Diagnosis and management of metabolic alkalosis.

Elevated pH and elevated plasma bicarbonate level above normal characterise metabolic alkalosis. When bicarbonate is elevated pCO2 must also be elevated to maintain pH to its normal range. Therefore with metabolic alkalosis, the compensation is to decrease alveolar ventilation, and increase pCO2. The causes of metabolic alkalosis are gastro-intestinal hydrogen and chloride loss and due to renal cause. For metabolic alkalosis to continue both generation and maintenance of high levels of bicarbonate are necessary. The diagnosis of metabolic alkalosis is established by noting pH, serum bicarbonate (elevated) and pCO2 (compensatory) elevation. To establish the causes it is necessary to determine intravascular volume, supine and standing blood pressure and renin angiotension alolosterone axis. In chloride responsive alkalosis in which the conditions are extracellular volume depletion, hypokalaemia and hypochloraemia correction of intravascular volume with sodium chloride is needed. In severe metabolic alkalosis of any cause dilute hydrochloric acid (0.1 N HCl) may be infused intravenously but haemolysis may be a complication. In emergency situation with severe hypokalaemia dialysis with higher K+, Cl- and low HCO3- bath will be appropriate.

Multiple functions of photosystem II.

The most important function of photosystem II (PSII) is its action as a water-plastoquinone oxido-reductase. At the expense of light energy, water is split, and oxygen and plastoquinol are formed. In addition to this most important activity, PSII has additional functions, especially in the regulation of (light) energy distribution. The downregulation of PSII during photoinhibition is a protection measure. PSII is an anthropogenic target for many herbicides. There is a unique action of bicarbonate on PSII. Decrease in the activity of PSII is the first effect in a plant under stress; this decreased activity can be most easily measured with fluorescence. PSII is a sensor for stress, and induces regulatory processes with different time scales: photochemical quenching, formation of a proton gradient, state transitions, downregulation by photoinhibition and gene expression.

Bicarbonate transport in microperfused pancreatic ducts

No abstract available.

CFTR, a rectifying, non-rectifying anion channel?

No abstract available.

Effect of omeprazole on gastric bicarbonate secretion in patients with duodenal ulcer.

BACKGROUND: Omeprazole, a H+/K+ ATPase inhibitor, has been shown to reduce gastric bicarbonate secretion in cats. However, there has been no study on the effect of omeprazole on bicarbonate secretion in patients with duodenal ulcer (DU). METHODS: Fifteen men with duodenal ulcer (mean age 38 years, range 22-57) were included. Baseline gastric acid output, bicarbonate secretion, and parietal and nonparietal secretions were estimated before and after omeprazole therapy (20 mg/day) for four weeks. RESULTS: Omeprazole administration did not significantly alter bicarbonate secretion (3.3 [1.2] vs 2.4 [0.4] mmol/h), though there was significant reduction in gastric acidity (44.2 [6.6] vs 20.7 [4.6] mmol/L, p < 0.01). CONCLUSION: Omeprazole reduces acid secretion but does not affect gastric bicarbonate secretion in patients with DU.

Comparative study of bentiromide test and endoscopic retrograde pancreatography in patients with chronic pancreatitis

We performed a bentiromide test in 25 patients with chronic pancreatitis and 7 normal controls to evaluate pancreatic exocrine function, and compared the test results of patients with their endoscopic retrograde pancreatography(ERP) findings. The cumulative 6-hour recovery rate of para-aminobenzoic acid(PABA) in the urine was significantly lower in patients with chronic pancreatitis(55.8 +/- 24.2%) than in controls(82.0 +/- 10.0%). Among 25 patients with chronic pancreatitis, however, 7 patients showed normal recovery rates of PABA. Pancreatograms of the patients represented 4 mild changes, 5 moderate changes, and 16 marked changes. The average 6-hour recovery rates of PABA of the groups were 56.9 +/- 21.6%, 78.4 +/- 10.5%, and 47.2 +/- 23.7%, respectively. Urinary PABA recovery rates were found subnormal as follows: 3(75%) in the mild changes group; 1(20%) in the moderate changes group; and 14(87.5%) in the marked changes group. We found hardly any correlation between the degree of functional impairment and the changes noted by ERP. These findings suggest that both the pancreatic function test and morphologic study are required to evaluate the degree of functional impairment in patients with chronic pancreatitis.

