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PubMed2004

[Acute confusional syndrome associated with obstructive sleep apnea aggravated by acidosis secondary to oral acetazolamide treatment].

Acute confusional syndrome, or delirium, is a transitory mental state characterized by the fluctuating alteration of awareness and attention levels. We present the case of a patient with acute confusional syndrome associated with obstructive sleep apnea syndrome (OSAS) aggravated by metabolic acidosis induced by oral acetazolamide treatment.A 70-year-old man with no history of neurological disease was referred with a clinical picture consistent with acute confusional syndrome presenting between midnight and dawn. During the admission examination infectious, toxic, and neurologic causes, or those related to metabolic or heart disease were ruled out. Arterial blood gases measured during one of the nighttime episodes of acute confusional syndrome showed mild hypoxia and hypercapnia with mixed acidosis. Signs and symptoms suggestive of OSAS had been developing over the months prior to admission, with snoring, sleep apnea, and moderate daytime drowsiness. Polysomnography demonstrated severe OSAS with an apnea-hypopnea index of 38. Mean arterial oxygen saturation was 83%; time oxygen saturation remained below 90% was 44%. The attending physician ordered the withdrawal of oral acetazolamide, which was considered the cause of the metabolic component of acidosis. Treatment with continuous positive airway pressure was initiated at 9 cm H2O, after a titration polysomnographic study. The patient continued to improve.OSAS, for which very effective treatment is available, should be included among diseases that may trigger acute confusional syndrome.

Acetazolamide↗
PubMed2001

Topiramate-induced metabolic acidosis: report of two cases.

Two children who presented with symptomatic metabolic acidosis after being put on topiramate (TPM) are reported. The first patient was an 11-year-old male with refractory complex partial epilepsy who was put on TPM for 13 months. He developed hyperventilation 1 week after increasing the dose to 300 mg/day. Arterial blood gas revealed hyperchloraemic metabolic acidosis with partial respiratory compensation: pH 7.36, PCO2 27.2 mmHg, bicarbonate 14.9 mEq/L, base excess -8.9 mmol/L. Hyperventilation and acidosis resolved after administration of sodium bicarbonate and reduction of the dose of TPM. The second patient was a female who developed increasing irritability at age 16 months and 21 months, each time associated with introduction of TPM and resolved promptly upon withdrawal of the drug. Venous blood gas taken during the second episode revealed pH 7.34, PCO2 37.4 mmHg, bicarbonate 20.4 mEq/L, base excess -4.2 mmol/L. The predominant mechanism of TPM-induced hyperventilation involves inhibition of carbonic anhydrase at the proximal renal tubule, resulting in impaired proximal bicarbonate reabsorption. The occurrence of hyperpnoea or mental status change in any patient who is on TPM should prompt an urgent blood gas sampling, with correction of the acid-base disturbances accordingly.

Acidosis↗
PubMed1995

Hearing impairment in association with distal renal tubular acidosis among Saudi children.

A follow-up of seven patients with the autosomal recessive inherited syndrome of distal renal tubular acidosis (RTA) and sensorineural hearing loss is described. Five patients were diagnosed as having primary distal renal tubular acidosis and rickets, four were found to have severe sensorineural hearing loss of over 80 dB: two of which are brothers. Two patients were diagnosed as having secondary distal renal acidosis due to a genetic disorder called osteopetrosis; they are brothers and their audiograms showed a mild conductive hearing loss of an average 35 dB bilaterally. All patients had growth retardation with improvement due to alkaline therapy but their hearing loss was not affected by the medication. The pedigrees of two families with half sibs showed the familial incidence for consanguineous marriage. Consanguinity was found to be positive in five out of the seven patients. The tribal tradition in Saudi Arabia fosters consanguineous marriages for cultural and social reasons and pre-arranged marriages are still seen.

Acidosis, Renal Tubular↗
PubMed2006

[Pathophysiology and diagnosis of renal tubular acidosis].

Intrinsic defects in tubular transport mechanisms of the kidney may cause impairment of urinary acidification or a loss of base equivalents, thereby inducing systemic metabolic acidosis. Different types of this disorder termed renal tubular acidosis (RTA) can be distinguished based on the localization of the disturbance along the nephron (proximal vs. distal) and their association with potassium transport (hypo-/hyperkalemic). Except for the proximal type RTA results in positive acid balance and negatively impacts on bone metabolism and the formation of kidney stones. The diagnosis is based on analysis of acid/base status, urinary pH and determination of ammonium excretion after an oral acid load. Both functional defects of specific tubular transport mechanisms and global impairment of renal tubular function can be causative of RTA. Their therapy is based on treatment of the primary disease process and correction of acidosis by alkali supplementation.

