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PubMed1996

Dilution acidosis: evidence for a role of intracellular pH in the control of ventilation.

Acute hyperosmolality results in an extracellular dilution acidosis and hypercarbia that does not stimulate ventilatory compensation. The osmotic stress is also associated with shifts in water and electrolyte balance and an increase in intracellular pH. The alkaline intracellular pH was hypothesized to have a role in preventing a normal respiratory response to the extracellular acidosis and hypercarbia. Therefore, this study examined the effect of ion-exchange blockade on intra- and extracellular pH and ventilation during acute hyperosmolality in the Pekin duck (Anas platyrhynchos) by using 31P-nuclear magnetic resonance spectroscopy. Both 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS) and amiloride inhibited the development of the intracellular alkalosis that normally develops in muscle during acute hyperosmolality. Instead, exposure to hyperosmotic stress during ion-exchange blockade resulted in a significant acidosis both intracellularly and extracellularly. Arterial pH decreased 0.10 +/- 0.04 pH unit with a sucrose infusion after either blocker, and intracellular pH decreased 0.11 +/- 0.06 and 0.16 +/- 0.04 pH units with a sucrose infusion after DIDS and amiloride, respectively. Ventilation increased 79 +/- 28 and 122 +/- 100%, respectively, during acute hyperosmolality after ion-exchange blockade with either DIDS or amiloride. The results suggest that intracellular pH may play a role in the ventilatory response to acid-base perturbations. The data also indicate that both Cl-/HCO3- and Na+/H+ exchanges are involved in the development of the intracellular alkalosis during hyperosmotically induced extracellular acidosis.

Acidosis↗
PubMed2001

Acidosis-stimulated neurons of the medullary raphe are serotonergic.

Neurons of the medullary raphe project widely to respiratory and autonomic nuclei and contain co-localized serotonin, thyrotropin-releasing hormone (TRH), and substance P, three neurotransmitters known to stimulate ventilation. Some medullary raphe neurons are highly sensitive to pH and CO(2) and have been proposed to be central chemoreceptors. Here it was determined whether these chemosensitive neurons are serotonergic. Cells were microdissected from the rat medullary raphe and maintained in primary cell culture for 13-70 days. Immunoreactivity for serotonin, substance P, and TRH was present in these cultures. All acidosis-stimulated neurons (n = 22) were immunoreactive for tryptophan hydroxylase (TpOH-IR), the rate-limiting enzyme for serotonin biosynthesis, whereas all acidosis-inhibited neurons (n = 16) were TpOH-immunonegative. The majority of TpOH-IR medullary raphe neurons (73%) were stimulated by acidosis. The electrophysiological properties of TpOH-IR neurons in culture were similar to those previously reported for serotonergic neurons in vivo and in brain slices. These properties included wide action potentials (4.55 +/- 0.5 ms) with a low variability of the interspike interval, a postspike afterhyperpolarization (AHP) that reversed 25 mV more positive than the Nernst potential for K(+), prominent A current, spike frequency adaptation and a prolonged AHP after a depolarizing pulse. Thus the intrinsic cellular properties of serotonergic neurons were preserved in cell culture, indicating that the results obtained using this in vitro approach are relevant to serotonergic neurons in vivo. These results demonstrate that acidosis-stimulated neurons of the medullary raphe contain serotonin. We propose that serotonergic neurons initiate a homeostatic response to changes in blood CO(2) that includes increased ventilation and modulation of autonomic function.

Acidosis↗
PubMed2005

[Treatment of symptomatic hyperlactatemia and lactic acidosis in HIV+ patients under nucleoside reverse transcriptase inhibitors].

BACKGROUND AND OBJECTIVE: We intended to find out the effectiveness of lactic acidosis therapy for mitochondrial toxicity. PATIENTS AND METHOD: HIV-patients receiving nucleoside reverse transcriptase inhibitors (NRTIs), hospitalized with lactic acidosis or symptomatic hyperlactatemia. Venous hyperlactatemia was considered at > 2.2 mmol/l. Treatment consisted of a daily vitamin regime of L-carnitine, thiamine, vitamin B6, hydroxicobalamine, and vitamin C; any glucose intake was discontinued. NRTIs treatment was stopped immediately. RESULTS: Nine patients on current therapy were identified who had symptomatic hyperlactatemia (n = 4) or lactic acidosis (n = 5) from 1/2001 to 9/2002. All were patients with AIDS, receiving NRTIs with a mean duration of 5 years: ddI (n = 7), d4T (n = 5), AZT(n = 3), 3TC (n = 2), abacavir (n = 1). Most common symptoms were tachypnea, slight fever, abdominal pain, nausea, vomiting and diarrhea. All patients had a favourable prognosis after administration of L-carnitine and vitamin complexes, with discontinuation of NRTIs and glucose intake. Clinical features lasted 7 days. After 15 (5) months of follow up, none had a recurrence of the syndrome. CONCLUSION: The application of this therapy could play a role in the treatment of NRTI - related lactic acidosis.

