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PubMed2001

Postnatal growth retardation exacerbates acidosis-induced retinopathy in the neonatal rat.

PURPOSE: We have previously described a metabolic acidosis-induced retinopathy in the neonatal rat, similar to retinopathy of prematurity (ROP). We also have reported exacerbation of oxygen-induced retinopathy by postnatal growth retardation, produced by raising newborn rats in 'expanded' litters. In the present study, we investigated the effect of postnatal growth retardation on the incidence and severity of acidosis-induced retinopathy. METHODS: 100 newborn Sprague-Dawley rats were randomly assigned to two expanded litters of 25 pups each and five standard control litters of 10 pups each. All rats were gavaged with 10 mM/kg NH(4)Cl twice daily from days two to seven. Following five days of recovery, retinal vasculature was assessed using ADPase staining, light microscopy, and computer-assisted image analysis. The presence of neovascularization (NV), severity of NV (clock hours), and vascularized retinal areas, were evaluated in a masked manner. RESULTS: NV occurred in 52% of rats in expanded litters versus 18% of rats in standard control litters (p = 0.005). Postnatal growth retardation of pups in expanded litters was confirmed by comparing total body weight of pups raised in expanded and standard control litters (10.8g vs 13.4g on day 8, p < 0.001; 20.8g vs 25.2g on day 13, p = 0.002). CONCLUSIONS: Postnatal growth retardation increases the incidence of acidosis-induced retinopathy in the neonatal rat. Our study provides further evidence that postnatal growth retardation is a risk factor for preretinal neovascularization in immature retinae and is consistent with the clinical observation that the smallest and sickest premature infants are more likely to suffer from ROP.

Acidosis↗
PubMed1994

The effect of acidosis on the labelling of urinary ammonia during infusion of [amide-15N]glutamine in human subjects.

In three experiments [amide-15N]glutamine was infused intravenously in male volunteers. After 4-8 h of infusion acidosis was achieved by an oral dose of CaCl2 (1 mmol/kg). In one subject acidosis was maintained for 5 d. The acid load produced an approximately 3-fold increase in urinary NH3 excretion, with a small (approximately 20%) and transient increase in the isotope abundance of urinary NH3. Estimates of glutamine production rate (flux) were obtained in two experiments. There was no evidence that it was increased in acidosis. The extra NH3 production by the kidney represented only a very small part, about 3%, of the total glutamine production rate.

Acidosis↗
PubMedDate not supplied

Metabolic acidosis and renal tubular injury due to pure toluene inhalation.

A 22-y-old woman was hospitalized for muscle weakness of her lower extremities after she sniffed approximately 6 l of pure toluene during the month prior to admission. The examinations on serum and urine revealed mixed hyperchloremic and high anion gap metabolic acidosis accompanied by impaired urinary acidification. Histopathological changes of the kidney were patchy areas of tubular injury. Acidosis normalized on the fourth day of admission, but both proximal and distal tubular dysfunction persisted. These findings indicate that toluene is a tubular toxin and may contribute to the development of distal renal tubular acidosis.

Acidosis↗
PubMed2005

Yeast mediates lactic acidosis suppression after antibiotic cocktail treatment in short small bowel?

During acidotic periods in a girl with a short small bowel, very high D-lactic acid concentrations were measured in blood and urine; the patient's characteristic faecal flora contained mainly lactobacilli, and during antibiotic cocktail treatment also many yeasts. In this case report we sought to understand the beneficial effect of the antibiotic cocktail. Microbiological analysis was performed in faecal samples. Total lactic acid in serum and urine was studied using capillary gas chromatography-mass spectrometry, and D- and L-lactic acid in serum and urine by enzymatic assay. The results were coupled to patient's condition. Antibiotic cocktail therapy reduced the acidosis-associated symptoms, faecal lactobacilli and D-lactic acid production, but simultaneously the antibiotic therapy strongly increased the percentage of yeast in the faecal flora. Four to six weeks after each course of treatment the percentage of yeast decreased, whereas the percentage of intestinal lactobacilli increased; D-lactic acid also simultaneously increased in blood and urine. The patient felt well and showed a high percentage of intestinal yeast, but she often suffered from acidosis owing to a high percentage of lactobacilli. The yeast was identified as the pathogenic Candida glabrata. From the mentioned data together with data from the literature it was concluded that during several weeks the selected pathogenic yeast, C. glabrata, acted as a microbiological and metabolic buffer. Shortly after the course of antibiotic treatment this intestinal yeast strongly competed with the intestinal lactobacilli and thus prevented renewed rapid growth, massive D-lactic acid production from glucose and consequently also D-lactic acid-associated acidosis. The emergence of this yeast led us to consider probiotic lactobacilli or yeast for therapeutic use. The lack of knowledge regarding bile acid-deconjugating activity in both lactobacilli and probiotic yeast means that a final recommendation is not yet possible.

