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PubMed1978

Acidosis and growth in nonuremic renal disease.

Our data demonstrate that correction of acidosis is sustained in children with type 1 RTA when alkali therapy is given in doses of 5 to 14 mEq/kg/day. The large doses are required as a result of renal bicarbonate-wasting. Children with type 1 RTA and acidosis who have significant growth impairment experience catch-up growth and attain normal stature for their age when correction of acidosis is sustained. Whether chronic acidosis impairs growth in any clinical condition except type 1 RTA is not settled. Whether sustained correction of acidosis with alkali therapy will allow attainment of normal stature in children with nonuremic diffuse renal disease is not yet determined. With the increasing availability of microchemistry and microgasometry and the new standards for growth based on mean-parent height [40], it can be anticipated that answers to these clinically important questions will be forthcoming.

Acidosis↗

PubMed1975

Intracellular pH and K+ of cardiac and skeletal muscle in acidosis and alkalosis.

The effects of a metabolic and respiratory acidosis and alkalosis on intracellular pH (pHi) and K+ have been compared in cardiac and skeletal muscle from the anesthetized rabbit. The extracellular space and pHi were calculated from the distribution volumes of [51Cr] EDTA and [14C]DMO, respectively. When pHe was varied by altering PCO2, the slope of the line relating pHi to the extracellular pH (pHe) was greater (P less than 0.05--0.001) than that obtained during metabolic changes of pHe in right and left ventricles, atria, diaphragm, and quadriceps. During metabolic acidosis and alkalosis, the slope of pHi/pHe line did not vary between tissues. During respiratory acidosis, there was no difference in slope between cardiac tissues, but it was less in left ventricle than quadriceps (P less than 0.001). In left ventricle intracellular K+ increased in a metabolic (P less than 0.05) or respiratory acidosis (P less than 0.02), whereas in diaphragm it decreased (P less than 0.02). Intracellular K+ correlated with pHe and pHE-PHi. Changes in pHi but not intracellular K+ could explain known differences in myocardial function in respiratory and metabolic acidosis.

Acidosis↗

PubMed1979

Biguanide-induced lactic acidosis in Finland.

Twenty-four patients with biguanide-induced lactic acidosis were reported to the Adverse Drug Reaction Register of the Finnish National Board of Health from 1974-1977. Of them, 23 had been treated with phenformin and one with metformin. The mean age of the patients was 71 years, and all but one were more than 65 years of age. The mortality rate was 63%. One patient had cirrhosis of the liver and one was already known tohave had impaired renal function. Fourteen of the patients had a normal serum creatinine concentration either before or after the development of lactic acidosis. Thus, in most patients it had not been possible to prevent development of lactic acidosis by observing the contraindications to biguanide therapy. Most patients had some form of co-existing cardiovascular disease. Tetracycline therapy was a probable precipitating factor in three cases. Based on the statistics of biguanide consumption in Finland, the annual incidence of biguanide-induced lactic acidosis in 1976 and 1977 was between 1/2000 and 1/3000 and that of fatal lactic acidosis was 1/4000.

Acidosis↗

PubMed1975

Lactic acid permeation rate in working gastrocnemii of dogs during metabolic alkalosis and acidosis.

In isolated, blood perfused, supramaximally stimulated, isotonically working gastrocnemii of dogs lactic acid (LA) output and O2-consumption (V O2) were measured according to the Fick principle. Simultaneously concentration of muscle tissue was determined at rest and at different times during exercise. In one series of experiments metabolic alkalosis was induced by infusions of THAM of Na bicarbonate. As a result arterial pH increased to about 7.5 and standard [HCO3-1] to 31-35 mmol per 1. In another group of experiments metabolic acidosis was induced by HCl infusions. In these experiments pH decreased to 7.0-7.1 and standard [HO301] to 8-11 mmol per 1. During the first 3-4 min after the onset of exercise LA concentration of muscle tissue rose to 18-19 mumol per g wet weight in both series of experiments. During acidosis the highest average values for LA release from the muscle were about 1.1 mumoles per g per minute. During alkalosis LA permeation rate was nearly three times as high. As a consequence of increased rate of permeation, LA concentration of muscle tissue decreased more rapidly in alkalosis than in acidosis. In both series of experiments work per time and VO2 were practically equal during the first 5-6 min of exercise. Thereafter work per time and VO2 decreased more rapidly in acidosis than in alkalosis, a result which probably is due to higher LA concentration in muscle at this time in acidosis. It is concluded that LA permeation rate across muscle cell membrane is increased by high extracellular HCO3- concentration in combination with low H+ activity and vice versa.