Acidosis, Lactic↗
PubMed2006

[D-lactic acidosis in an 11-year-old patient with short bowel syndrome].

The short bowel syndrome is the result of a congenital or acquired loss of a large part of the small intestine. The most frequent causes of surgical resection of the intestine in infants are arterial or venous thrombosis, intestinal volvulus, necrotizing enterocolitis, and Crohn's disease. Symptoms include nutrient and electrolyte malabsorption, steatorrhea and diarrhea, which can result in failure to thrive. The consequences of extensive small bowel resections consist of nutritional deficiencies, gastric acid hypersecretion, nephrolithiasis, cholelithiasis and lactic acidosis. Of these, D-lactic acidosis is an infrequent but important complication because of the symptoms that it can produce. D-lactic acid in the human organism is generated by intestinal bacteria, D-lactate ingestion, or endogenous production in the methyl glycoxylase pathway. Neurological symptoms such as somnolence, ataxia or altered behavior in a patient with short bowel syndrome should make us think of D-lactic acidosis caused by bacterial overgrowth. We present the case of an 11-year-old boy with short bowel syndrome secondary to multiple resections during the postnatal period who was admitted to hospital for episodes of confusion and altered behavior. The diagnosis was lactic acidosis. Outcome was favorable due to prompt instauration of treatment.

Acidosis, Lactic↗
PubMed2001

Direct effect of the correction of acidosis on plasma parathyroid hormone concentrations, calcium and phosphate in hemodialysis patients: a prospective study.

BACKGROUND: Metabolic acidosis contributes to renal osteodystrophy and together with hyperphosphatemia, hypocalcemia and altered vitamin D metabolism may result in increased levels of intact parathyroid hormone (iPTH) and metastatic calcifications. However, the impact of the correction of metabolic acidosis on iPTH levels and calcium-phosphate metabolism is still controversial. STUDY DESIGN: The effects of the correction of metabolic acidosis on serum concentrations of iPTH, calcium (Ca), phosphate (PO(4)) and alkaline phosphatase were prospectively studied. Twelve uremic patients on maintenance hemodialysis (HD) for 49 months (median; range 6-243 months) with serum bicarbonate levels < or =20 mmol/l were studied before and after 3 months of oral sodium bicarbonate supplementation. Predialysis serum bicarbonate, arterial pH, ionized calcium, plasma sodium, plasma potassium, serum creatinine, hemoglobin, K(t)/V, postdialysis body weight, predialysis systolic and diastolic blood pressure were also evaluated before and after correction. RESULTS: Serum bicarbonate levels and arterial pH increased respectively from 19.3 +/- 0.6 to 24.4 +/- 1.2 mmol/l (p < 0.0001) and 7.34 +/- 0.03 to 7.40 +/- 0.02 (p < 0.001). iPTH levels decreased significantly from 399 +/- 475 to 305 +/- 353 pg/ml (p = 0.026). No changes in total serum Ca, plasma PO(4), serum akaline phosphatase, K(t)/V, serum creatinine, hemoglobin, body weight, predialysis systolic and diastolic blood pressures were observed. iCa decreased significantly. CONCLUSIONS: Our study demonstrates that the correction of metabolic acidosis in chronic HD patients reduces iPTH concentrations in HD patients with secondary hyperparathyroidism possibly by a direct effect on iPTH secretion.

Acid-Base Equilibrium↗
PubMed1998

Metabolic acidosis and protein catabolism: mechanisms and clinical implications.

Metabolic acidosis increases protein degradation resulting in muscle wasting and a negative nitrogen balance. The branched-chain amino acids serve as useful markers of these changes and their catabolism is increased in acidosis, particularly for the spontaneous acidosis associated with renal failure. As a result, the neutral nitrogen balance is compromised and malnutrition results. Glucocorticoids mediate these changes through the recently discovered ATP-dependent ubiquitin-proteasome pathway. Therapy necessitates correction of the underlying acidosis either through adjustment of the alkalinity of the dialysate for the patient on dialysis or through dietary protein restriction and sodium bicarbonate supplements for the predialysis patient.

Acidosis↗
PubMed2003

Oxidative stress in a novel model of chronic acidosis in LLC-PK1 cells.