Acidosis, Lactic↗
PubMed1988

The role of tissue acidosis in ischaemic tissue injury: the concept of the pH integral.

Cerebral cortical tissue pH was monitored with an extracellular glass electrode in 32 rats subjected to total global cerebral ischaemia produced by ligation of the basilar and carotid arteries with systemic hypotension for periods of 8 to 60 min. The totality of the ischaemia, and its duration were confirmed by monitoring with a brain tissue O2 electrode. Reperfusion was induced by hypertension and maintained thereafter to exclude delayed ischaemia during 3 h survival after which the rats were sacrificed by perfusion fixation. The severity of tissue pH change was varied by inducing hyperglycaemia in some of the rats. Quantitative counts were made of neurons demonstrating changes reflecting severe ischaemic injury within 500 microns of the electrode tip. For the criterion of an ischaemically injured neuron count greater than 20%, there appeared to be a threshold at about 30 min, and more than 0.8 units change in pH. For quantitative assessment of the ischaemic insult a more satisfactory index was found by combining both time and acidosis as the integral of the pH change during the period of ischaemia. This was found to have a strong correlation with the histologic changes. There was a less strong correlation between the acidosis during reperfusion and the histologic change. Comparing these results with those for 3 rats subjected to 215 min of ischaemia without reperfusion, it appears that most of the effect of acidosis in aggravating ischaemic injury takes place during the first hour of ischaemia with little further aggravation for longer periods.

Acidosis↗
PubMed2006

Effect of acidosis on isolated porcine retinal vessels.

PURPOSE: To study the effect of normocapnic (NA) and hypercapnic acidosis (HA) on the tone, the intracellular calcium level ([Ca(2 +)](i)), and the membrane potential of smooth muscle cells in porcine retinal arterioles. METHODS: Twenty-four porcine retinal arterioles were mounted in a wire myograph for isometric recording of the wall tension. The vessels were precontracted with 0.3 microM U46619 and were exposed to NA (pH = 7.0) and HA (pH = 7.0). Intracellular calcium was measured using the fluorophore Fura-2AM (n = 12). In six vessels, 0.1 mM NG-nitroarginine methyl ester (L-NAME) was added to block NO synthesis. The membrane potential of smooth muscles cells was measured in situ with sharp glass electrodes (n = 12). RESULTS: NA and HA induced both a decrease in wall tension from 1.04 +/- 0.06 N/m to 0.65 +/- 0.1 N/m (p < 0.01) (NA) and 0.56 +/- 0.1 N/m (p < 0.01) (HA) and a decrease in [Ca(2 +)](i) as evidenced from the change in the Fura-2 fluorescence emission ratio from 0.66 +/- 0.03 to 0.57 +/- 0.05 (p = 0.005) (NA) and 0.56 +/- 0.05 (p = 0.002) (HA). These results were unaffected by inhibition of NO-synthesis. NA and HA also both induced hyperpolarization of the smooth muscle membrane from -18 +/- 0.7 mV during precontraction to -26 +/- 1.9 mV (p = 0.002) (NA) and -24 +/- 2.6 mV (p = 0.02) (HA). CONCLUSIONS: Acidosis-induced relaxation of the tone in preconstricted isolated porcine retinal arterioles is associated with a decrease in intracellular calcium and a hyperpolarization of the smooth muscle cells. The acidosis-induced relaxation is independent of CO(2) and is not mediated through NO.

Acidosis↗
PubMed1998

In vitro activation of complement and contact system by lactic acidosis.

