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Biomedical subjects

A Bidani

Publications and source records attributed to A Bidani.

At least 109 records · Page 6Linked to original sources
PubMed1988

Effect of indomethacin and of prostaglandins on extrarenal erythropoietin production in rats.

Indomethacin elevates the plasma erythropoietin titer of hypoxic anephric rats and probably does so by increasing extrarenal erythropoietin production. Because indomethacin is a potent cyclooxygenase inhibitor, we postulated that it alters extrarenal erythropoietin production via its effects on tissue prostaglandin levels. Studies were, therefore, performed to determine the effects of indomethacin on hepatic prostaglandin E2 (PGE2) and prostaglandin F2 alpha (PGF2 alpha) titers. Indomethacin significantly decreased the PGF2 alpha level but its effects on the PGE2 level were, in most experiments, insignificant. We next studied the effects of infusing PGF2 alpha and PGE2 on the plasma erythropoietin levels of hypoxic rats. PGF2 alpha significantly reduced the plasma erythropoietin titer of anephric rats and neutralized the effect of indomethacin when both substances were administered. PGE2 infusion, on the other hand, did not significantly affect the plasma erythropoietin level of anephric rats. The data support the conclusion that PGF2 alpha is a potent inhibitor of extrarenal erythropoietin production, and that indomethacin enhances the rate of extrarenal erythropoietin production by reducing the PGF2 alpha titer in the liver.

Animals↗
PubMed1987

Renal effects of selective adenosine receptor agonists in anesthetized rats.

Exogenous adenosine affects renal hemodynamics, renal tubular transport processes, and the secretion of renin. However, adenosine is not a selective agonist; it activates both A1 and A2 cell-surface receptors and it binds to an intracellular P-site that inhibits adenylate cyclase activity. Recent in vitro studies have suggested that activation of A1- and A2- adenosine receptors results in opposite effects on renin secretion. The purpose of these experiments was to examine the renal effects of A1- and A2-adenosine receptor agonists in vivo. 5'-N-ethylcarboxamide adenosine (NECA), 2-chloroadenosine (2-CLA), and N6-cyclohexyladenosine (CHA) were infused intravenously at rates that produced comparable decreases in systemic arterial blood pressure. All three of these adenosine analogues produced comparable decreases in para-aminohippurate (PAH) and inulin clearances and in Na and K excretion rates. CHA, an A1-selective agonist, markedly decreased plasma renin concentration (PRC), whereas NECA, an A2-selective agonist, markedly increased PRC; 2-CLA, a nonselective agonist, produced a smaller increase in PRC. Taken together, these results suggest that occupation of A1- and A2-receptors inhibits and stimulates renin secretion in vivo, independently of the effects of these adenosine receptor agonists on arterial blood pressure, renal hemodynamics, and tubular Na and K transport.

Adenosine↗
PubMed1986

Electrolyte and acid-base disorders.

An overview of the principles of the diagnosis and management of severe electrolyte and acid-base problems in the critically ill is presented, stressing a pathophysiologic approach to an understanding of the problem in the individual patient.

Acid-Base Imbalance↗
PubMed1986

Effects of dextran-bound inhibitors on carbonic anhydrase activity in isolated rat lungs.

Effects of macromolecular Prontosil-dextran inhibitors (PD) on carbonic anhydrase (CA) activity in isolated rat lungs were studied. Isolated lungs were perfused with Krebs-Ringer bicarbonate (KRB) solutions containing no inhibitor, PD 100,000 (mol wt 100,000), PD 5,000 (mol wt 5,000), or low-molecular-weight inhibitors (Prontosil or acetazolamide). The time course of effluent perfusate pH equilibration was measured in a stop-flow pH electrode apparatus. Pulmonary CO2 excretion (Vco2) was monitored by continuously recording expired CO2 concentration. The lungs were ventilated with room air and perfused at 37 degrees C with KRB prebubbled with 5% CO2- 20% O2- 75% N2. The results obtained show that both the low-molecular-weight inhibitors and PD's caused postcapillary pH disequilibria (delta pH) in effluent perfusate. However, only acetazolamide and Prontosil caused a reduction in Vco2. These results suggest that there is an intravascular CA, presumably associated with endothelial cell membranes, that is accessible to all inhibitors used and is responsible in part for equilibration of the CO2- HCO3- -H+ reactions in the perfusate but, under the conditions used, does not affect CO2 excretion; and there is an extravascular (possibly intracellular) CA that can be inhibited by low-molecular-weight inhibitors, is primarily responsible for enhanced CO2 transfer across the alveolar-capillary barrier (perhaps via facilitation of CO2 diffusion), and is in part responsible for pH equilibration.

Acetazolamide↗
PubMed1985

Determinants of CO2 generation and maintenance in the renal cortex: role of metabolic CO2 production and diffusive CO2 transfer.