Acidosis, Renal Tubular↗
PubMed2002

Bicarbonate attenuates intracellular acidosis.

BACKGROUND: This study was prompted by concern that administration of bicarbonate for correction of lactate acidosis aggravates a low intracellular pH (pHi). In healthy subjects we evaluated skeletal muscle pHi using 31P-magnetic resonance spectroscopy during 5-minute rhythmic handgrip to provoke intracellular acidosis. METHODS: Subjects were randomized to treatment with bicarbonate or saline infused intravenously in a cross-over study design with 1 h between trials. RESULTS: In response to rhythmic handgrip, muscle venous O(2) hemoglobin saturation decreased from 51 +/- 4% to 36 +/- 2% and lactate increased from 1.0 +/- 0.1 to 4.9 +/- 0.5 mmol/l with a reduction in pH from 7.43 +/- 0.01-7.23 +/- 0.01 (P<0.05). pHi decreased from 7.06 +/- 0.02-6.36 +/- 0.08 (P<0.05). Infusion of bicarbonate increased the arterial blood concentration from 26 +/- 1 to 39 +/- 1 mmol/l (P<0.05). The arterial CO(2) partial pressure decreased from 5.6 +/- 0.2 to 5.2 +/- 0.3 kPa during rhythmic handgrip, whereas it increased to 5.9 +/- 0.2 kPa (P<0.05) during infusion of bicarbonate. Bicarbonate treatment also increased pH of arterial and venous blood (7.55 +/- 0.01 vs. 7.44 +/- 0.02 and 7.31 +/- 0.01 vs. 7.23 +/- 0.02, respectively; P<0.05). In the last min of rhythmic handgrip the decrease in pHi was attenuated by the administration of bicarbonate (6.60 +/- 0.11 vs. 6.40 +/- 0.12; P<0.05). CONCLUSION: During exercise-induced metabolic acidosis, intravenous administration of bicarbonate increased the buffering capacity of blood and attenuated the decrease in intracellular muscle pH, although there was a small increase in the arterial carbon dioxide pressure.

Acidosis↗
PubMed2003

Lactic acidosis following convulsions.

Lactic acidosis is a common cause of metabolic acidosis and is usually connected with high mortality. However, changes in the level of lactate and pH can also be seen after generalized epileptic attacks, due to local muscle hypoxia during the seizures. Although these changes can be quite marked, the condition is self-limiting and usually does not call for any specific treatment. We report five cases of lactic acidosis following convulsions from our centre.

Acidosis, Lactic↗
PubMed1981

Brain lactic acidosis and ischemic cell damage: 1. Biochemistry and neurophysiology.

This study explores the influence of severe lactic acidosis in the ischemic rat brain on postischemic recovery of the tissue energy state and neurophysiological parameters. Severe incomplete brain ischemia (cerebral blood flow below 5% of normal) was induced by bilateral carotid artery clamping combined with hypovolemic hypotension. We varied the production of lactate in the tissue by manipulating the blood glucose concentrations. A 30-min period of incomplete ischemia induced in food-deprived animals caused lactate to accumulate to 15-16 mumol g-1 in cortical tissue. Upon recirculation these animals showed: (1) a considerable recovery of the cortical energy state as evaluated from the tissue concentrations of phosphocreatine, ATP, ADP, and AMP; and (2) return of spontaneous electrocortical activity as well as of somatosensory evoked response (SER). In contrast, administration of glucose to food-deprived animals prior to ischemia caused an increase in tissue lactate concentration to about 35 mumol g-1. These animals did not recover energy balance in the tissue and neurophysiological functions did not return. In other experiments the production of lactate during 30 min of complete compression ischemia was increased from about 12 mumol g-1 (normoglycemic animals) to 20-30 mumol g-1 by preischemic hyperglycemia and, in separate animals, combined hypercapnia. The recovery of the cortical energy state upon recirculation was significantly poorer in hyperglycemic animals. It is concluded that a high degree of tissue lactic acidosis during brain ischemia impairs postischemic recovery and that different degrees of tissue lactic acidosis may explain why severe incomplete ischemia, in certain experimental models, is more deleterious than complete brain ischemia.