Interactions of ANP and ANG II in tubular nephron acidification

In order to examine the effects and the interaction of angiotensin II (ANG II, 1 pM) and atrial natriuretic peptide (ANP, 1 muM) on the kinetics of bicarbonate reabsorption in the rat middle proximal tubule, we performed in vivo experiments using a stopped-flow microperfusion technique with the determination of lumen pH by Sb microelectrodes. These studies confirmed that ANG II added to the luminal or peritubular capillary perfusion fluid stimulates proximal bicarbonate reabsorption and showed that ANP alone does not affect this process, but impairs the stimulation caused by ANG II. We also studied the effects and the interation of these hormones in cortical distal nephron acidification. Bicarbonate reabsorption was evaluated by the acidification kinetic technique in early (ED) and late (LD) distal tubules in rats during in vivo stopped-flow microperfusion experiments. the intratubular pH was measured with a double-barreled microelectrode with H+ -sensitive resin. The results indicate that ANG II acted by stimulating Na+/H+ exchange in ED (81 per cent) and LD (54 per cent)segments via activation of AT1 receptors, as well as vacuolar H+ -ATPase in LD segments (33 per cent). ANP did not affect bicarbonate reabsorption in either segment and, as opposed to what was seen in the proximal tubule, did not impair the stimulation caused by ANG II. To investigate the mechanism of faction of these hormones in more detail, we studied cell pH dependence on ANG II and ANP in MDCK cells using the fluroescent probe BCECF. We showed that the velocity of cell pH recovery was almost abolished in the absence of Na+, indicating that it is dependent on Na+/H+ exchange. ANP (1 muM) alone had no effect on this recovery but reversed both the acceleration of H+ extrusion at low ANG II levels (1 pM and 1 nM), and inhibition of H+ extrusion at higher ANG II levels (100 nM). To obtain more information on the mechanism of interation of these hormones, we also studied their effects on the regulation of intracellular free calcium concentration, [Ca2+]i, monitored with the fluorescent probe Fura-2 in MDCK cells in suspension. The data indicate that the addition of increasing concentrations of ANG II (1 pM to 1 muM) to the cell suspension led to a progressive increase in [Ca2+]i to 2-3 times the basal level.In contrast, the addition of ANP (1 muM) to the cell suspension led to a very rapid 60 per cent decrease in [Ca2+]i and reduced the increase elicited by ANG II, thus modulating the effect of ANG II on [Ca2+]i. These results may indicate a role of [Ca2+)i in the regulation of the H+ extrusion process mediated by Na+/H+ exchange and stimulated/impaired by ANG II. The data are compatible with stimulation of Na+/H+ exchange by increases of [Ca2+]i in the lower range, and inhibition at high [Ca2+]i levels.