We have developed a mathematical model utilizing steady-state mass balance considerations in a compartmental analysis of bicarbonate reabsorption in the superficial proximal tubule and associated vasculature in order to describe quantitatively the determinants of the elevated PCO2 in the renal cortex. This analysis demonstrated for the first time that diffusive transfer of CO2 between vascular segments coupled with metabolic CO2 production could account for the PCO2 measured experimentally. In the present study the predictive value of the model was extended by comparing model-predicted and measured values for PCO2 before and after administration of metabolic and transport inhibitors. In control conditions diffusive CO2 transfer (FCO2) in combination with accepted levels of metabolic CO2 production (MCO2) can account for an elevation in PCO2 to 60 mm Hg. During rotenone and DNP administration the model predicts values for PCO2 which approximate closely the value measured in vivo. In addition, the model demonstrates that the reduction in PCO2 after rotenone and increase in PCO2 after DNP can be accounted for by parallel changes in MCO2 alone as expected. In each case a significant contribution from FCO2 is necessary, however. Therefore, this study demonstrates close agreement in both the magnitude and direction of predicted and determined values in cortical PCO2 in a variety of experimental conditions, thus, supporting a dual role for the major determinants: metabolic CO2 production and diffusive vascular to vascular CO2 transfer.

Animals↗
PubMed1984

Role of metabolic CO2 production in the generation of elevated renal cortical PCO2.

Several possible explanations for the elevated CO2 tension observed in structures of the renal cortex have been proposed. The present study was designed to investigate the contribution of renal metabolic CO2 production and removal and the role of incomplete equilibration of the CO2 added to peritubular plasma in an environment devoid of carbonic anhydrase. PCO2 was measured in vivo with PCO2 microelectrodes in early (EP) and late proximal (LP) tubules and stellate vessels (SV) during control conditions and after hyperoncotic albumin, aortic constriction, vanadate, rotenone, or 2,4-dinitrophenol (2,4-DNP) per renal artery, and carbonic anhydrase infusion. In all groups values for PCO2 in EP, LP, and SV sites were indistinguishable but significantly higher than systemic arterial PCO2. PCO2 increased to 71.4 +/- 1.4 mmHg with hyperoncotic albumin and to 87.0 +/- 1.8 mmHg after 2,4-DNP (P less than 0.001). During aortic constriction, vanadate infusion, and rotenone per renal artery, PCO2 fell to 53.7 +/- 0.9, 55.2 +/- 2.5, and 57.3 +/- 1.3, respectively (P less than 0.001). Renal O2 consumption decreased significantly after rotenone (-38.1 +/- 5.6 to -13.3 +/- 2.7 mumol X min-1 X kg-1) and increased significantly after 2,4-DNP (-35.7 +/- 5.9 to -75.9 +/- 6.9 mumol X min-1 X kg-1). These findings demonstrate that renal energy utilization and metabolic CO2 production represents an important source of renal cortical PCO2. Carbonic anhydrase infusion resulted in a decrease in PCO2 to 58.2 +/- 1.2 mmHg (P less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1984

Analysis of the determinants of renal cortical PCO2.

Recent studies employing Pco2 microelectrodes demonstrated CO2 tensions in the renal cortex (60-65 mmHg) that are significantly greater than systemic arterial Pco2. Three sources for CO2 generation have been proposed: 1) luminal production from H+ and HCO-3,2) addition of HCO-3 to peritubular plasma with disequilibrium for H+/HCO-3/CO2, and 3) metabolic CO2 production. None of these mechanisms alone can adequately explain the findings. The purpose of this study was to examine mechanisms of elevated renal cortical Pco2 generation and maintenance by developing a mathematical model for the reaction and transport processes involved in proximal tubule HCO-3 reabsorption. Steady-state calculations of pH, Pco2, and [HCO-3] for luminal, cellular, and vascular compartments employing simple mass balance considerations are presented. Besides exploring the role of metabolic CO2 production in the genesis and maintenance of elevated renal cortical Pco2, we also propose and examine the additional mechanism of diffusive transfer of CO2 between renal cortical venular and afferent arteriolar capillaries. Our results show that the required magnitude of either metabolic CO2 production or diffusive CO2 transfer alone is large (3 mmol/liter RBF). However, vascular-vascular exchange of CO2 gas in combination with accepted levels of metabolic CO2 production can adequately explain the findings of an elevated renal cortical Pco2 of approximately 65 mmHg as measured experimentally in vivo.

Absorption↗
PubMed1983

The effect of denervation diuresis on the severity of glycerol-induced acute renal failure in rats.