Acidosis↗
PubMed1985

Influence of acidosis on lipid peroxidation in brain tissues in vitro.

To study the influence of acidosis on free radical formation and lipid peroxidation in brain tissues, homogenates fortified with ferrous ions and, in some experiments, with ascorbic acid were equilibrated with 5-15% O2 at pH values of 7.0, 6.5, 6.0, and 5.0, with subsequent measurements of thiobarbituric acid-reactive (TBAR) material, as well as of water- and lipid-soluble antioxidants (glutathione, ascorbate, and alpha-tocopherol) and phospholipid-bound fatty acids (FAs). Moderate to marked acidosis (pH 6.5-6.0) was found to grossly exaggerate the formation of TBAR material and the decrease in alpha-tocopherol content and to enhance degradation of phospholipid-bound, polyenoic FAs. These effects were reversed at pH 5.0, suggesting a pH optimum at pH 6.0-6.5. It is concluded that acidosis of a degree encountered in ischemic brain tissues has the potential of triggering increased free radical formation. This effect may involve increased formation of the protonated form of superoxide radicals, which is strongly prooxidant and lipid soluble, and/or the decompartmentalization of iron bound to cellular macromolecules like ferritin.

Acidosis↗
PubMed1985

Lactic acidosis and recovery of mitochondrial function following forebrain ischemia in the rat.

The effect of different degrees of lactic acidosis on the recovery of brain mitochondrial function, measured as respiratory activity in isolated mitochondria or cortical concentrations of labile phosphates and carbohydrate substrates, was studied during 30 min of recirculation following 15 min of near-complete forebrain ischemia in rats. During ischemia, there was a marked decrease in mitochondrial State 3 respiration in vitro and a depletion of energy stores (i.e., phosphocreatine, ATP, glucose, and glycogen) in vivo that was similar in the high- and low-lactate ischemia groups. However, lactate concentrations differed markedly (20 and 10 mumol g-1, respectively). During recirculation, there was a near-complete recovery of both respiratory activity in vitro and adenylate energy charge (EC) in vivo regardless of the differences in lactic acidosis during ischemia. Respiratory activity and EC were well correlated. The changes in Ca2+ homeostasis during ischemia, an increase in tissue and a decrease in mitochondrial Ca2+ content, were reversed rapidly after ischemia in both high- and low-lactate ischemia animals and did not hinder an early recovery of mitochondrial function. It is concluded that lactic acidosis, with lactate levels reaching 20 mumol g-1 during 15-min ischemia, does not adversely affect early postischemic recovery of mitochondrial function.

Acidosis↗
PubMed1985

Brain tissue acidosis and changes of energy metabolism in mild incomplete ischemia--topographical study.

Regional changes of brain tissue pH and its correlation to energy metabolism were studied in various degrees of incomplete ischemia for 5 and 60 min in the unilateral common carotid occlusion of normally fed mongolian gerbils. The degree of ischemia was evaluated by the severity of neurological deficits following 60 min of occlusion, and animals were divided into three groups: symptomatic, borderline, and asymptomatic. Changes of NADH and ATP distribution corresponded well to the degree of ischemia. On the other hand, acidosis developed more clearly and extended in wider areas than the changes of NADH and ATP distribution. These changes were already seen at 5 min of occlusion. From the results of this experiment, it was suspected that acidosis in mild incomplete ischemia was due to stimulated anaerobic glycolysis that might supplement NADH oxidation and ATP yields. Further, acidosis without energy failure was considered not to be detrimental to neuronal cells.

Acidosis↗
PubMed1989

The effects of extracellular acidosis on neurons and glia in vitro.