The activation of complement and contact systems occurs in reperfusion injuries with initial tissue hypoxia, and lactic acidosis such as mycardial infarction and birth asphyxia. The aim of our experiment was the formal proof of activation by sole lactic acidosis. Lactic acid was added to blood and plasma samples from 10 healthy volunteers. C5a and factor XIIa were measured by EIA after incubation at 37 degrees C for 1 h. Both concentrations increased (P < 0.0001 by Friedman analysis) in blood and plasma samples with increasing amount of added lactic acid. Lactic acidosis can activate C5 from the complement system and factor XII from the contact system directly, even in the absence of cellular components.

Acidosis, Lactic↗
PubMed1999

Acidosis and tissue hypoxia in the critically ill: how to measure it and what does it mean.

We routinely monitor blood gases to determine the adequacy of ventilation and the presence of acid-base abnormalities. Changes in the blood are easily assessed, but of more importance is the abnormality at tissue level. Defects in acid-base homoeostasis have major effects on protein function, thus affecting tissue and organ performance. We concentrate on the changes seen in critically ill patients with acidosis because they form a large portion of the workload of the average intensive care unit. In addition, such patients have significant morbidity and mortality. The development of acidemia in the critically ill is often attributed to reductions in oxygen utilization, which in the past has generally been regarded as dysregulation of tissue blood supply. Resulting tissue hypoperfusion leads to anaerobic metabolism and lactic acidosis. Carbon dioxide production increases as anaerobically produced hydrogen ions are buffered by extracellular bicarbonate. The effectiveness of tissue perfusion is the target of much research, and in this review we outline factors that affect tissue acid-base status, techniques to measure tissue acid-base status, and explore the relationship between tissue acidosis and hypoxia in the critically ill. However, things are not always as simple as they may first appear.

Acid-Base Equilibrium↗
PubMed2002

Hypoglycaemia and lactic acidosis in a MALT non Hodgkin's lymphoma.

Hypoglycaemia associated with lactic acidosis is a rare complication of lymphomas; only four cases have been previously reported. Recent studies provide evidence of direct consumption of glucose by the tumour cells, leading to lactic acidosis. We report the case of a 64-year-old patient with a gastric diffuse large B cell non-Hodgkin's lymphoma transformed from an indolent mucosa associated lymphoid tissue (MALT) lymphoma, admitted to our department for acute renal failure due to a tumour lysis syndrome. After recovery from renal failure, she developed severe hypoglycaemia and lactic acidosis refractory to therapy. She died after the onset of shock and coma.

Acidosis, Lactic↗
PubMedDate not supplied

Effect of metabolic acidosis on white-tailed deer antler development.

Metabolic acidosis can result when herbivores consume browse diets high in plant secondary compounds. One mechanism for buffering excess acid is the mobilization of calcium and other alkaline salts from the skeletal system. White-tailed deer (Odocoileus virginianus) and other cervids consuming browse during antler formation may use minerals essential for antler development as buffers, resulting in altered antler characteristics. Our research objectives were to examine the effects of metabolic acidosis on mineral metabolism, acid-base homeostasis, and antler development in white-tailed deer. Fifteen male white-tailed deer were assigned to one of three diets: 2% NH(4)Cl, 3% commercial tannic acid, or a basal ration without additive. Two feeding trials were completed on each deer to determine nutrient use. Urine pH and the percentage of urinary nitrogen excreted as NH+4 varied by diet. No significant diet or trial effects occurred for nitrogen, calcium, phosphorus, magnesium, or sodium use. Urinary calcium excretion varied between diets. No dietary differences were observed for antler characteristics. The NH(4)Cl diet induced metabolic acidosis but did not alter antler development in white-tailed deer. Skeletal mineral reserves and mineral intake appeared sufficient to buffer excess acids and support antler development.

Acidosis↗
PubMed2001

Emerging role of riboflavin in the treatment of nucleoside analogue-induced type B lactic acidosis.

Type B lactic acidosis is a rare and often fatal complication seen in patients receiving the nucleotide analogues zidovudine, stavudine, didanosine, and lamivudine. We describe a case of a 51-year-old human immunodeficiency virus (HIV)-positive woman receiving three nucleotide analogues. She presented with nausea, vomiting, abdominal pain, and hepatic steatosis. Signs of mitochondrial toxicity were demonstrated by diffuse myopathy and pancreatitis. Serum riboflavin levels documented a deficiency that was treated with 50 mg of riboflavin daily. Immediately after treatment, serum blood urea nitrogen level, lactic acid levels, and arterial blood pH all returned to normal values. Her signs of mitochondrial toxicity also improved after treatment with riboflavin. Successful reversal of the patient's type B lactic acidosis after riboflavin therapy suggested that riboflavin deficiency plays a direct role in the development of nucleotide analogue-induced lactic acidosis. It is impossible to predict which patients are predisposed to the development of this syndrome. For this reason, it may be important to screen and treat riboflavin deficiency in patients on nucleoside analogues.