Chronic metabolic acidosis occurs commonly in chronic renal failure (CRF). The proximal renal tubular cell is the site in the kidney of high oxidative metabolic activity and in CRF is associated with adaptive hypertrophy and hypermetabolism. We hypothesised that chronic acidosis may lead to increased generation of reactive oxygen species due to increased oxidative activity. We developed a novel model of chronic acidosis in LLC-PK1 cells and measured markers of oxidative stress and metabolism. Acidosis led to a reduction in cellular total glutathione and protein thiol content and an increase in glutathione peroxidase activity and NH3 generation. The expression of constitutively expressed heat stress protein (HSP) HSC70 and HSP60 increased at pH 7.0.

Acidosis↗
PubMed2006

Proximal renal tubular acidosis in pregnancy. A case report and literature review.

Renal tubular acidosis is usually associated with chronic renal conditions and is rarely encountered in pregnancy. It may be inherited causing osteomalacia and rickets in children or acquired following autoimmune diseases or following exposure to nephrotoxic agents. It is known to worsen during pregnancy and if left untreated may cause maternal and foetal morbidity or death. We report a 28-year-old woman, gravida 3 para 2, who presented at 30 weeks gestation with lethargy, weakness and generalized myalgia. Investigation revealed severe hypokalaemia and a systemic metabolic acidosis due to proximal renal tubular acidosis. Her previous pregnancies were both complicated by foetal losses at term. Following prompt correction of her electrolyte disturbance and metabolic acidosis, she went on to deliver a healthy female infant at term. Regular evaluation up to 1 year post-partum revealed mild persistence of her hypokalaemia. At 1 year, the infant showed no signs of the disorder and is growing normally.

Acidosis, Renal Tubular↗
PubMed1986

Hypertension, mineralocorticoid-resistant hyperkalemia, and hyperchloremic acidosis in an infant with obstructive uropathy.

An 8-week-old infant with hypertension, hyperkalemia, and hyperchloremic acidosis, presumably due to chloride shunt type of distal renal tubular acidosis, is described. The patient's renin-aldosterone axis was intact. The infant was also found to have an obstructed solitary kidney. Despite correction of the obstruction and improvement in the glomerular filtration rate accompanied by normal development, hyperkalemia and renal tubular acidosis persisted. The defect was still demonstrable 9 months following relief of the obstruction. We conclude that neonatal obstructive uropathy can result in renal tubular acidosis of the chloride shunt type. The reversibility of this defect is, as yet, unknown.

Acid-Base Equilibrium↗
PubMed1988

Captopril-induced metabolic acidosis with hyperkalemia.

Hyperreninemic hypoaldosteronism was diagnosed in a 34-year-old woman with hypertension who was receiving captopril therapy. Renal biopsy revealed an advanced stage of IgA nephropathy, and her creatinine clearance was 40 ml/min. Elevation of serum potassium from 4.7 to 5.8 mEq/l and development of hyperchloremic metabolic acidosis with laboratory findings of pH 7.285, HCO3- 13.5 mEq/l, Na 141, and Cl 114 mEq/l were observed after captopril therapy. When captopril was withdrawn, elevated serum potassium levels and metabolic acidosis returned to normal. Challenge with captopril resulted in a decrease in plasma aldosterone levels, an increase in plasma renin activity, and development of hyperkalemic, hyperchloremic metabolic acidosis which is corrected with mineralocorticoid replacement. This case study demonstrates that captopril can cause hyperreninemic hypoaldosteronism with the laboratory finding of hyperkalemic, hyperchloremic metabolic acidosis.

Acidosis↗
PubMed1995

Acidosis and glucocorticoids interact to provoke muscle protein and amino acid catabolism.

Malnutrition and a loss of lean body mass frequently complicate chronic renal failure. Muscle wasting in uremia is caused by increased protein degradation, decreased protein synthesis and increased branched-chain amino acid oxidation. Acidosis and glucocorticoids are pivotal in these pathophysiologic aberrations. When the acidosis of chronic renal failure is corrected by feeding bicarbonate, protein degradation and amino acid oxidation normalize. Likewise, if patients and animals with normal renal function are made acidotic, protein degradation and amino acid oxidation increase. In adrenalectomized, acidotic rats, proteolysis increases only when they are supplemented with physiologic concentrations of glucocorticoids, suggesting that glucocorticoids are necessary for increased proteolysis. Acidosis stimulates the ATP-dependent proteolytic process involving ubiquitin and the 26S proteasome. Thus, acidosis evokes a glucocorticoid-dependent catabolic response in muscle that can account for the protein wasting associated with uremia.