Cerebral lactic acid, a product of ischemic anaerobic glycolysis, may directly contribute to ischemic brain damage in vivo. In this study we evaluated the effects of extracellular acid exposure on 7-day-old cultures of embryonic rat forebrain. Mixed neuronal and glial cultures were exposed to either lactic or hydrochloric acid to compare the toxicities of relatively permeable and impermeable acids. Neurons were relatively resistant to extra-cellular HCl acidosis, often surviving 10-min exposures to pH 3.8. In the same cultures, immunochemically defined astrocytes survived 10-min HCl exposures to a maximum acidity of pH 4.2. Similarly, axonal bundles defasciculated in HCl-titrated media below pH 4.4, although their constituent fibers often survived pH 3.8. Cell death occurred at higher pH in cultures subjected to lactic acidosis than in those exposed to HCl. Over half of forebrain neurons and glia subjected for 10 min to lactic acidification failed to survive exposure to pH 4.9. Longer 1-h lactic acid incubations resulted in cell death below pH 5.2. The potent cytotoxicity of lactic acid may be a direct result of the relatively rapid transfer of its neutral protonated form across cell membranes. This process would rapidly deplete intracellular buffer stores, resulting in unchecked cytosolic acidification. Neuronal and glial death from extracellular acidosis may therefore be a function of both the degree and the rapidity of intracellular acidification.

Acidosis↗
PubMed1994

Acidosis induced by hypercapnia exaggerates ischemic brain damage.

Although preischemic hyperglycemia is known to aggravate damage due to transient ischemia, it is a matter of controversy whether or not this is a result of the exaggerated acidosis. It has recently been reported that although tissue acidosis of a comparable severity could be induced in normoglycemic dogs by an excessive rise in arterial CO2 tension, short-term functional recovery was improved, rather than compromised. In the present experiments we induced excessive hypercapnia (PaCO2, approximately 300 mm Hg) in normoglycemic rats before inducing forebrain ischemia of 10-min duration. This reduced the brain extracellular pH to values normally encountered in hyperglycemic rats subjected to ischemia. The events induced by hypercapnia clearly enhanced ischemic brain damage, as assessed histologically after 7 days of recovery. We hypothesize that the decisive event was an exaggerated decrease in extra- and intracellular pH and that the results thus demonstrate an adverse effect of acidosis. However, since postischemic seizures did not occur in the hypercapnic ischemic rats, the results also demonstrate that changes in intra-extracellular pH and bicarbonate concentrations modulated ischemic damage in an unexpected way.

Acidosis↗
PubMed1978

Mechanism of the metabolic acidosis of selective mineralocorticoid deficiency.

The mechanism of generation of metabolic acidosis in selective mineralocorticoid deficiency was investigated in bilaterally adrenalectomized (ADX) rats treated with dexamethasone and in sham-operated (S) rats. ADX rats had significantly lower plasma sodium and bicarbonate concentrations and significantly higher plasma potassium concentrations than S rats did. ADX rats developed negative sodium balance when fed a "zero" sodium diet. The minimum urine pH achieved during sodium sulfate infusion and during ammonium chloride administration was not significantly different between ADX and S rats. Bicarbonate reabsorption and urine minus blood PCO2 gradient were not different between ADX and S rats. For any given urine pH, absolute ammonium excretion was significantly lower in ADX than it was in S rats, both during sodium sulfate infusion and during chronic ammonium chloride administration. Glomerular filtration rate (GFR) was significantly lower in ADX than it was in S rats; ammonium excretion corrected for GFR was not different between the two groups. To determine the role of decreased distal sodium delivery (secondary to decrease in GFR and enhanced proximal sodium reabsorption which resulted from distal sodium chloride wastage) on ammonium excretion, ADX rats were fed 0.9% sodium chloride in an effort to keep body weight constant. Salt-loaded ADX rats had a plasma bicarbonate concentration higher than did S rats. Salt-loading also led to a significant increase in GFR; absolute ammonium excretion was significantly higher than that of other ADX rats with the same degree of acidosis. At comparable levels of GFR, there was no difference in ammonium excretion between ADX and S rats. Ammonium excretion was linearly related to GFR. ADX rats fed a zero potassium diet had significantly greater ammonium excretion than did all other groups of ADX or S rats receiving a normal potassium intake. These data suggest that volume contraction is a major factor responsible for the acidosis of selective mineralocorticoid deficiency.

Acidosis↗
PubMed1982

Effect of metabolic acidosis on renal brushborder membrane adaptation to low phosphorus diet.