Regulation of nephron acidification by costicosteroids

The present paper reviews work from our laboratories evaluating the importance of adrenal cortical hormones in acidification by proximal and cortical distal tubules. Proximal acidification was determined by stationary microperfusion, and measurement of bicarbonate reabsorption using luminal pH determination was performed with H+ -ion-sensitive microelectrodes. Rats were adrenalectomized (ADX) 48 h before the experiments, and corticosteroids (aldosterone(A), corticosterone(B), and 18-OH corticosterone (18-OH-B)) were injected intramuscularly 100 and 40 min before the experiments. In ADX rats stationary pH increased significantly to 7.03 as compared to sham-operated rats (6.78). Bicarbonate reabsorption decreased from 2.65 + 0.18 in sham-operated rats to 0.50 + 0.07 mmol cm-2 S(-1) after ADX. The administration of the three hormones stimulated proximal tubule acidification, reaching, however, only 47.2 per cent of the sham values in aldosterone-treated rats. Distal nephron acidification was studied by measuring urine minus blood pCO2 differences (U-B pCO2) in bicarbonate-loaded rats treated as above. This pCO2 difference is used as a measure of the distal nephron ability to secrete H+ ions into an alkaline urine. U-B pCO2 decreased significantly from 39.9 + 1.26 to 11.9 + 1.99 mmHg in ADX rats. When corticosteroids were given to ADX rats before the experiment, U-B pCO2 increased significantly, but reached control levels only when aldosterone (two 3-mug doses per rat) plus corticosterone (220 mug) were given together. In order to control for the effect of aldosterone on distal transepithelial potential difference one group of rats was treated with amiloride, which blocks distal sodium channels. Amiloride-treated rats still showed a significant reduction in U-B pCO2 after ADX. Only corticosterone and 18-OH-B but not aldosterone increased U-B pCO2 back to the levels of sham-operated rats. These results show that corticosteroids stimulate renal tubule acidification both in proximal and distal nephrons and provide some clues about the mechanism of action of these steroids.

Acetate enhances the chemosensory response to hypoxia in the cat carotid body in vitro in the absence of CO2-HCO3-

To determine if intracellular acidosis enhances hypoxic chemoreception in the absence of CO2-HCO3- at pH 7.4, the effects of sodium acetate (30 mM) were studied on the chemosensory responses of the cat carotid body to hypoxic, stagnant and cytotoxic hypoxia. Carotid bodies were perfused and superfused in vitro with Tyrode's solution, free of CO2-HCO3-, buffered with HEPES-NaOH, pH 7.40, at 36.5 +/d- 0.5 degrees C and equilibrated at PO2 of 125 Torr (perfusate) and < 20 Torr (superfusate). In the absence of acetate, hypoxia (PO2 25 Torr), flow interruption and NaCN (0.01-100 micrograms) augmented the chemosensory discharges. However, in the presence of acetate, the half-excitation time of these responses decreased and their amplitude increased. Thus, acetate enhances the chemosensory response to hypoxic, stagnant and cytotoxic hypoxia. It is suggested that that intracellular acidosis induced by acetate contributes to this potentiation by correcting the alkaline pHi caused by the absence of HCO3-(-)HCO2 in the perfusate

Effect of sucralfate on gastric bicarbonate secretion in patients with duodenal ulcer.

BACKGROUND: Sucralfate is known to protect gastroduodenal mucosa and thereby facilitate healing of peptic ulcer. The mechanism of action of this drug is still not fully known. METHODS: We studied the effect of sucralfate treatment on gastric bicarbonate secretion in 16 patients with duodenal ulcer. RESULTS: Sucralfate administration (3 g daily for 4 weeks) stimulated bicarbonate secretion from 3.1 +/- 1.2 mmol/h to 4.6 +/- 2.0 mmol/h (p < 0.05). Gastric juice volume as well as non-parietal volume secretion also increased significantly after sucralfate therapy (p < 0.05). CONCLUSION: Sucralfate causes stimulation of non-parietal volume-dependent gastric bicarbonate secretion.

Impaired pancreatic bicarbonate secretion in chronic malnutrition.

Twenty three children with recurrent episodes of diarrhea and chronic malnutrition were studied for pancreatic duct function. Those children were subjected to pancreatic stimulation with pancreozymin and secretin. Grade I malnourished children, as per Gomez classification, formed the control group. The water output from pancreas increased in malnourished children (p < 0.05). It correlated significantly to cationic transport (p < 0.01). Sodium and potassium together accounted for significant proportion of water output in pancreatic fluid. Potassium transport increased with increasing severity of malnutrition and may be responsible for the hypokalemia observed in malnourished children. Pancreatic secretion of bicarbonate decreased in severe malnutrition inspite of increased flow rate of pancreatic secretion. This is probably due to defective bicarbonate secretion likely to be located at pancreatic duct epithelial cell membrane.