Acidosis, Lactic↗
PubMed1983

Evaluation of whole body nitrogen kinetics in acute metabolic acidosis.

The data obtained after a pulse dose of L-[15N] alanine and [13C] urea in control and acidotic conscious dogs were analyzed to compute the whole body nitrogen turnover rates. Acute acidosis was induced and maintained by continuous HCl infusion. On the basis of a four pool model, the mean daily protein synthesis rate in the normal dog was calculated to be 10.8 g/kg compared to 7.6 g/kg in acidosis. Since all dogs were in negative nitrogen balance, the daily catabolic rate of protein was greater than the synthetic rate and the mean daily catabolic rate was 14.4 g protein/kg in normal dogs compared to 10.5 g protein/kg in acidotic dogs. The body urea pool size and excretion rates were decreased by 24 and 27%, respectively, due to acute acidosis, without any change in the fractional turnover rate. Thus the adaptive response to the induced acid challenge appears to be a reduction in the synthesis and breakdown rates of protein and also a decrease in the production and excretion rate of urea.

Acidosis↗
PubMed2001

Multiple acyl-CoA dehydrogenase deficiency: a rare cause of acidosis with an increased anion gap.

Metabolic acidosis is encountered frequently in intensive care and common causes include lactic acidosis, ketoacidosis, or renal failure. We describe a patient presenting to intensive care with a rare cause of metabolic acidosis associated with an increased anion gap: multiple acyl-CoA dehydrogenase deficiency. The pathophysiology of this condition is discussed along with potential treatment options.

Acid-Base Equilibrium↗
PubMed1994

Age related differences in the response to acidosis, hypoxia, and hyperkalaemia in canine cardiac Purkinje fibers.

OBJECTIVE: In the clinical setting, the response of adult and neonatal cardiac rhythms to hypoxia and to acidosis differs, the former leading to tachyarrhythmias and the latter to bradyarrhythmias. In this study, the aim was to determine whether a cellular electrophysiological substrate could be identified to explain the clinical observation. METHODS: Conventional microelectrode techniques were used to study the electrophysiological responses of automatic Purkinje fibres to acidosis, hypoxia, and hyperkalaemia individually. RESULTS: Adult Purkinje fibres showed decreases in maximum diastolic potential, activation voltage, and automaticity as pH was decreased from 7.3 to 6.1. Triggered activity due to early afterdepolarisations developed in 70% of adult Purkinje fibres at pH 6.1. Neonatal Purkinje fibres showed decreased automaticity as pH decreased and, in contrast to adults, quiescence occurred at pH 6.1 At PO2 < 2.9 kPa automaticity decreased significantly in adult Purkinje fibres, whereas neonatal fibres were unaffected. The effect of raising [K+]o was comparable at both ages. CONCLUSIONS: The response to acidosis and to hypoxia differs significantly between neonatal and adult Purkinje fibres and may explain some developmental differences in the expression of cardiac arrhythmias.

Acidosis↗
PubMed1994

Acidosis and arrhythmias in cardiac muscle.

Acidosis is a well recognised consequence of myocardial ischaemia. In this brief article we have reviewed the consequences of acidosis that might be arrhythmogenic. These include early afterdepolarisations and triggered activity, delayed afterdepolarisations, pulsus alternans, and reentry. In each case we have described the evidence that acidosis can provoke such behaviour and then discussed the possible mechanisms and consequences of each behaviour. It seems likely that changes of pH may contribute to arrhythmogenesis during ischaemia by these mechanisms.

Acidosis↗
PubMed1983

Failure of dietary-casein-induced acidosis to explain the hypercholesterolemia of casein-fed rabbits.

