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PubMed1976

Urinary excretion of beta2-microglobulin in renal stone patients under normal conditions and during acidosis and alkalosis.

The urinary excretion of beta2-microglobulin was studied under normal conditions and during acidosis and alkalosis in 65 patients with renal stones. Eleven patients were studied under two of these conditions. Four out of 51 patients examined under normal conditions had an increased excretion of beta2-microglobulin in their urine. Four out of five patients with distal acidification defects were found to have an increased excretion of beta2-microglobulin during induced acidosis. During alkalosis, four out of eight patients with acidification defects increased their excretion of the protein. The tubular proteinuria that could be provoked during acute acidosis and alkalosis was considered to be secondary to changes in the acid-base status and may indicate a renal tubular defect.

Acidosis↗
PubMed1996

[Acidosis in severe acute asthma].

On admission to intensive care units, the acid-base profile in acute severe asthma appears to be more diverse than previously. Especially a mixed or less frequently metabolic acidosis is eventually observed, which is not always caused by elevated lactate. On the other hand, hyperlactatemia is actually rather common, not necessarily accompanied by acidosis. This finding is as a rule related to massive doses of beta 2 adrenergic agents given parenterally: subsequent elevated lactate is in no way a marker of cellular hypoxia and has no pejorative meaning in this event. Hypercapnia with severe respiratory acidosis implies less and less mechanical ventilation; however, when mandatory, it has to be carried out using permissive hypercapnia, giving more favorable outcome while lowering side-effects.

Acidosis↗
PubMed2002

Evaluation of prescribing practices: risk of lactic acidosis with metformin therapy.

BACKGROUND: The risk of lactic acidosis during metformin therapy is linked to specific and well-documented conditions that constitute contraindications or precautions to use of the agent. We conducted a retrospective evaluation of metformin use to determine whether prescribing practices are in accord with published contraindications and precautions. METHODS: All patients admitted to the hospital during a 6-month period who received at least 1 dose of metformin were identified through hospital pharmacy records. Patient demographics and clinical characteristics were then evaluated to determine whether metformin was prescribed to patients possessing any of the risk factors associated with development of lactic acidosis. RESULTS: We identified 263 hospitalizations involving 204 patients who received at least 1 dose of metformin during inpatient admission. Patients had at least 1 absolute contraindication to metformin therapy in 71 admissions (27%). In 29 (41%) of these 71 admissions, treatment with metformin continued despite the contraindication. The most common contraindication, elevated serum creatinine concentration, was present or developed during 32 admissions (12%); however, metformin use was appropriately discontinued in only 8 (25%) of these 32 patients. Of the precautions against metformin use, concomitant administration of cationic agents was the most common, occurring in 97 admissions (37%). CONCLUSIONS: Many patients are treated with metformin despite having clinical conditions that place them at risk for developing lactic acidosis. To minimize this risk, it is essential that prescribers develop a better understanding of the prescribing guidelines for metformin.

Acidosis, Lactic↗
PubMed1992

Fluorescein and acidosis. Implications for flap perfusion studies.

The visual fluorescein technique underpredicts survival of a skin flap during the first 24 hours after raising the flap. This problem limits its use as a research and clinical tool. There is no compelling explanation for this observation, but two facts are known: fluorescein is a derivative of phthalein, a pH indicator, and ischemic tissues become acidotic, with the pH falling below 7.0. These observations lead to the hypothesis that acidosis quenches fluorescence in distal skin flaps. No data could be found regarding this effect. Therefore, the effect of acidosis on sodium fluorescein was studied in vitro. A spectrophotometer was used to measure the intensity of the fluorescence of sodium fluorescein in buffered solutions of different hydrogen ion concentrations. Two studies were performed at different concentrations of fluorescein. At a concentration of 10(-5) g/mL, there is a drop of 26% in fluorescence intensity from pH 7.5 to 7.0, and 51% between pH 7.5 and 6.5. At 10(-7) g/mL, there is a 43% decrease in fluorescence between pH 7.5 and 6.5. This study supports our hypothesis that acidosis quenches the fluorescence of fluorescein. This effect must be considered when interpretating basic studies of skin flap microcirculation.

