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Biomedical subjects

A Bidani

Publications and source records attributed to A Bidani.

10 recordsLinked to original sources
PubMed1979

Sodium-chloride-induced protection in nephrotoxic acute renal failure: independence from renin.

It has been shown that the severity of experimentally induced acute renal failure (ARF) is inversely related to dietary sodium chloride intake, and the effects have been attributed to the concurrent changes in renal renin. In the current study, renal renin of rats was increased by chronic sodium deprivation and decreased by chronic sodium loading and DOCA administration. In two nephrotoxic models (mercuric chloride, uranyl nitrate), giving previously sodium-deprived rats 1% sodium chloride to drink for 48 hours prior to ARF induction greatly attenuated the severity without any reduction in their high renal renin. Conversely, giving previously sodium-loaded rats tap water to drink for 4 to 5 days prior to AFR induction greatly enhanced the severity without any increase in their subnormal renal renin. Therefore, the changes in severity of ARF resulting from changes in dietary sodium are not mediated by changes in renal renin. Significant inverse correlations were found between mean peak BUN values during the follow-up period (5 to 7 days) and the 24-hour urinary sodium excretions prior to ARF induction in both models, suggesting that sodium intake and/or excretion at the time of induction is a good predictor of the severity. The effects of sodium chloride in both models were predominantly expressed during the maintenance phase, and consisted of attenuation of the severity (both models) and hastening of the recovery (mercuric chloride model). Possible mechanisms by which dietary sodium produced its effects, independently of its effects on the renin-angiotensin system, are discussed.

Acute Kidney Injury↗
PubMed1979

Peritoneal dialysis of theophylline.

The use of peritoneal dialysis as an adjunct to management of theophylline intoxication is presented. Due to the nature of the case, detailed pharmacokinetic explanation was not possible. The data indicate that appreciable quantities of theophylline can be removed using peritoneal dialysis.

Humans↗
PubMed1978

Analysis of the effects of pulsatile capillary blood flow and volume on gas exchange.

Blood flow into the pulmonary capillaries and the volume of blood within the capillary bed are both pulsatile with the cardiac cycle. We have developed a quantitative model of diffusional gas exchange in the lung to investigate the effects of coupling between these two time-varying parameters on lung O2 and CO2 exchange. For normal man breathing room air at rest, the computed results agree well with previous predictions for the constant flow and volume case, and for the case of pulsatile flow alone. When coupled time-varying pulmonary capillary blood flow and volume are included, using the best data available in the literature to define these parameters, diffusional O2 exchange is improved over the cases of pulsatile flow or volume alone, and closely approximates that obtained for the hypothetical constant flow and volume case. CO2 exchanges, and O2 exchange during hypoxia, are not affected by pulsatile flow and/or volume. These results suggest that O2 exchange is efficient in the presence of coupled blood flow and blood volume pulsations as they exist in the lung capillaries, and that these conditions may be optimal for gas exchange under certain physiological (or pathological) conditions.

Blood Volume↗
PubMed1978

Analysis of postcapillary pH changes in blood in vivo after gas exchange.

A quantitative description of the reaction and transport processes that take place in blood during and after gas exchange in capillaries is developed and used to interpret recently reported experimental results. Included in the computation are 1) CO2-H2CO3 hydration-dehydration reactions in plasma and erythrocytes, 2) CO2 reactions with hemoglobin, 3) O2 binding to hemoglobin, 4) buffering of H+ intra- and extracellularly, 5) HCO3- Cl- exchange across the red cell membrane, 6) diffusion of gases between alveolar gas and blood, and 7) transcellular movement of water. Ion and water fluxes are described assuming passive diffusion down their electrochemical potential gradients. Recent data on the magnitude of the Bohr and Haldane shifts and on carbamate formation in the presence of 2,3-diphosphoglycerate are used. The analysis is used to examine the direction, magnitude, and time course of plasma pH changes in blood leaving the pulmonary capillaries and is shown to preduct results that agree very closely with recently reported experimental measurements in vivo. The time computed for plasma pH equilibration after gas exchange when carbonic anhydrase activity is absent from plasma is so great that blood may never be in complete electrochemical equilibrium as it travels around the circulation in normal man.

Bicarbonates↗
PubMed1978

Slow postcapillary changes in blood pH in vivo: titration with acetazolamide.

