either hormone alone produced no change. With 21 days treatment, however, estrogen but not progesterone caused a 4-fold increase in hepatic carbonic anhydrase. Similar results were obtained when ovariectomized rats were treated with estrogen or progesterone. The male rat contained a mixture of isoenzymes of which only 20 percent of enzyme was sensitive and the remainder refractory to inhibition by sulfonamides. Castration yielded 70 percent of enzyme sensitive, whereas castration plus progesterone yielded enzyme totally sensitive to sulfonamides without any change in total activity of hepatic carbonic anhydrase. Estrogen treatment of male rats yielded not only 100 percent sensitive enzyme but also caused a 2-fold increase in hepatic carbonic anhydrase. It is concluded that estrogen induces hepatic carbonic anhydrase of the sulfonamide-sensitive type in both males and females. This isoenzyme is normally present in female rats, but in males it replaces the sulfonamide-resistant type normally identified.

Animals↗