Acidosis↗

PubMed1978

Cellular changes in the toad urinary bladder in response to metabolic acidosis.

The urinary bladder of Bufo marinus excretes H+ and NH+4, and the H+ excretion is increased when the animal is placed in metabolic acidosis. The mitochondria-rich (MR) cells mediate the H+ excretion by the bladder. The purpose of this study was to determine if there is a change in MR cells of the bladder during metabolic acidosis. Bladders from normal toads and from toads that had been placed in metabolic acidosis were used. The bladders were mounted between plastic chambers and H+ excretion measured. The bladder was then fixed and prepared for scanning (SEM) and transmission (TEM) electron micrograph studies. SEM's at low magnification were used to count the various cell types and the TEM's were used to confirm the different cell types. Fields were randomly selected and a total of 2500 cells counted in each group. The bladders from toads in metabolic acidosis had a consistently higher ratio of MR cells to granular cell than did the normal bladders. These results indicate that during metabolic acidosis there is an increased number of MR cells in the bladder, and this increased the bladder's capacity to excrete H+.

Acidosis↗

PubMed1979

Familial absorptive hypercalciuria and renal tubular acidosis.

Hypercalciuria was considered as a secondary condition when associated with familial renal tubular acidosis. Later studies suggested that hypercalciuria could lead to renal tubular acidosis and nephrocalcinosis. Selected members of a family spanning five generations were studied. Renal tubular acidosis was present in eight subjects in three consecutive generations. Increased 24-hour urinary calcium excretion was present in nine subjects in three consecutive generations, alone in the younger generation, and in combination with renal tubular acidosis and nephrocalcinosis in the older generation. Calcium loading tests showed the absorptive nature of hypercalciuria in nine of 18 subjects studied. This report suggests that in this family the absorptive hypercalciuria is an autosomal dominant genetic defect with complete penetrance and variable expressivity which leads to renal tubular acidosis and nephrocalcinosis.

Acidosis, Renal Tubular↗

PubMedDate not supplied

Nephrology rounds, University of Iowa Hospitals: renal tubular acidosis.

We have discussed two patients who had renal tubular acidosis complicated by hypokalemia. The first patient had a distal acidifying defect. Circumstantial evidence has been presented suggesting that exposure to toluene-diisocyanate or toluene-diamine played a role in the pathogenesis. The acidosis and the hypokalemia of this patient were easily corrected by the administration of small amounts of sodium bicarbonate without potassium supplementation. The second patient had an interstitial nephritis of unknown etiology and presented with moderate renal insufficiency, renal tubular acidosis, and proximal as well as distal acidifying defects. The proximal tubular dysfunction was associated with general aminoaciduria and glucosuria. This patient required large quantities of both alkali and potassium to correct the electrolyte abnormalities. The mechanisms of potassium wasting in proximal and distal renal tubular acidosis are reviewed. A classification is presented of cellular defects that may underlie the different renal acidifying defects. Attempts to distinguish between pump and permeability defects from urinary pCO2 levels must take into account the simultaneous HCO-3 concentration, since large pCO2 elevations require the presence of ample HCO-3 in the urine. Permeability defects may impair urinary acidification by either abnormal back flux of H+ out of the lumen or increased influx of HCO-3 into the lumen. In studies of acidification in vitro, amphotericin B causes increased H+ permeability and has little effect on HCO-3 permeability. Toluene-diamine causes a marked permeability defect which is reversible, but remains to be defined in terms of the ion species, HCO-3 or H+, affected. At times, hyperchloremic acidosis is caused by distal defects in net acid excretion that occur without impairment of the H+ gradient. In certain patients with hypoaldosteronism, for example, distal H+ secretion may be reduced without change in the force of the H+ pump.

Acidosis, Renal Tubular↗

PubMed1975

The effect of propranolol and phentolamine on serum gastrin concentration in response to respiratory acidosis in normal man.

