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At least 793 records · Page 44Linked to original sources
PubMed1995

Modulation of sodium-hydrogen exchange activity in cardiac myocytes during acidosis and realkalinisation: effects on calcium, pHi, and cell shortening.

OBJECTIVE: The aim was to examine the effects of the Na+/H+ exchange inhibitor methylisobutylamiloride (MIA) as well as protein kinase C, a putative regulator of Na+/H+ exchange, on intracellular calcium, intracellular pH, and unloaded cell shortening in isolated guinea pig cardiac myocytes subjected to lactic acid induced acidosis followed by realkalinisation. METHODS: Calcium transient amplitude and cell shortening were measured simultaneously in single isolated myocytes loaded with fura2-AM. Intracellular pH was measured in cells loaded with BCECF-AM. RESULTS: Exposure of cells to 5 min of lactate (20 mM) acidosis (pH 6.8) caused an increase in calcium transient amplitude and a decrease in cell shortening and intracellular pH. During realkalinisation (pH 7.3), the calcium transient gradually decreased while intracellular pH became more alkaline than pre-acidosis values. The cells underwent transient hypercontractility as evidenced by a marked increase in systolic cell shortening and a decrease in diastolic cell length. Inhibition of sodium/hydrogen exchange with MIA (1 microM) caused a significant attenuation of the increase in calcium transient amplitude during acidosis and further depressed cell shortening as well as intracellular pH. In addition, MIA significantly attenuated hypercontractility and abolished cell contracture upon realkalinisation. In contrast, phorbol 12-myristate 13-acetate (10(-12) M) exerted no effects on the response to acidosis; however, this treatment exacerbated cell hypercontractility and reduced functional recovery upon realkalinisation. CONCLUSIONS: Inhibition of Na+/H+ exchange activity during acidosis/realkalinisation enhances recovery of cell function.

Acidosis↗
PubMed1995

[Renal tubular acidosis in the kidney transplant].

UNLABELLED: Renal tubular acidosis is a syndrome of disordered renal acidification, we have studied a group of patients transplanted. Their cases clinic patients have been analyzed with no-present infectious disease, or tubulointerstitial diseases or urinary infection, immunosuppression with prednisone and azatioprine only, no have to ingest cyclosporine and period graft superior 3 months. We haven't neither patient with proximal renal tubular acidosis. We have been reported 7 cases of distal renal tubular acidosis. All the patients have make the furosemide test. Only one case hyperkalemia renal tubular acidosis. Histologic kidney had been chronic rejection. CONCLUSION: renal tubular acidosis is not infrequent of kidney transplantation and this syndrome connect with chronic rejection.

Acidosis, Renal Tubular↗
PubMedDate not supplied

[Mechanisms of renal adaptation to disorders of water-electrolyte balance in metabolic acidosis].

The albino rat experiments have demonstrated that despite the type, metabolic acidosis causes an increase in plasma and urinary osmolarity, hyperkalemia and hypernatremia, enhanced urinary excretion of potassium, phosphates, and titrated acids with a tendency for the glomerular filtration rate and urinary pH to be lowered with the increased concentrations of plasma vasopressin and insulin and renal cortical PGE2. Hyperchlorinemic acidosis without increases in the anion difference is accompanied by severe chloremia, natriuresis, chloruresis, ammoniuresis without diuretic changes with the inhibited renin-aldosterone system and progesterone synthesis. Lactate acidosis with a growing anion difference leads to lower diuresis, Na+ and Cl- excretion without enhancing ammonium excretion in the presence of elevated plasma levels of renin, aldosterone, and progesterone. It is concluded that in metabolic acidosis, adaptation to water-electrolytic exchange derangements greatly depends upon the type of metabolic acidosis and it is mediated by hormones to a considerable extent.

Acidosis↗
PubMed1994

Correction of intramyocardial hypercarbic acidosis with sodium bicarbonate.