Acidosis, Renal Tubular↗
PubMed1978

Urinary sulfate excretion in children with classic renal tubular acidosis.

These studies quantitat the significantly elevated sulfate excretion in the urine of children with classic renal tubular acidosis as compared to six weight-matched controls (1.4 +/-0.5 vs. 0.7 +/- 0.2 mEq/kg/day;p less than 0.05). This sulfate loss may result in a subclinical sulfate deficiency which may contribute to a chondroitin sulfate metabolic disorder.,and thus contribute to the growth failure in children with real tubular acidosis. Futhermore, elevated urinary sulfate excretion may be an early diagnostic finding in infancy prior to the manifestation of renal acidification defects. It is not known whether the sulfate loss is related to a primary renal tubular defect or secondary to metabolic acidosis, although the increased sulfate excretion persisting after correction of metabolic acidosis would tend to suggest a primary defect. However, the normal plasma sulfate concentration and the relatively short period of study permit no definitive answer at this time.

Acidosis, Renal Tubular↗
PubMed1985

Hyperkalemia during acute ammonium chloride acidosis in man.

The relationship between acid base parameters and serum potassium concentration was studied in controls and in patients during acute ammonium chloride-induced metabolic acidosis. Serum potassium was best correlated with serum bicarbonate during control (r = -0.323; p less than 0.01) and acidosis (r = -0.437; p less than 0.001). The slopes and intercepts were similar in both instances and the combined correlation was highly significant (r = -0.493; p less than 0.001). Examination of the 95% joint confidence region revealed that during acidosis serum potassium was rarely above 5.0 mEq/l when serum bicarbonate was greater than 16 mEq/l. It is probably not sound clinical practice to ascribe hyperkalemia to acute mild metabolic acidosis.

Acidosis↗
PubMed1986

Renal bicarbonate handling in low birth weight infants during metabolic acidosis.

We studied the fractional excretion of bicarbonate (FE HCO-3) in 10 low birth weight infants aged 1-6 days during metabolic acidosis (base excess greater than or equal to -5 mEq/l) and during subsequent sodium HCO-3 infusion. The mean birth weight was 1,095 g; the mean gestational age was 29 weeks. The ability to decrease urine pH to less than 5.5 and FE HCO-3 to less than 1% during metabolic acidosis was not limited by low gestational age or birth weight. After HCO-3 therapy, all infants corrected their negative base excess, and plasma HCO-3 increased significantly. All infants with blood pH less than or equal to 7.22 or PaCO2 greater than or equal to 50 mm Hg had minimal or absent FE HCO-3. Infants with elevated PaCO2 and mild or absent acidosis also had complete HCO-3 tubular reabsorption. These results suggest that the HCO-3 tubular reabsorption is adequate during metabolic and/or respiratory acidosis in low birth weight infants.

Acidosis↗
PubMed1991

Effects of NH4Cl metabolic acidosis on proximal and distal tubular sodium reabsorption in newborn infants.

The present study was undertaken to assess the influence of acute metabolic acidosis on proximal and distal tubular sodium reabsorption in a group of 7 one-week-old neonates with a mean birth weight of 2,164 g (range: 1,300-3,750 g) and a mean gestational age of 34 weeks (range: 28-40 weeks) undergoing an NH4Cl loading test. Free water clearance during water diuresis was used to estimate separately the proximal and distal sodium reabsorption. In response to NH4Cl metabolic acidosis urine flow rate (p less than 0.01) and free water clearance (p less than 0.025) increased significantly, and there was a general tendency for creatinine, osmolar and sodium clearance to increase without achieving statistical significance. The absolute amount of sodium delivered to (p less than 0.01) and reabsorbed in the distal nephron (p less than 0.01) increased significantly in spite of the constant fractional distal reabsorption. The enhanced distal sodium reabsorption during acidosis is assumed to be related to the acidosis-induced increase in aldosterone production.

Acidosis↗
PubMed1986

The combined effects of hypoxia, high K+, and acidosis on the intracellular sodium activity and resting potential in guinea pig papillary muscle.