Serum gastrin concentration and basal acid secretion were studied in normal subjects under the influence of respiratory acidosis induced by CO2 rebreathing. During the intragastric instillation of 100 ml/h 0.5 M bicarbonate a significant increase of gastrinaemia from 133 to 158 pg/ml (p less than 0.01) occurred in ten subjects during respiratory acidosis (pCO2 62 torr, pH 7.25). Under the intragastric instillation of 100 ml/h 0.1 N HCl the rise of gastrin concentration in response to CO2 rebreathing (pCO2 68 torr, pH 7.20) was not significant. The relationship between the decrease of pH and the increase of the gastrin concentration was shifted in the direction of a greater systemic acidosis compared to the results performed in the presence of a neutral intragastric pH. 50 mug/kg propranolol intravenously produced a decrease of gastrin concentrations from 145 to 127 pg/ml (p less than 0.01) and a total suppression of hypergastrinaemia in response to CO2 rebreathing, suggesting activation of beta-cell receptors in respiratory acidosis. The infusion of phentolamine in a dose of 0.6 to 1.8 mg/min. resulted in a rise of gastrin concentration from 140 to 165 pg/ml (p less than 0.01) which was not further elevated during respiratory acidosis. The basal acid secretion showed a significant rise in response to CO2 rebreathing, which was abolished by the administration of propranolol.

Acidosis, Respiratory↗

PubMed1979

Effects of acidosis on mechanical function and Ca2+ exchange in rabbit myocardium.

The effects of acidosis on myocardial function and calcium exchange have been studied in the isolated but arterially perfused interventricular septum of the rabbit. Temperature was 28 degrees C and stimulation rate 48 beats/min. Acidosis was induced either by increase of the perfusate PCO2 (pH reduced from 7.35 to 6.68) or by decrease of the bicarbonate-chloride ratio (pH 7.35 to 6.72). The effect on calcium efflux was assessed by introduction of acidosis at different times during the washout of 45Ca2+ from the muscle. The uptake of 47Ca2+ was recorded directly with a NaI crystal and counter. An increase of perfusate PCO2 caused a rapid fall in developed tension. The efflux of slowly exchanging 45Ca2+ and the uptake of 47Ca2+ were inhibited. There was no rapid displacement of calcium from the muscle. Decrease of the bicarbonate-chloride ratio caused a slower fall of developed tension and neither the efflux nor uptake of calcium were altered. These results suggest that developed tension and calcium exchange in the myocardium are more responsive to acidosis within the cell or cell membrane than to extracellular acidosis.

Acidosis↗

PubMed1975

Inotropic and intracellular acid-base changes during metabolic acidosis.

Experiments in isolated, Ringer-perfused isovolumic rabbit hearts showed that metabolic acidosis resulted in a decrease in peak left ventricular pressure and dP/dt. Concomitantly, the decrease in extracellular pH from 7.28 plus or minus 0.02 to 6.82 plus or minus 0.02 at constant PaCO2 was associated with a negative av HCO3- difference that lasted throughout the duration of acidosis. This negative av HCO3- difference indicated that either HCO3- moved into the intravascular space or H+ moved in the opposite direction during acidosis. During perfusion with normal pH solution av HCO3- was not significantly different from zero. Washout of the extracellular space with the acid solution can account for only 32 percent of the total amount of HCO3-recovered in the venous perfusate during the 30 min of acidosis. The remaining 68 percent (10.7 plus or minus 3.1 mmol times kg-1 of cardiac tissue) must then have originated in the cellular fluid. When intracellular fluid volume is taken into account, it can be calculated that 21.3 plus or minus 6.1 mmol of HCO3- moved into the vascular space per liter of intracellular water. The magnitude of this HCO3- flux suggests that significant myocardial cellular acid-base changes are associated with metabolic acidosis.

Acidosis↗

PubMed1976

Dual contribution theory of regulation of CSF HCO3 in respiratory acidosis.