Although it has been hypothesized that exogenously administered bicarbonate can exacerbate intramyocardial acidosis and compromise contractile function, this phenomenon has not been demonstrated in an intact model in which intramyocardial pH (pH(int)), regional venous pCO2, and regional contractile function have been simultaneously monitored. In 20 anesthetized dogs, we studied the effects of intracoronary infusions of sodium bicarbonate NaHCO3 30 mEg over 15 min, on regional pH(int), (glass electrode) and regional stroke work (SW, sonomicrometry) before and after creating systemic hypercarbic acidosis by hypoventilation. During NaHCO3 administration, regional coronary venous pCO2 increased rapidly during the first minute (eucapnea; 34 +/- 7 to 55 +/- 18 mm Hg; hypercapnea: 70 +/- 15 to 98 +/- 23 mm Hg, P < 0.05 for both increases). Regional venous pH rose from 7.36 +/- .04 to 7.55 +/- .06 (P < 0.05) after the first minute of NaHCO3 infusion during eucapnea and from 7.09 +/- .09 to 7.22 +/- .09 (P < 0.05) during hypercapnea. During the first minute of NaHCO3 infusion, pH(int) declined minimally. However, during the remaining 14 min of each infusion, pH(int) increased significantly (eucapnea: 7.19 +/- 0.10 to 7.43 +/- 0.12; hypercapnea: 6.86 +/- 0.14 to 7.02 +/- 0.15, P < 0.05 for both changes). Regional SW decreased significantly during the first minute of infusion, both during eucapnea (23,400 +/- 7,400 to 18,000 +/- 6,300 ergs/cm2, P < 0.05) and hypercapnea (27,000 +/- 9,100 to 25,000 +/- 10,000 ergs/cm2, P < 0.05). The first minute of contractile dysfunction was followed by recovery and ultimately supranormal contractile function during the remainder of each bicarbonate infusion. To test the hypothesis that transient intracellular acidosis during bicarbonate infusions was underestimated by measurements of pH(int), measurements of intracellular pH using the pH-sensitive dye, BCECF, were performed in isolated guinea pig papillary muscles incubated in vitro. These measurements confirmed the presence of transient intracellular acidosis during bicarbonate infusion. In conclusion, (1) the intracoronary administration of sodium bicarbonate causes a transient depression in myocardial contractile function that is related to transient intracellular acidosis; and (2) despite exacerbating hypercarbia, sodium bicarbonate ultimately neutralizes intracellular acid and augments myocardial contractile function.

Acidosis↗
PubMed1994

The role of chronic anion gap and/or nonanion gap acidosis in the osteodystrophy of chronic renal failure in the predialysis era: a minority report.

Chronic renal failure (CRF) due to (1) glomerulopathies, vascular and tubulointerstitial disorders, and (2) chronic nonazotemic renal tubular disorders creates sustained acidosis in the untreated state. Number 1 represents a mixture of anion and nonanion gap acidosis and number 2 a pure nonanion gap acidosis. There remains significant uncertainty as to the role of the acidosis (CRF) in the associated osteodystrophy. In general, little attention has been given to this subject in recent monographs. It is the purpose of this review ('minority report') to 'reexamine' the information available on this subject in humans and animals. The author has concluded that the chronic metabolic acidosis of CRF may well contribute to the development and maintenance of the osteodystrophy, and that its treatment should be included along with the other modalities of therapy. The subject is not a 'dead issue' but one definitely deserving further investigation. The response of the skeleton to acid loads clearly represents another 'trade-off' in ion metabolism in CRF.

Acidosis, Renal Tubular↗
PubMed1996

Metabolic acidosis as a uremic toxin.

Patients with chronic renal failure suffer from a muscle wasting syndrome that is characterized by loss of lean body mass and negative nitrogen balance. Evidence is provided indicating that metabolic acidosis plays a major role in initiating these adverse effects. In particular, we discuss findings suggesting that metabolic acidosis mitigates its effects by activating the cytosolic ubiquitin proteasome proteolytic pathway. Additional evidence that metabolic acidosis alters vitamin D and parathyroid hormone levels is provided. Therapy that includes correction of the metabolic acidosis with alkali in the form of sodium bicarbonate supplements has significant therapeutic implications for uremic patients with even mild degrees of metabolic acidosis.

Acidosis↗
PubMed1977

Renal tubular acidosis due to the milk-alkali syndrome.

A 60-year-old man with a history of excessive ingestion of calcium carbonate presented with azotemia, hypercalcemia and hyperphosphatemia. His acid-base status was initially normal. Following the cessation of calcium carbonate treatment, the hypercalcemia and azotemia disappeared, and the patient was found to be in metabolic acidosis with blunted acid excretion and a urine pH of 6.1. Kidney biopsy showed focal tubular calcification; the tubular damage was apparently caused by hypercalcemia and had resulted in renal tubular acidosis. During the three months of observation since that time there has been a tendecy for spontaneous remission of the renal tubular acidosis. Impaired renal hydrogen ion excretion prevented the development of metabolic alkalosis despite ingestion of alkali initially, and was later responsible for the metabolic acidosis. Renal tubular acidosis occurring as a sequel to the milk-alkali syndrome may aggravate the danger of nephrocalcinosis in this syndrome.