Efecto del bicarbonato de sodio sobre la actividad colinesterasa en cerebro, eritrocitos, plasma e higado de ratas intoxicadas con paratión

El presente trabajo se realizó con la finalidad de evaluar el efecto que tiene el bicarbonato sobre la actividad de la acetil colinesterasa de diversos tejidos, en animales de experimentación intoxicados con paratión. Para ello se formaron cuatro grupos de diez ratas cada uno. El grupo A sirvió de control . Los grupos B y C recibieronm por vía intraperitoneal paratión y además este último recibió bicarbonato de sodio luego de quine minutos de ser administrado el organofosforado. El grupo D recibió únicamente bicarbonato de sodio. Se dosaron las actividades colinesterásicas de los cuatro grupos en plasma , eritrocito, cerebro e hígado, por el método de Ellman modificado, y se compararon las actividades en los diferentes tejidos entre los grup[os de estudio con el fin de ver como variaba la actividad de la enzima inhibida por el paratión, por efecto del bicarbonato. Se encontró que la inhibición de la actividad colinesterásica, por el efecto del paratión, era significativa a nivel plasmático, cerebral y hepático, mas no a nivel eritrocítico; además se vió que el bicarbonato por si solo inhibia la actividad de la enzima en los mismos tejidos, de manera significativa. Por otro lado se encontró que la actividad colinesterásica inhibida por el órgano fosforado, se recuperó luego de la administración del bicarbonato de sodio. Con los resultados obtenidos se propone que la acción del bicarbonato sería desactivando al insecticida mismo y no sobre la colinesterasa.

Effect of pentagastrin on gastric bicarbonate secretion in patients with duodenal ulcer & healthy controls.

We studied the gastric acid and bicarbonate secretion rates in 12 patients with duodenal ulcer and 6 age matched healthy controls. Measurements of gastric juice volume (nonparietal and parietal), acidity and osmolality were done. The ulcer patients secreted more acid, parietal and nonparietal fluid than controls under basal conditions and after subcutaneous pentagastrin injection (6 micrograms/kg body weight). However, the gastric bicarbonate secretion was similar in the duodenal ulcer patients and controls, both under basal state as well as after pentagastrin stimulation. The gastric acidity was similar in ulcer patients and control subjects under both the states (49.3 +2- 4.5 vs 50.0 +/- 6.0 mmol/l basally, 85.2 +/- 8.9 vs 63.4 +/- 6.6 mmol/l after pentagastrin injection respectively). Thus, gastric bicarbonate secretion was similar, whereas parietal and nonparietal volume secretions were increased in patients with duodenal ulcer as compared to controls.

Efecto de la alcalinización y el calentamiento de las soluciones anestésicas sobre el periodo de latencia en el bloqueo de plexo axilar vía axilar / Effects of anesthetic Warming and alcalinization upon the latency period in axilary blockade through axilary approach

Se estudiaron tres grupos de 10 pacientes cada uno, de ambos sexos, edad promedio de 34.8 ñ 8.8 años, peso promedio de 68.8 ñ 2.3 zkg. talla promedio de 156 ñ cm. y estados físicos 1 y 2, programados para cirugía electiva ortopédica o reconstructiva del miembro toráxico. A todos ellos se les administró lidocaína al 2 por ciento con epinefrina para bloqueo de plexo braquial vía axilar a dosis de 7 mg/kg. al grupo I sin modificaciones , al grupo II se adicionó bicarbonato de sodio y al grupo III se aumentó la temperatura a 37ºC, para reducir el tiempo de latencia. El tiempo promedio de latencia observado para el grupo I fue de 15.2 ñ 7.3 minutos y para el grupo II fue de 9.1 ñ 1.9 minutos, existiendo diferencias significativas estadísticamente p<0.01. El tiempo promedio de latencia para el grupo III fue de 2.4 ñ 1.3 minutos y en comparación con los dos grupos previos se aprecia una diferencia significativa estadísticamente (P<0.005). En suma, tanto la alcalinización como el calentamiento de las soluciones anestésicas con eficaces para disminuir el tiempo de la latencia