Regulation of CSF HCO3-in respiratory acidosis was studied in light of the "dual contribution theory," which proposed that there were two sources for the CSF HCO3-increase: 1) HCO3-by diffusion from plasma and 2) HCO3-generated in the CNS and catalyzed by the local carbonic anhydrase (J. Appl. Physiol. 38: 504-512, 1975). In anesthetized dogs with an increase in Paco2 of 30 mmHg for 4 h the plasma HCO3 increased 2 meq/1 and CSF 6 meq/1. In combined respiratory and metabolic acidosis, plasma HCO3-did not increase but CSF HCO3-increased 6 meq/1. In combined acidosis and intraventricular injections of acetazolamide no increase in plasma or CSF HCO3-occurred. In combined respiratory acidosis and metabolic alkalosis and intraventricular acetazolamide, plasma HCO3-increased 15 meq/1 but CSF HCO3-increased 6 meq/1. Brain and CSF ammonia increased linearly and selectively with the increase in the relative contribution of CNS HCO3-increase. Therefore regulation of CSF HCO3-in respiratory acidosis depends on both components of the dual contribution theory, where each component can provide the total CSF HCO3-increase under appropriate experimental conditions. The control mechanism may be sensitive to changes in [H+] on the brain side of the blood-brain barrier.

Acid-Base Equilibrium↗

PubMed1979

Respiratory response to HCl acidosis in dogs after carotid body denervation.

To test the participation of the carotid bodies in the respiratory response to metabolic acidosis, six dogs were infused with HCl for 2 h followed by HCl feeding to prolong the acidosis to 48 h. This protocol was repeated after carotid body denervation (CBD). Mean control PCO2 rose by 7.3 Torr after CBD. PCO2 fell comparably during acidosis before and after CBD at all time periods from 30 to 48 h and returned to control levels by 72 h. The pH ranged from 7.10 to 7.30 during acidosis pre- and post-CBD. The decreases in pH and bicarbonate concentration did not differ significantly at any time interval between the pre- and post-CBD studies. This study indicates that in dogs moderately severe HCl acidosis stimulates ventilation acutely and chronically through a central mechanism in the absence of the carotid bodies.

Acidosis↗

PubMed1978

Effect of acidosis on heart cAMP-dependent protein kinase.

The effect of acidosis on cAMP-dependent protein kinase activity in perfused hearts from normal and reserpinized rats has been investigated. The results were compared to the effect of acidosis on myocardial contractility under the same conditions. The results showed that acidosis increases the cAMP-dependent protein kinase activity in normal hearts. This increase was abolished when the hearts were depleted of norepinephrine by previous treatment with reserpine. As regards myocardial contractility, there was a similar decrease by acidosis either in normal hearts with increased cAMP-dependent protein kinase activity or in reserpinized hearts in which the increase in protein kinase activity was prevented. Two alternative hypotheses are suggested: (1) a dissociation between contractility and cAMP levels, or (2) a "blockade" by acidosis of the mechanical effect of increasing cAMP-dependent protein kinase activity.

Acidosis↗

PubMed1976

Lactic acidosis in childhood.

Children with chronic metabolic acidosis should be investigated to determine the presence of an organic acid, especially when the plasma electrolyte profile shows a deficiency of anion. One of the organic acids that should be looked for in such a patient is lactic acid. Lactic acidosis due to tissue hypoxia is a well-known phenomenon (e.g., in shock and cardiopulmonary disease) and has not been discussed in this essay; nor has lactic acidosis due to exogenous causes like infusion of fructose or sorbitol, or admiministration of phenformin. Chronic lactic acidosis in infancy is a rare condition. It may be associated with glycogen storage disease Type 1, fructose diphosphatase deficiency, methylmalonic acidemia, propionic acidemia, pyruvate carboxylase or dehydrogenase deficiency and Leigh's subacute necrotizing encephalomyelopathy (SNE). Some patients with chronic lactic acidosis do not have nay of these diseases and comprise an "idiopathic" group. This is a heterogeneous group, probably having several different causes for the metabolic error. In Leigh's SNE, a metabolic block in the formation of thiamine triphosphate in brain has been demonstrated and has been attributed to the presence of an inhibitor of thiamine pyrophosphate-adenosine triphosphate (TPP-ATP) phosphoryl transferase in body fluids. The inhibitor has also been encountered in cases of intermittent cerebellar ataxia and of primary hypoventilation (Ondine's curse), which may represent variants of Leigh's disease. Increased blood levels of lactate, pyruvate and alanine frequently are encountered in SNE, but it still is not clear whether they are due to a primary or secondary disturbance in the catabolism of pyruvate. Disturbed lactate and pyruvate metabolism has also been encountered in isolated cases of mental retardation and growth failure, in mitochondrial myopathies and in polyneuropathies, and may be expected to occur in Wernicke's encephalopathy. Finally, it has been noted in malignancy and in association with other rare metabolic disorders.