A stopped-flow pH electrode apparatus was used to investigate the mechanisms underlying slow changes in plasma pH (pHO) after blood leaves the pulmonary capillaries in carbonic anhydrase-inhibited animals. After acetazolamide was administered to an anesthetized dog or cat, arterial blood was withdrawn through the electrode apparatus into a syringe. Syringe movement was then suddenly stopped. Temperature and pHO of the blood in the electrode chamber were monitored both before and after blood withdrawal ceased. After stopping flow, pHO of the blood in the electrode chamber a) rose 0.02 after a dose of about 1 mg/kg acetazolamide; b) did not change after a dose of about 2 mg/kg acetazolamide; and c) fell 0.10 after a dose greater than about 5 mg/kg acetazolamide. With reasonable red cell and plasma carbonic anhydrase activities assumed for each dose level of acetazolamide, a computer model of the reaction and transport processes occurring in blood after gas exchange in the lung yielded predicted time courses of pHo that were in good agreement with the experimental results. The observed slow pHo changes are largely a result of disequilibrium of [H+] between red blood cells and plasma as blood leaves the pulmonary capillaries.

Acetazolamide↗
PubMed1978

Analysis of PCO2 differences during rebreathing due to slow pH equilibration in blood.

A quantitative analysis of the reaction and transport processes that occur in blood during and after gas exchange has been used to investigate mechanisms that might account for positive alveolar-mixed venous (A-V) and alveolar-arterial (Aa) PCO2 differences during rebreathing. The analysis was used to determine PCO2 changes that take place in blood as it travels from veins to arteries under conditions in which no CO2 is exchanged in the lung. The predicted A-V and Aa PCO2 differences are all positive and lie within the range of reported measured values. The differences are due to disequilibrium of [H+] between plasma and red blood cells, and to disequilibrium of the reactions CO2 in equilibrium HCO3- + H+ in plasma, as blood leaves the tissue and/or lung capillaries. The differences are increased with exercise and with continued O2 uptake in the lung, the latter due to the Haldane shift. We conclude that the two disequilibria and the Haldane shift contribute to the reported PCO2 differences in rebreathing animals but may not fully account for them. These mechanisms cannot explain any PCO2 differences that might exist during net CO2 elimination from blood in the lung.

Acid-Base Equilibrium↗
PubMed1978

Slow postcapillary pH changes in blood in anesthetized animals.

To investigate the hypothesis that blood pH and PCO2 continue to change after the blood leaves an exchange capillary, we used a rapidly responding, pressure-insensitive, stopped-flow pH electrode apparatus. Arterial blood from an anesthetized dog or cat is drawn through the apparatus into a syringe. Syringe movement is then suddenly stopped. Temperature and pH of the blood in the electrode assembly are continuously monitored, both before and after blood withdrawal ceases. Hemolysis was reduced by coating all blood contact surfaces with silicone and fasting the animal overnight, anesthetizing it with crystalline pentobarbital sodium, and allowing it to ventilate spontaneously. After stopping withdrawal, pH of blood in the electrode chamber continued to change, rising 0.01 unit with t1/2 of 4.4 s. After lysed blood was returned to the animal to provide carbonic anhydrase to the plasma, no pH change was seen after stopping the flow. The small pH rise occurring in arterial blood in vivo is probably due in large part to disequilibrium of [H+] between red blood cells and plasma at the end of the pulmonary capillary, the equilibration process being rate-limited by the extracellular CO2 hydration-dehydration reaction.

Acid-Base Equilibrium↗
PubMed1978

HgCl2-induced acute renal failure in the Goldblatt rat.

These experiments were designed to test the hypothesis that renal renin is an important determinant of the severity of acute renal failure in rats. Two-kidney "Goldblatt rats" were prepared by constricting the left renal arteries with silver clips and leaving the contralateral arteries untouched. After 2 to 5 weeks, the clips were removed, and HgCl2 was injected in 13 rats (1 ml/kg body weight of 4.7 mg of HgCl2 per milliliter of 140 mM NaCl). These rats exhibited the characteristic features of acute renal failure 24 hr later. As compared with a group of seven similarly treated rats injected with 140 mM NaCl without HgCl2, GFR, V, and UNaV were reduced, and %FE H2O and %FE Na were increased. As assessed by these parameters, severity of functional impairment was equal in both kidneys. However, cortical renin was 28 times higher in the left kidney than in the right. These results are inconsistent with the hypothesis.

Acute Kidney Injury↗
PubMed1977

Postcapillary changes in blood pH in vivo during carbonic anhydrase inhibition.

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.

Acetazolamide↗