In previous in vitro studies the level of oxidized nicotinamide adenine dinucleotide (NAD+) in renal cortex changed parallel to changes in gluconeogenesis and NAD+ inhibited phosphate transport by renal cortical brushborder membrane (BBM) vesicles. To determine whether or not changes in renal gluconeogenesis in vivo were accompanied by altered renal handling of phosphate, possibly related to NAD+ action on BBM phosphate transport in vivo, renal gluconeogenesis was stimulated in rats by metabolic acidosis. Chronic acidosis in rats previously adapted to low phosphorus diet was associated with increased UPiV (controls, 68 +/- 19; acidotic, 1055 +/- 428 nmoles/mg creatinine; P less than 0.05) without changes in plasma phosphate and creatinine (Cr) and in UCrV compared to controls. The initial rate of sodium gradient-dependent transport of phosphate by renal cortical BBM vesicles was lower in acidotic TPTX rats compared to TPTX controls (controls, 3.10 +/- 0.16; acidotic, 1.50 +/- 0.06 nmole/mg protein/0.5 min; P less than 0.001), attributed to a decrease in the apparent Vmax. In renal cortex, gluconeogenesis and the NAD+/NADH ratio were increased in acidosis. Decreased BBM transport of phosphate in proximal tubules of acidotic rats may explain the increased UPiV. This change indicates reversal of the adaptation of the BBM phosphate transport system to dietary phosphorus deprivation and may be related to increases in gluconeogenesis and the NAD+/NADH ratio in renal cortex.

Acidosis↗
PubMed1986

Na+-H+ exchange in luminal-membrane vesicles from rabbit proximal convoluted and straight tubules in response to metabolic acidosis.

Na+-H+-exchanger activity of pars convoluta and pars recta luminal-membrane vesicles prepared from the proximal tubule of acidotic and control rabbits were assayed by a rapid-filtration technique and an Acridine Orange method. Both experimental approaches revealed the existence of an antiporter, sensitive to metabolic acidosis, in pars convoluta membrane vesicles. Kinetic data, obtained with the pH-sensitive dye, showed that the Km for Na+ transport was unchanged by acidosis, whereas Vmax. for exchanger activity was increased, on an average, by 44%. The fluorescence method, in contrast with the rapid-filtration technique, was able to detect exchanger activity in pars recta membrane vesicles. The Km value for the antiporter located in pars recta is comparable with that calculated for pars convoluta membrane vesicles. By contrast, the Vmax. of this exchanger is only about 25% of that found for pars convoluta. Furthermore, metabolic acidosis apparently does not increase Na+-H+-exchanger activity of pars recta luminal-membrane vesicles.

Acidosis, Renal Tubular↗
PubMed1975

Adaptations in urea ammonium excretion in metabolic acidosis in the rat: a reinterpretation.

1. The effects of oral hydrochloric acid, ammonium chloride, sodium bicarbonate and ammonium bicarbonate on urea and ammonium excretion in rats on a constant diet were studied. 2. Hydrochloric acid acidosis significantly reduced urea excretion in the rat, with an equimolar increase in NH+4 excretion and no change in their sum. In ammonium chloride acidosis, most of the additional nitrogen intake is excreted as NH+4 and a small percentage as urea. The converse holds true after administration of ammonium bicarbonate. The physiological significance of this is discussed. 3. The shift in nitrogen excretion from urea to NH+4 in acidosis is interpreted on the basis of bicarbonate production and utilization. Urea formation utilizes HCO-3. For amino acid sources, this utilization is offset by the metabolism of the carbon skeleton, which gives rise to HCO-3. When waste nitrogen is excreted as NH+4, no bicarbonate is utilized and the new HCO-3, generated by the carbon skeleton, hels to maintain hydrogen ion homeostasis.

Acidosis↗
PubMed1976

The ventilatory response in severe metabolic acidosis.

1. The ventilatory response to severe metabolic acidosis was studied by measuring arterial blood carbon dioxide tension and pH in sixty-seven patients with blood pH less than 7-10, none of whom had hypercapnia, pulmonary oedema, or chronic pulmonary insufficiency. The results were compared with those previously found in patients with uncomplicated diabetic ketoacidosis. 2. By that comparison, fifty-two of the sixty-seven patients with blood pH less than 7-10 were judged to have "appropriate hypocapnia", and fifteen had "submaximal hypocapnia". Thirteen of the latter fifteen had circulatory failture and/or acute hypoxia, and seven of nine in whom it was measured had plasma lactate greater than 9 mmol/1. 3. Hyperventilation was therefore usually well sustained in these patients with severe metabolic acidosis, except in most of those with acute tissue hypoxia. The latter may have had insufficient time to achieve maximum hyperventilation in response to their acidosis, or perhaps their submaximal hypercapnia presaged imminent failure of the hyperventilatory response.

Acidosis↗