Several reports have shown that electrical and ionic changes occurring in acute myocardial ischemia can be closely mimicked by exposure of tissue to hypoxic, acid-, and glucose-free solutions at elevated [K+]o. In the present work, this approach was chosen to distinguish between the combined effects of hypoxia, substrate withdrawal, and acidosis, and the effects of two different levels of [K+]o (4.7 mM and 11.5 mM) on intracellular sodium activity and resting membrane potential. Measurements were made with microelectrodes in isolated guinea pig papillary muscles. In normoxia at 4.7 mM [K+]o, intracellular sodium activity was 7.5 mM (+/- 1.9 mM, SD) during stimulation at 1 Hz. Combined hypoxia, substrate withdrawal, and acidosis increased intracellular sodium activity significantly, by 3-4 mM in 4.7 mM [K+]o and by approximately 2 mM in 11.5 mM [K+]o, after 9-10 minutes. Increasing [K+]o in normoxic solution decreased intracellular sodium activity by 1.9 mM (+/- 1.3 mM, SD). The transition from normal (4.7 mM [K+]o) Tyrode's solution to "ischemic solution" (hypoxia, acidosis, substrate withdrawal, 11.5 mM [K+]o) was associated with a small initial increase and a subsequent decrease of intracellular sodium activity. The steady state level after 12 minutes was not significantly different from the level in normal Tyrode's solution. The secondary decrease of intracellular sodium activity coincided with the gradual development of inexcitability and was absent in quiescent preparations. Combined hypoxia, acidosis, and glucose-withdrawal produced a depolarization by 7-10 mV at 4.7 mM and at 11.5 mM [K+]o, probably reflecting cellular potassium loss and extracellular potassium accumulation in the restricted extracellular space.(ABSTRACT TRUNCATED AT 250 WORDS)

Acidosis↗
PubMed1989

Contractile shortening response of ventricular cells to extracellular acidosis. Evidence for two-site control of H+-Ca2+ interaction.

The effect of extracellular acidosis on contraction of single isolated ventricular cells from rabbit was measured in a system in which pHo could be changed in less than 200 msec. The contractile response to acidotic levels was complete within 25 seconds. The response was measured 30 seconds after pHo was decreased to 7.0, 6.5, 6.0, and 5.5 at each of 8 [Ca]o levels (0.125-4.0 mM). Cell shortening versus [Ca]o was plotted to construct a curve for each pHo level, with each point relative to shortening at pH 7.5, [Ca]o = 1 mM (100% value). Calcium current (1 mM [Ca]o) was also measured 30 seconds after pHo was decreased from 7.5 to 6.5 with single-cell patch clamp technique. The contractile response to extracellular acidosis is accurately predicted by assuming two (probably sarcolemmal) sites at which H+ ions affect calcium binding and/or flux: (equation; see text) The first factor represents a set of sites that are proposed to control access, dependent on the degree of their ionization, to sites represented by the second factor. The latter sites are proposed to accept calcium according to mass-action law. The response of calcium channel current to extracellular acidosis was also complete and reversible within 25 seconds. The current response indicates that the two-site model could be predictive for the effect of extracellular acidosis on calcium current in ventricular cells.

Acidosis↗
PubMed1991

Role of intrarenal angiotensin II and alpha-adrenoceptors in renal vasoconstriction with acute hypoxemia and hypercapnic acidosis in conscious dogs.

To evaluate our previous observation of renal vasoconstriction during combined acute hypoxemia and hypercapnic acidosis preceded by acute hypoxemia, we studied 13 conscious mongrel uninephrectomized dogs with chronic renal catheters and controlled sodium intake (80 meq/day for 4 days). Five dogs were studied during combined acute hypoxemia (PaO2, 37 +/- 1 mm Hg) and hypercapnic acidosis (PaCO2, 59 +/- 1 mm Hg; pH 7.20 +/- 0.01). Each dog was studied during infusion of 1) the intrarenal vehicle (n = 5), 2) the intrarenal alpha 1-antagonist prazosin (0.2 micrograms.kg-1.min-1, n = 5), 3) intrarenal [Sar1,Ala8]angiotensin II (70 ng.kg-1.min-1, n = 5), and 4) intrarenal prazosin and [Sar1,Ala8]angiotensin II (n = 4). Immediate induction of combined hypoxemia and hypercapnic acidosis after control measurements during intrarenal vehicle infusion resulted in a decrease in effective renal plasma flow and glomerular filtration rate, increase in renal vascular resistance, and decrease in filtered sodium load in the first 20 minutes of the blood gas derangement. Intrarenal administration of [Sar1,Ala8]angiotensin II failed to reverse the effects of the combined blood gas derangement on renal function. In contrast, intrarenal prazosin administration either alone or in combination with [Sar1,Ala8]angiotensin II abrogated the increase in renal vascular resistance, decrease in glomerular filtration rate, and fall in filtered sodium load. These studies identify a major role for alpha 1-adrenoceptors in the renal vasoconstriction during combined hypoxemia and hypercapnic acidosis.

Acidosis↗