Acidosis↗

PubMed1977

[Blood picture in lactate acidosis. Part 2: acid-base equilibrium and lactate].

A differentiation between lactate emia (lactic acid emia) and lactate acidosis (lactic acidosis) is made. The normal value for blood lactate concentration is 1-2 mmol/1. The term lactate emia is used for lactate values between 2-6 mmol/1. The limiting value for the diagnosis of lactate acidosis should be more than 7-8 mmol/1 for the blood lactate concentration. Furthermore the different buffer mechanisms are evaluated in respect to their influence on the pH of the blood and to lactate metabolism. Especially the mechanism of respiratory compensation for metabolic acidosis is discussed. It is stated that for the diagnosis of lactate acidosis the blood-pH and the bicarbonate concentration should be measured.

Acid-Base Equilibrium↗

PubMed1977

[Chronic metabolic acidosis in dairy cows].

Complex clinical and clinico-biochemical examination of the blood, urine and rumen liquor in a herd of dairy cows revealed chronical metabolic acidosis accompanied by rumen dysfunction and by a reduced butterfat content of milk. During the first examination of the acid-base state of the blood was almost at a standard level. An increased level of urea in blood plasma and a higher GOT transaminase activity testified to an excessive load on the liver. Urine pH was considerably deviated towards the acidic side and inorganic phosphorus was present in urine in a greater concentration. The pH of rumen liquor was slightly shifted towards alkalinity owing to the release of NH3 from urea in the food ration. The diagnosis--suspect chronical metabolic acidosis--was determined on the basis of the first examination. Chronical metabolic acidosis was definitely proved by the second examination when urea had been excluded from the feed ration. Repeated examinations revealed chronical metabolic acidosis which had originally been accompanied by a higher rumen liquor pH. On the basis of case histories and mechanisms of chronical acidosis, measures were proposed, resulting in an increase of the butterfat content of milk. Chronical metabolic disorders often follow a long-lasting latent pattern, manifesting themselves as a reduced milk yield and lower resistance; the clinical form of disease appears only at a later stage. The system of preventive diagnostics provides information on the changes in the composition of internal medium and of the faeces before a drop occurs in milk and fat production. These measures prevent metabolic disorders and high losses of produce which otherwise remain hidden for a long time.

Acidosis↗

PubMed1978

Hyperchloremic acidosis during the recovery phase of diabetic ketosis.

We have studied 35 patients to find the occurrence of hyperchloremic acidosis during the recovery phase of diabetic ketoacidosis. At admission the patients had typical normochloremic acidosis, with increased anion gap exactly balancing decreased serum bicarbonate. In contrast, in 18 patients with phenformin-induced lactic acidosis, the increase in anion gap at admission was much greater than the decrease in bicarbonate. The difference between lactic acidosis and ketoacidosis may be explained by a slower rate of excretion of lactate than of ketone anions. After the patients with ketoacidosis were treated, the acidosis became predominantly hyperchloremic with normal anion gap. Failure to normalize serum bicarbonate is attributed to excretion of ketone anions in the urine.

Adolescent↗

PubMed1979

Carbonic anhydrase isoenzyme B in erythrocytes of subjects with chronic acidosis.

A specific and quantitative immunological method for determination of human erythrocyte carbonic anhydrase isoenzyme B has been used to ascertain the contents of this enzyme in the erythrocytes of healthy persons and of subjects with chronic metabolic and respiratory acidosis. The investigations have shown significant increase of carbonic anhydrase type B in the erythrocytes of patients suffering from renal failure with chronic acidosis, and in patients with chronic obstructive lung disease and chronic respiratory acidosis. The erythrocytes of acidotic uremic patients have a significantly higher content of erythrocyte carbonic anhydrase isoenzyme B than do the erythrocytes of uremic subjects without chronic acidosis. In chronic obstructive lung disease, the content of this enzyme in erythrocytes was significantly higher in the hypercapnic patients than in the normocapnic ones. In renal failure, significant correlation was found between carbonic anhydrase isoenzyme B and standard bicarbonate. In chronic obstructive lung disease no significant correlation was found between carbonic anhydrase and pCO2.

Acidosis↗