Acidosis, Renal Tubular↗
PubMed1996

Two survival cases of alcoholic lactic acidosis complicated with diabetes mellitus and alcoholic liver disease.

We have experienced two patients with alcoholic lactic acidosis complicated with liver disease and diabetes mellitus who were successfully treated. They developed hypoglycemia, dehydration, lactic acidosis, and renal failure after drinking a large volume of alcohol without eating for 1 week before onset. Acidosis was thought to be directly related to excessive alcoholic intake, because it was no associated with severe liver failure and rhabdomyolysis. During monitoring of respiratory and circulatory functions, a rapid infusion of fluids adjusting to water and electrolyte imbalance was performed. A mixture of physiological saline and 5% glucose solution was thought to be effective in these cases. Patients recovered from renal failure and lactic acidosis without hemodialysis. Our experience will hopefully provide a key to successful treatment of fatal alcoholic lactic acidosis.

Acidosis, Lactic↗
PubMed1995

[Lactic acidosis induced by phenformin: a still forgotten iatrogenic complication].

Phenformin, a drug used in the treatment of diabetes mellitus frequently associated with potentially fatal cases of lactic acidosis, has been removed from market in the USA and several European countries. However, cases of lactic acidosis are still reported in countries where phenformin is available, either because well-known contraindications for its use are not observed, or because the prodromic syndrome of the lactic acidosis is not diagnosed. This study describes two cases of lactic acidosis, the treatment used and the final outcome. The authors point out that plainly evident contraindications were ignored in both cases, while the prodromic syndrome remained unrecognized even by specialists. The management of lactic acidosis continues to be a challenge. There is no optimal treatment and early recognition is essential. The authors call for greater attention in the use of phenformin and its eventual removal from market, especially in the light of alternative therapies which prove to be equally valid and easier to administer.

Acidosis, Lactic↗
PubMed1997

New autosomal-recessive syndrome of Leber congenital amaurosis, short stature, growth hormone insufficiency, mental retardation, hepatic dysfunction, and metabolic acidosis.

We report on a new autosomal-recessive syndrome in 4 Japanese children in 2 families. The key manifestations are Leber congenital amaurosis, short stature, growth hormone insufficiency, mental retardation, hepatic dysfunction, metabolic acidosis, and autosomal-recessive inheritance. There were no consanguineous marriages. Abnormal eye movements were noticed neonatally, and ophthalmological examinations showed no visual acuity, pigmentary retinal degeneration, and nonrecordable electroretinograms in all cases. Inadequate weight gain and short stature gradually became apparent after birth, and at present the height range is -4.6 - -7.2 SD (standard deviations). Developmental delay was noted at age 4 months, and the developmental quotient is 50-70 at present. Deterioration of development and convulsions were not recognized. Elevated serum aminotransferase levels and metabolic acidosis were also found at age 4 months. Proximal renal tubular acidosis was clarified by bicarbonate tolerance tests in 1 case, and may have caused metabolic acidosis. Growth hormone secretion was insufficient by insulin tolerance test in 3 cases. One year of growth hormone therapy in 2 cases did not affect growth velocity. Hepatic dysfunction and metabolic acidosis ameliorated later. No renal cysts were found. A cranial computed tomographic scan and magnetic resonance imaging showed normal findings. Amino acids, organic acids, and very long chain fatty acid levels in plasma were all normal in the 3 cases examined. Histopathological and mitochondrial DNA analyses showed no evidence of mitochondrial disorders.

Acidosis↗
PubMed1997

Pathogenesis of cardiac dysfunction during metabolic acidosis: therapeutic implications.

Based on work performed in many laboratories including our own, we suggest the following schematic shown in Figure 4 to explain metabolic acidosis and the effects of alkalinization therapy. Metabolic acidosis induces prompt and substantial decreases in cardiac functional performance. This is mediated by an intracellular acidosis which impairs cardiac function directly as well as leads to an impairment of cardiac energy metabolism which further impairs cardiac function. Attempts to alkalinize the cell with sodium bicarbonate therapy lead to a paradoxical intracellular acidosis and further impairment of cardiac function, whereas Carbicarb may correct the intracellular acidosis and improve physiological function. However, at the time which this paper was written, Carbicarb was not available for clinical use in the United States.

Acidosis↗
PubMed1997

[Insufficient correction of blood bicarbonate levels in biguanide lactic acidosis treated with CVVH and bicarbonate replacement fluids].