The partial replacement of casein by a mixture of gelatin, fish protein and soy protein in cholesterol-free semipurified diets of rabbits reduced the hypercholesterolemic response. The partial replacement of casein by the protein mixture also increased the feed intake and alleviated or reversed the weight loss observed from the casein diet. The data indicate that casein alone is not an ideal protein source for rabbits probably because of the imbalance of the amino acid composition. When KCl in the semipurified diets was replaced by KHCO3, a higher feed intake and a better growth were obtained, irrespective of the protein source in the diet. In addition, the feeding of semipurified diets containing KCl resulted in acidosis, which could be prevented by its replacement with KHCO3. A semipurified diet containing casein and KCl produced a more severe acidosis and higher serum cholesterol levels than the diet containing the protein mixture. Nevertheless, the correction of the acidosis by the replacement of KCl in the diet by KHCO3 did not lead to an abrogation of the casein-induced hypercholesterolemia.

Acidosis↗
PubMed2001

Both L- and D-lactate contribute to metabolic acidosis in diarrheic calves.

Diarrhea in neonates is often complicated by metabolic acidosis. We used blood gas analysis and HPLC to determine whether bacterial fermentation might contribute to acidosis in diarrheic calves. Diarrheic calves (n = 21) had significantly lower pH, PCO(2), HCO(3)(-) and a higher anion gap than healthy calves (n = 21). Serum concentrations (mean +/- SD, mmol/L) of DL-, L- and D-lactate were also significantly higher in diarrheic (8.9 +/- 5.1, 4.1 +/- 3.4 and 5.2 +/- 5.7) than in healthy calves (1.7 +/- 1.2, 2.0 +/- 1.1 and too low to quantify). D- and L-lactate accounted for 64% anion gap increase in diarrheic calves. Fecal D- and L-lactate concentrations were also significantly higher in diarrheic calves (9.4 +/- 3.0 and 11.9 +/- 2.7 mmol/L) than healthy calves (1.1 +/- 0.1 and 1.6 +/- 0.1 mmol/L). The elevated concentrations of serum and fecal D-lactate suggest gut bacterial fermentation contributes to the development of acidosis in diarrhea.

Acid-Base Equilibrium↗
PubMed2000

Prevalence and characterization of renal tubular acidosis in patients with osteopenia and osteoporosis and in non-porotic controls.

BACKGROUND: Chronic metabolic acidosis may increase alkali mobilization from the bone and thus promote the development of osteoporosis. The objective of the current study was to compare urinary acidification in patients with reduced bone mineral content with that in control subjects with normal bone density. METHODS: Forty-six subjects (41 females, 5 males) with osteopenia or osteoporosis were studied. In none of the subjects were overt metabolic acidosis, derangement of potassium homeostasis, or renal insufficiency present. Distal tubular acidification was studied by means of oral ammonium chloride loading test (0.1 g/kg body weight) and the oral frusemide test (40 mg). In addition the frusemide test was performed in 20 healthy age- and sex-matched controls (17 females, 3 males). RESULTS: In all control subjects a urinary pH <5. 5 was observed following the ingestion of 40 mg frusemide. In contrast, in patients with reduced bone mineral density incomplete renal tubular acidosis type I (RTA I) was diagnosed in 10 of 46 subjects (22%) by oral ammonium chloride loading test. Disorders possibly related to RTA I were detected in eight of these 10 patients. Thirty-six patients had a normal urinary pH response following oral ammonium chloride loading. Oral frusemide, 40 mg, failed to lower urinary pH <5.5 in sixteen patients (35%), these included 10 subjects with incomplete RTA I, and six subjects with a normal oral ammonium chloride loading test. An abnormal frusemide test was found in 35% of patients with reduced bone mass and in none of the normal controls (chi(2)=7.39; P<0.01). With the ammonium chloride test as the gold standard for diagnosis of distal RTA, the frusemide test showed a sensitivity of 1.0 (95% CI, 0.69-1.0) and a specificity of 0.89 (95% CI, 0.78-0.96) for the diagnosis of distal RTA. Patients with incomplete RTA I were younger than those without incomplete RTA I (42+/-16 vs 54+/-14 years; P=0.025; mean+/-SD). Basal serum bicarbonate concentrations and capillary pH did not differ between the groups. CONCLUSION: Incomplete RTA I may be prevalent in a significant proportion of patients suffering from osteopenia or osteoporosis. The outcome of the frusemide test suggests either a defect of the H(+)ATPase in the cortical collecting tubule (CCT) or a defective Na(+) reabsorption in the CCT. Prospective studies are needed to further elucidate the impact of incomplete RTA I on the development of reduced bone mineral content.

Acidosis, Renal Tubular↗