Acidosis↗
PubMedDate not supplied

Controversies in lactic acidosis. Implications in critically ill patients.

Lactic acidosis is common in critically ill patients and is usually caused by tissue perfusion that is inadequate to meet metabolic demand. However, it has also been noted in conditions in which tissue perfusion is apparently adequate. Hyperlactatemia can occur in the absence of acidosis, usually in the setting of hypermetabolic disease. Numerous areas of controversy exist regarding the pathogenesis of lactic acidosis, as well as certain of its diagnostic, therapeutic, and prognostic features. Knowledge of these areas of controversy should facilitate the clinician's approach to diagnosis and management.

Acidosis, Lactic↗
PubMed1998

Extracellular acidosis and high levels of carbon dioxide suppress synaptic transmission and prevent the induction of long-term potentiation in the CA1 region of rat hippocampal slices.

Long-term potentiation (LTP) is a long-lasting increase in synaptic strength induced by high frequency stimulation. LTP may participate in learning and memory formation. In many synaptic systems, LTP is dependent on intact function of N-methyl-D-aspartate (NMDA) receptors. NMDA receptors may be inhibited in different conditions involving also extracellular acidosis. A decrease in the extracellular pH accompanies many pathological states such as ischemia, hypoxia, and the CNS injury. The study was designed to determine whether comparable extracellular acid-base imbalances are able to interfere with the LTP induction. Hippocampal slices from adult rats were stimulated with high frequency stimulation (1 x 100 Hz/1 s) at Schaffer collateral-commissural synaptic system in the environment with different pH (6.7-7.8) and the field responses were recorded in CA1. Acidosis was achieved by supplying excessive CO2 or by HCO3-decrease in standard bicarbonate-containing buffer or by a direct acidification of the buffer containing Na-HEPES. Invariably, all forms of acidification suppressed the efficacy of normal, low frequency synaptic transmission and prevented the induction of LTP in a reversible manner; i.e., after reperfusion of the slices at pH 7.3 and restimulation, there was a return of synaptic transmission back to baseline, and a significant amount of LTP occurred. In contrast, alkalization to pH 7.8, although enhancing synaptic transmission efficacy, did not further increase the LTP magnitude compared to control environment with pH 7.3. The results suggest that extracellular acidosis associated with several pathological conditions in the CNS may significantly diminish the LTP induction, and thus negatively affect all physiological processes that utilize LTP.

Acidosis↗
PubMed1981

Chronic lactic acidosis in a patient with cancer: therapy and metabolic consequences.

Lactic acidosis is a life-threatening disorder in some cases. Treatment should be directed at the primary cause. Sodium bicarbonate should be added if the acidosis is very severe, or if the rate of hydrogen ion production is very rapid and not controlled. In contrast, with moderate degrees of steady state lactic acidosis and poor dietary intake, the risks of therapy with sodium bicarbonate or dichloroacetate may actually outweigh the benefits in a cachectic patient unless a dietary glucose and/or protein load is given.

Acidosis↗
PubMed1995

Myopathy, lactic acidosis, and sideroblastic anemia: a new syndrome.

We describe 2 sibs (brother and sister) with myopathy, sideroblastic anemia, lactic acidosis, mental retardation, microcephaly, high palate, high philtrum, distichiasis, and micrognathia. Very low levels of cytochromes a, b, and c were detected in the patients' muscle mitochondria. Deposition of iron within the mitochondria of bone marrow erythroblasts was observed on electron microscopy. Irregular and enlarged mitochondria with paracrystalline inclusions were also seen on electron microscopy of the patients' muscle specimen. Examination of DNA from the affected sibs showed no deletions in the mitochondrial DNA nor the mutations identified in the syndromes of mitochondrial myopathy, encephalopathy, lactic acidosis, and strokelike episodes (MELAS) or myoclonus, and epilepsy associated with rugged-red fibers (MERRF). Since the parents were first cousins and 2 of 6 sibs (male and female) were affected, we suggest that the syndrome expressed by our patients represents a previously unknown autosomal recessive disorder that includes mitochondrial myopathy, lactic acidosis, and sideroblastic anemia.