Transepithelial pH gradients in cortical distal tubules during metabolic alkalosis

1. The cortical distal tubule of the rat kidney participates in the regulation of acid-base balance, showing bicarbonate reabsorption, secretion or absence of transport under different experimental conditions. In the present study, we measured differences in transepithelial pH using double ion-exchange resin/reference microelectrodes in control and alkalotic (chronic plus acute) male Wistar rats and in alkalotic rats receiving a K+ supplement in diet and infusion. 2. pH was measured in the tubule lumen during stationary microperfusion with 25 mM bicarbonate Ringer solution, and in peritubular vessels next to the perfused tubules. 3. Differences in transepithelial pH were 0.70 +/- 0.12 (N = 16) pH units in early distal tubules (ED) and 1.03 +/- 0.050 (N = 15) in late distal tubules LD) of control rats, 0.22 +/- 0.056 (N = 17) in ED and 0.25 +/- 0.050 (N = 20) in LD of alkalotic rats, and -0.02 +/- 0.039 (N = 24) in ED and -0.02 +/- 0.040 (N = 24) in LD of K(+)-supplemented alkalotic rats. 4. In control rats, the transepithelial potential difference (PD) (-8.9 +/- 1.45 mV (N = 16) in ED and -32.7 +/- 2.99 mV (N = 15) in LD) was not large enough to explain transepithelial H+ and HCO3- gradients, suggesting the presence of an active transport mechanism responsible for their maintenance. 5. The present data show that the cortical distal tubule is able to establish transepithelial pH (HCO3-) differences, that these differences are reduced by alkalosis and abolished by alkalosis plus K+ supplementation, and that, although inversion of pH gradients (evidence for bicarbonate secretion) was observed in individual tubules, this inversion was not significant in the groups studied

Esvaziamento gástrico e acidose metabólica: II. estudo, num modelo experimental em ratos, da retençäo gástrica de uma soluçäo de bicarbonato de sódio / Gastric emptying and metabolic acidosis: II. study in an experimental model in rats, of the gastric retention of a sodium bicarbonate solution

O esvaziamento gástrico (EG) de 2ml/100g de peso do animal de uma soluçäo de bicarbonato de sódio 0,25 M, acrescida de fenol vermelho (6 mg/dl) foi estudado em ratos com acidose metabólica induzida por infusäo orogástrica prévia de volume igual de uma soluçäo de cloreto de amônio 0,5 M. Como grupos controles foram utilizados animais com infusäo prévia de 2ml/100g de peso do animal de soluçäo de cloreto de sódio 0,5M e de água. As retençöes (RG) foram avaliadas 6 horas após a infusäo das refeiçöes prévias nos tempos de 5, 10, 20 e 30 minutos. Os resultados mostrtam que as RG da soluçäo de bicarbonato de sódio nos animais com acidose metabólica foram significativamente menores que as apresentadas pelos animais com infusäo prévia de água (aos 20 minutos) e áquelas apresentadas pelos animais metabólica acelera o esvaziamento gástrico de uma soluçäo de bicarbonato de sódio, havendo evidências de que este fato ocorra devido a aumento de secreçäo de ácido pela mucosa gástrica

Products of non-reductive CO2 assimilation in the halophilic archaebacterium Haloferax mediterranei.

The products of CO2 fixation by heterotrophically grown Haloferax mediterranei were analysed. The main 14C-labelled alpha-ketoacid detected following incubation with NaH14CO3 and pyruvate or propionate was pyruvate. In presence of these organic acids and NH4+, 14CO2 was incorporated into glutamic and aspartic acids and alanine.