BACKGROUND: In the course of Continuous Veno-Venous Hemofiltration (CVVH), bicarbonate buffer instead of lactate is suitable for the treatment of combined renal and hepatic failure and for patients suffering from lactic acidosis, type A or B, joined with acute renal failure (ARF). METHODS: We applied the CVVH buffered with bicarbonate for the treatment of two patients affected by ARF and severe lactic acidosis type B (due to biguanide intoxication) and we evaluated its ability to correct the acid-base balance. RESULTS: Clinical and laboratory data show that this technique, performed in standard conditions (plasma flow: 70 ml/min, ultrafiltration: 25 ml/min, bicarbonate concentration in the infusion fluid: 30 mEq/L), was inadequate to compensate for the high requirement of bicarbonate (approximately 280 mEq/hr during the first 6 hours of observation) and the severe metabolic acidosis, thus additional bicarbonate infusion was needed. CONCLUSIONS: In particular, from ascertained data and theoretical considerations, in the course of lactic acidosis caused by biguanide, in order to correct acidosis a positive balance of bicarbonate could be obtained only by means of a bicarbonate-based replacement fluid and of a continuous high flow hemofiltration, such as to assure an ultrafiltrate volume exceeding 150 ml/min.

Acidosis, Lactic↗
PubMed1997

[Pathogenesis and diagnosis of systemic acidosis in animals with conclusions for effective forms of therapy].

Intermediary metabolism produces daily approximately 285 mmol hydrogen ions per kilogramm metabolic body weight (BWkg 0.75). If the lung fails to eliminate the volatile acid H2CO3 sufficiently and/or if the kidneys do not eliminate the also produced nonvolatile acids a retention of acids in the organism results. This way, as well as increased acid production through metabolic processes, leads to a systemic acidosis. Systemic acidosis develops after a primary dysfunction of an organ. If there is only one cause of an acid-base-disturbance, e.g. metabolic acidosis, the organism will respond with compensation by the correspondent organ, e.g. the lung, which reduces the drop in the pH. If metabolic and respiratory acidosis occur simultaneously normal compensation is impaired and the fall in the pH is greater by additive effects. This can lead to a severe, life-threatening decline in the blood-pH (< 7.00). If the pH falls from normal value of 7.40 below 7.20, buffer therapy is necessary. Most alkalinizing agents in veterinary medicine, such as bicarbonate, lactate or acetate are only effective after increased pulmonary elimination of CO2 produced in buffer reactions. These substances are not suitable and are even contraindicated in therapy of primary respiratory or mixed respiratory-metabolic acidosis. New buffer agents, e.g. an equimolar mixture of NaHCO3 and Na2CO3 (= Carbicarb) open new promising possibilities in the treatment of acidotic disorders in animals. However clinical trials to determine the efficacy of Carbicarb in animals are still to be conducted.

Acid-Base Equilibrium↗
PubMed1976

Phenformin and lactic acidosis.

All patients admitted with severe lactic acidosis to a university teaching hospital during a 17-month period were taking phenformin hydrochloride. Serum phenformin concentration was measured in one patient and found to be four to nine times the usual therapeutic concentration. Prerenal azotemia was present at the time of admission in all but one of these patients, but renal function was normal at the time of discharge in those patients with phenformin-associated lactic acidosis who survived. Phenformin-associated lactic acidosis accounted for 7% of the episodes of metabolic acidosis and 27% of deaths due to metabolic acidosis in diabetics.

Acidosis↗
PubMed1976

Pulmonary oedema associated with acidosis in patients with cholera.

Five patients with severe acidosis and pulmonary oedema complicating cholera were seen at the Cholera Research Laboratory, Dacca, in a two-year period. All had had inadequate treatment. Their disease resulted in acidosis prior to admission; only the two who subsequently survived received volumes of sodium bicarbonate solutions sufficiently large to repair completely their acidosis. Saline alone worsened pulmonary congestion, while alkali appeared to relieve it despite the accompanying volume expansion. These observations are consistent with the known redistribution of blood to the central circulation in acidosis. Timely and proper treatment of cholera will avert this syndrome, when use of isotonic sodium bicarbonate sufficient to correct acidosis may be very helpful.

Acidosis↗
PubMed1998

[Lactate metabolism and lactic acidosis].