5-Aminolevulinate Synthetase↗
PubMed1983

Mitochondrial cytochrome deficiency presenting as a myopathy with hypotonia, external ophthalmoplegia, and lactic acidosis in an infant and as fatal hepatopathy in a second cousin.

Fatal infantile mitochondrial myopathy with lactic acidosis, morphologically abnormal mitochondria, deficient cytochromes aa3 and b, and a Fanconi-like aminoaciduria has been described. We report two infants, second cousins, with a similar fatal mitochondrial disorder, the cytochrome deficiency limited to skeletal muscle in one child and to liver in the other. The first child at 3 months of age had weight loss, hypotonia, external ophthalmoplegia, and a severe lactic acidosis with a high lactate/pyruvate ratio. Electron microscopy of muscle showed marked proliferation of enlarged mitochondria, many containing concentric rings of cristae. In skeletal muscle mitochondria, cytochromes aa3 and b were not detectable but cytochrome cc was found to be normal by spectroscopy. Cytochrome c oxidase activity was less than 1% of normal. Mitochondria from kidney, liver, heart, lung, and brain examined postmortem had normal cytochromes and preserved cytochrome c oxidase activity. The second cousin at 5 months of age had weight loss and hepatomegaly but no systemic lactic acidosis. Liver biopsy showed hepatocytes packed with enlarged mitochondria. The liver mitochondria showed deficient cytochromes aa3 and b postmortem, and cytochrome c oxidase activity was less than 10% of normal. Kidney mitochondria had normal cytochromes. Muscles was not studied. The mitochondrial abnormality in the two cousins presumably is related. Unexplained are the mode of genetic transmission or environmental exposure and the apparent involvement of a single different organ in each child.

Acidosis↗
PubMed1984

The induction and reversibility of cerebral acidosis in thiamine deficiency.

Regional cerebral pH was determined autoradiographically using carbon 14-labeled dimethyloxazolidinedione in normal rats, following various durations of thiamine deficiency and replenishment with thiamine when the clinical sequelae of the deficiency appeared. In our model the clinical sequelae of thiamine deficiency (opisthotonus) appeared on the average on day 18. Regional cerebral pH on day 12 was comparable to that in controls and ranged between 7.02 +/- 0.03 and 7.09 +/- 0.03 (mean +/- SEM) in gray matter structures. On day 14 the pH in the inferior colliculus was 6.85 +/- 0.08 and relative acidosis also appeared in thalamic structures. At opisthotonus the pH was 6.48 +/- 0.17 in the mamillary body, 6.43 +/- 0.14 in the vestibular nucleus, and 6.36 +/- 0.14 in the medial dorsal nucleus of the thalamus (p less than 0.01). One dose of thiamine replenishment at this stage transiently raised the pH in the inferior colliculus to 7.25 +/- 0.19 and in the medial dorsal nucleus to 7.20 +/- 0.13 (p less than 0.01). Cerebral regions showing significant acidosis during thiamine deficiency coincided largely with those known to be histologically vulnerable and those previously reported to show a focal rise in local cerebral glucose utilization between days 11 and 14 of thiamine deficiency. This focal acidosis shown to occur in thiamine deficiency may be one mechanism contributing to the selective histological vulnerability in this model.

Acidosis↗
PubMed1975

Metastatic reticulum cell sarcoma and lactic acidosis.

The clinical course of a woman with metastatic reticulum cell sarcoma and intractable lactic acidosis is described. Although her illness was dominated by a myelopathy, she developed severe lactic acidosis which could not be related to decreased tissue oxygen delivery. Necropsy showed extensive hepatic replacement with tumor and widespread disease. This and other possible pathogenetic factors causing lactic acidosis are discussed.

Acidosis↗
PubMed1999

Prolonged lactic acidosis after extended hepatectomy under in situ hypothermic perfusion.