The results of several previous studies suggest that high urine flow rate has a protective effect in several models of experimentally induced acute renal failure. However, the methods employed to alter urine flow precluded a paired experimental design, left kidney vs. right kidney in the same experimental animal. The purpose of the present studies was to determine whether the unilateral diuresis that results from renal denervation has a protective effect on that kidney in glycerol-induced acute renal failure. Eight groups of rats were studied. The left kidneys of all were either denervated or sham-denervated; 3 to 5 days later, rats were injected with either 150 mM NaCl (controls) or glycerol; then either 3 or 24 hr after injection, renal function was measured in acute experiments. In saline-injected rats, the inulin clearances of right and left kidneys were virtually identical, whether the left kidney was denervated or not; however, in rats with denervated left kidneys, left kidney urine flow exceeded that of the right kidney whereas the opposite was true in rats with sham-denervated left kidneys. In contrast with saline-injected rats, there were highly significant differences in inulin clearances of right and left kidneys in glycerol-injected rats at both 3 and 24 hr after injection; left kidney inulin clearance exceeded that of the right in rats with denervated left kidneys, whereas right kidney inulin clearance exceeded that of the left in rats with sham-denervated left kidneys. Since the kidney with the higher urine flow had the higher inulin clearance at 3 and 24 hr after glycerol, whether or not the kidney was denervated, these results suggest that urine flow per se has a protective effect in glycerol-induced acute renal failure in rats.

Acute Kidney Injury↗
PubMed1982

Effects of salicylate on HCO-3/Cl- exchange across the human erythrocyte membrane.

Changes in extracellular pH (pHo) in human red cell suspensions were monitored in a stopped-flow rapid reaction apparatus. A 20% suspension of washed human RBC in saline at pH 7 containing NaHCO3 and extracellular carbonic anhydrase was mixed with an equal volume of buffered saline solution at pH 6.7. Sodium salicylate, when present, was added to both the erythrocyte suspension and the buffer solution. The effects of salicylate in the therapeutic to toxic concentration range on HCO-3/Cl- exchange were studied at 37 degree C. HCO-3/Cl- exchange flux was estimated using the extracellular buffer capacity and the difference between dpHo/dt using a control RBC suspension and that using a suspension of RBC whose anion exchange pathway was markedly inhibited. The results show that salicylate competitively decreases the rate of HCO-3/Cl- exchange, with inhibition increasing as salicylate concentration increases. KI is approximately 2.4 mM. At a salicylate concentration of 10 mM, HCO-3/Cl- exchange under the conditions of our experiments was inhibited by more than 70%. These findings are consistent with the possibility that CO2 transfer in capillary beds in vivo may be diminished in the presence of salicylate due to slowing of red cell HCO-3/Cl- exchange.

Bicarbonates↗
PubMed1982

Analysis of the effects of hematocrit on pulmonary CO2 transfer.

A mathematical model of the chemical and transport events in blood during and after gas exchange has been used to examine the rates of CO2 excretion (Vco2) and O2 uptake (Vo2) in the lung at different levels of hematocrit (Hct), assuming fixed mixed venous blood O2 and CO2 contents and alveolar gases and constant cardiac output. The results show that a reduction in Hct from 45 to 30% leads to approximately 25% reduction in Vco2 compared with approximately 30% reduction in Vo2. Reduction of Hct from 45 to 15% results in approximately 50% reduction in Vco2 and approximately 63% reduction in Vo2. An increase in Hct from 45 to 60% results in approximately 25% increase in Vco2, accompanied by approximately 30% increase in Vo2. These fractional changes in gas exchange are only slightly affected by the extent of catalysis of the plasma CO2-H2CO3 hydration-dehydration reactions in the pulmonary vasculature. The reduction in Vco2 with reductions in Hct are due to 1) decrease in the total quantity of Bohr protons released during diminution of Vo2, 2) decrease in the size of the high buffer capacity intraerythrocytic pool, and 3) decrease in the total surface area available for HCO-3/Cl- exchange across the red cell membrane. We conclude that hitherto unrecognized changes in Vco2 (in addition to the well-known changes in Vo2) may occur as a consequence of alterations in Hct.

Capillaries↗
PubMed1981

Effects of red blood cell HCO3(-)/Cl- exchange kinetics on lung CO2 transfer: theory.

A mathematical model has been used to study the influences of the kinetics of erythrocyte HCO3(-)/Cl-- exchange on CO2 elimination in the lung. In addition to the chloride shift, the model includes 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) red cell volume changes; and 6) diffusion of gases between alveoli and blood. Carbonic anhydrase activity was assumed to be available to plasma as it passes through the lung capillaries. The results show that a reduction of PHCO3(-) leads to a reduction in pulmonary CO2 elimination of up to 30%, whether or not carbonic anhydrase activity is available to plasma. Characteristic slow downstream pH and PCO2 changes predicted for each case may represent an explanation for the apparent discrepancy between in vivo and in vitro slow downstream pH changes reported previously. We conclude that red cell HCO3(-)/Cl- exchange partially limits CO2 elimination from blood in the lung and may have a major influence on capillary gas transfer when its speed is abnormally slow.

Bicarbonates↗