Lactate can be viewed as a metabolic dead end in that it can only be produced or utilized via pyruvate. Lactate production is determined primarily by pyruvate concentration and to a lesser extend by the redox state. Increased lactate production may result from tissue hypoxia, alkalosis, catecholamine and alanine transamination to pyruvate. Hyperlactatemia is observed in many pathological conditions. Current diagnostic criteria for lactic acidosis are a pH less than 7.35 and lactate concentration greater than 5 to 6 mmol/l. In our study series, malignancy was the most common underlying disease accompanied by lactic acidosis. Organ failure, cardiovascular disease and diabetes mellitus were also common. The prognosis of patients with these diseases were grave. In cases of lactic acidosis associated with diabetes mellitus, alcoholic liver disease, rhabdomyolysis and diabetic comas were noticeable as complications. Alcohol abuse was the most common cause of lactic acidosis associated with diabetes mellitus. In these cases, laboratory data showed prominent hyperlactatemia, hyperglycemia and acidemia and elevated anion gap. The mortality rate in these cases was 36% and higher in cases with organ failure. Treatment of lactic acidosis consists of alkalization by sodium bicarbonate with carbicarb, insulin-glucose-infusion, dichloroacetate therapy, tham administration, bicarbonate-buffered peritoneal dialysis and high bicarbonate-containing dialysis.

Acidosis, Lactic↗
PubMed1996

Swelling, intracellular acidosis, and damage of glial cells.

Cerebral ischemia and severe head injury among others are associated with a limited availability of oxygen, leading to cell catabolism as well as anaerobic glycolysis. Resulting metabolites, such as arachidonic- and lactic acid, can be expected to leak into perifocal brain areas, contributing there to cytotoxic swelling and damage of neurons and glia. Since elucidation of mechanisms underlying cell swelling and damage in the brain is difficult in vivo, respective investigations were carried out in vitro using suspended glial cells. Thereby, effects of arachidonic acid (AA) and of lactacidosis on glial cell volume, intracellular pH (pHi), and cell damage were analyzed utilizing flow cytometry. AA led to an immediate, dose dependent swelling and intracellular acidosis of glial cells. A concentration of 0.1 mM increased cell volume to 110% of control and decreased pHi to 7.05. Whereas glial swelling was permanent, pHi recovered to baseline after 90 min. Cell viability of 90% remained unchanged after addition of AA up to 0.1 mM, while at 0.5 mM it was significantly decreasing. Glial swelling from AA was nearly completely inhibited by the aminosteroid U-74389F or by using a Na(+)-free suspension medium for the experiment. Acidification of the medium to pH 6.8 or 6.2 led to a cell volume of 110% or 120% of control without affecting cell viability. The cells were not capable to defend their normal pHi during lactacidosis of the suspension medium but became acidotic as well. Addition of amiloride or utilization of Na(+)-free medium inhibited cell swelling from lactacidosis, while intracellular acidosis was even more pronounced. The results indicate that AA as well as acidosis are potent mediators of glial swelling and damage at levels found under pathophysiological conditions in the brain in vivo. Whereas intracellular acidification caused by AA was reversible, glial cells were unable to regulate their pHi during maintenance of extracellular acidosis. Concerning the mechanisms of glial swelling by AA, the production of oxygen- and lipid radicals might play a major role in the swelling process. The results indicate a role of the Na+/H(+)-antiporter in acidosis-induced glial swelling, whereas the exchanger has a limited significance for maintenance of pHi. As seen, the final pathway of glial swelling from both, AA and lactacidosis, requires a net influx of Na(+)-ions, probably together with Cl-ions, and osmotically obliged water.

Acid-Base Equilibrium↗
PubMed1993

Acidosis slows the response of oxidative phosphorylation to metabolic demand in isolated rabbit heart.

The purpose of this study was to investigate the effect of acidosis on the mean response time of mitochondrial oxygen consumption to steps in heart rate and in left ventricular balloon volume. The mean response time may be viewed as the average delay between a change in adenosine triphosphate (ATP) hydrolysis and oxygen consumption. The mean response time is calculated by subtracting the transport time, required for diffusion of oxygen and for convective transport through the coronary vessels, from the response time measured in the coronary venous effluent. Eight isolated rabbit hearts were perfused according to Langendorff using Tyrode solution at 28 degrees C. Arterial perfusate pH was lowered from 7.30 +/- 0.03 (mean +/- SD) to 6.59 +/- 0.02 by increasing the CO2 tension. At pH 7.3 the mean response time was 12.6 +/- 1.6 s, independent of the time after isolation of the heart. During acidosis, applied 40-75 min after isolation of the heart, the mean response time was 21.4 +/- 0.7 s and increased to 32.6 +/- 4.3 s during acidosis, 85-120 min after isolation. Thus the retardation of the metabolic response by acidosis might depend on the condition of the heart. A decrease of mitochondrial ATP synthetic capacity during acidosis may contribute to the retardation of the metabolic response. Since determination of the mean response time at 37 degrees C is not yet feasible, the experiments were done at 28 degrees C. Extrapolation of our findings to 37 degrees C appears premature.

Adenosine Triphosphate↗