A 46-year-old woman underwent right extended hepatectomy under total vascular occlusion with in situ hypothermic perfusion for colorectal metastasis. Immediately after surgery, she developed severe lactic acidosis, which required correction with sodium bicarbonate solution and ventilatory support for 36 hours. After 2 days, her lactate normalized, and the acidosis was corrected. She made an uneventful recovery. Persistent lactic acidosis after major hepatic resection under in situ hypothermic perfusion is a rare but reversible problem.

Acidosis, Lactic↗
PubMed1990

Hemodynamic and hepatic pH responses to sodium bicarbonate and Carbicarb during systemic acidosis.

Rats subjected to ammonium chloride-induced metabolic acidosis were given alkalinization therapy with either sodium bicarbonate or Carbicarb. Ammonium chloride-induced severe metabolic acidosis had minimal effect on mean arterial blood pressure and cardiac output. This acidosis resulted in a small but statistically significant fall in intracellular liver pH (pHi) as measured with 31P magnetic resonance spectroscopy (7.01 +/- 0.05 vs 7.08 +/- 0.04, p less than 0.05). Sodium bicarbonate treatment resulted in systemic alkalinization and increases in arterial pCO2 as well as transient but extreme decreases in cardiac output and mean arterial pressure. Alkalinization with sodium bicarbonate also resulted in a transient but significant decrease in intracellular liver pH (7.02 +/- 0.06 at 5 min vs 7.09 +/- 0.06 at baseline, p less than 0.05). Carbicarb therapy resulted in systemic alkalinization without major changes in arterial pCO2, cardiac output, or mean arterial blood pressure. Moreover, Carbicarb effected a sustained intracellular alkalinization of the liver (phi = 7.12 +/- 0.07 at 5 min, p less than 0.05, pHi = 7.19 +/- 0.07 at 10 min, p less than 0.01, pHi = 7.16 +/- 0.06 at 15 min, p less than 0.01, vs baseline pHi = 7.05 +/- 0.06). These data suggest that Carbicarb may be a more effective buffer than sodium bicarbonate during conditions where ventilation is limited and hemodynamic instability is present.

Acidosis↗
PubMed1995

Increase of GPC levels in cultured mammalian cells during acidosis. A 31P MR spectroscopy study using a continuous bioreactor system.

The purpose of this study was to study the metabolic events during a slow acidosis in three different cell lines by combining 31P magnetic resonance spectroscopy and hollow fiber bioreactor technology. The rate of change in intracellular pH, glycerophosphorylcholine (GPC), phophorylcholine (PCho), and nucleoside-triphosphate (NTP) levels were measured during 8 h of acidosis and 16 h of recovery in EPO, EAT, and RN1a cells, three cultured mammalians cell lines. Our results show a significant increase in GPC levels to 330 +/- 21.540 +/- 25, and 220 +/- 21% of their initial value correlated to a decrease of PCho levels to 57 +/- 14.58 +/- 17 and 45 +/- 15% of their initial value in EAT, RN1a, and EPO cells, respectively. These changes are discussed in terms of perturbation of energetic metabolism in cells undergoing a slow acidosis.

3T3 Cells↗
PubMed1998

Difference in the mechanisms for compensating ischemic acidosis in diabetic rat hearts.

To elucidate the difference in the mechanisms for alkalization during ischemic acidosis between diabetic and non-diabetic hearts, intracellular pH (pHi) was measured by phosphorus-31 magnetic resonance spectroscopy. Diabetes was induced by the injection of streptozotocin. The accumulation of proton ion (DeltaH+) during 15 min global ischemia at 37 degreesC was calculated from pH i. There were no significant differences in DeltaH+ between diabetic (DM: 0. 54+/-0.03 micromol/l,n=6; mean+/-s.e.m.) and non-DM hearts (0.57+/-0.04, n=6), when perfused with bicarbonate buffer. However, perfusion with HEPES buffer revealed a significant increase of DeltaH+ in DM (0.85+/-0.07, n=5) compared with non-DM (0.61+/-0.06, n=5P<0.05). On the contrary, the addition of a Na+/H+ exchange inhibitor (EIPA; 1 micromol/l) to bicarbonate buffer significantly increased DeltaH+ in non-DM (1.09+/-0.10, n=4) compared with DM (0.71+/-0.03, n=5P<0.01). Perfusion with HEPES buffer and EIPA equally increased DeltaH+ in both groups (DM 1.13+/-0.13, n=4; non-DM 1.15+/-0.14, n=4). Thus, the activity of Na+/H+ exchanger during ischemic acidosis, assessed as the increase of DeltaH+ induced by addition of EIPA to bicarbonate buffer, was higher in non-DM (0.52) than DM (0.17). In contrast, the contribution of bicarbonate-dependent systems evaluated by the deference of DeltaH+ between the bicarbonate buffer and the HEPES buffer was markedly bigger in DM (0.31) than non-DM (0.04). These results indicate that Na+/H+ exchange is a major mechanism to compensate ischemic acidosis in non-DM hearts, whereas bicarbonate-dependent systems compensate the depressed activity of Na+/H+ exchange in DM.

Acidosis↗
PubMed1997

Effect of mild and moderate hypothermia on the acidosis-induced swelling of glial cells.

The effect of mild (32 degrees C) and moderate (27 degrees C) hypothermia was analyzed on the cell volume and intracellular pH (pHi) of C6 glioma cells at normal pH and during lactacidosis at pH 6.2 in vitro. The cells were suspended in an incubation chamber under continuous control of pH, PO2 and temperature. Cell swelling was quantified by an advanced Coulter-system. pHi was measured by flow cytometry using the fluorescent dye bis-carboxyethyl carboxyfluorescein (BCECF). Following a control period at 37 degrees C, the ambient temperature was decreased to 32 degrees C for 30 min, and subsequently to 27 degrees C for another 30 min. Hypothermia alone led to an immediate and significant cell volume increase of 107.3 +/- 0.4% (mean +/- SEM) of control after 30 min at 32 degrees C, and further swelling to 110.5 +/- 0.9% after 30 min at 27 degrees C. Yet, hypothermia (27 degrees C) afforded partial protection against the acidosis-induced cell swelling at pH 6.2, which was reaching to 120.4 +/- 0.9% in the normothermic control group after 60 min, while only to 111.3 +/- 0.9% at 27 degrees C. Hypothermia, however, was associated with a more pronounced decrease of the pHi during acidosis (6.3 +/- 0.04) as compared to that of the normothermic control falling then to 6.5 +/- 0.03. The results demonstrate that mild and moderate hypothermia induce glial cell swelling, but simultaneously inhibit cell swelling from acidosis. The protection against cell swelling, however, has its price as indicated by the enhancement of the intracellular acidification.

Acidosis, Lactic↗
PubMed1989

A possible involvement of oxygen free radicals in the development of myocardial acidosis during coronary occlusion in dogs.

The present study was designed to examine whether free radical scavengers attenuate myocardial acidosis induced by partial occlusion of the coronary artery in dogs. The myocardial pH was determined by a micro glass pH electrode inserted in the endocardial layers of the left ventricular wall perfused by the left anterior descending coronary artery. The left anterior descending coronary artery was occluded for 90 min incompletely so that the flow would be 1/2-1/3 the original flow. The myocardial pH before partial occlusion was 7.54-7.55. Partial occlusion decreased the flow in the left anterior descending coronary artery by 49.3-64.9% and the myocardial pH by 0.71-0.76, and increased the ST segment (surface electrocardiogram) by 6.3-9.3 mV. Saline (0.5 ml/kg), recombinant human superoxide dismutase (70,000 or 210,000 U/kg), or catalase (55,000 or 165,000 U/kg) was injected intravenously 30 min after partial occlusion. The injection of recombinant human superoxide dismutase or catalase alone did not restore the myocardial pH that had been decreased by coronary occlusion. The combined injection of recombinant human superoxide dismutase (70,000 U/kg) + catalase (55,000 U/kg), however, restored the myocardial pH without restoration of ST segment. In conclusion, recombinant human superoxide dismutase + catalase attenuated myocardial acidosis during ischaemia, suggesting a possible involvement of oxygen free radicals in the development of myocardial acidosis (especially in the endocardial layers) during ischaemia.

Acidosis↗