The Prevalence of Metabolic Acidosis in Patients with Different Stages of Chronic Kidney Disease: Single-Centre Study.

BACKGROUND: Metabolic acidosis (MA) is one of the most common consequences of CKD. MA is also a risk factor of CKD progression and increased mortality in these patients. AIM: The aim of this retrospective, cross-sectional study was to assess the prevalence of MA in different stages of CKD and renal replacement therapy (RRT) modalities - haemodialysis (HD) and peritoneal dialysis (PD). Additionally, the relationship between the prevalence of MA and aetiology of kidney disease was analysed. METHODS: One thousand five patients in different stages of CKD, or modalities of RRT were enrolled into this single-centre cross-sectional study. Forty-one patients were ruled out because of oral bicarbonate supplementation. In the remaining 964 patients (698 CKD stages 1-5, 226 HD, 40 PD), venous blood HCO3- concentration, as well as serum Cr and urea concentrations were assessed. MA was diagnosed when blood HCO3- concentration was below 22 mmol/L. RESULTS: The prevalence of MA increased among all stages of CKD. Patients on HD had lower prevalence of MA in comparison with CKD 5 patients with no RRT (38.5 vs. 56.0%; p = 0.02) In PD patients, the prevalence of MA was significantly lower than in HD patients (2.5 vs. 38.5%; p < 0.001). In the whole study group, there were no significant differences in the prevalence of MA between different aetiologies of CKD (glomerulonephritis 24%, hypertension 23%, diabetes 25%, and tubule-interstitial diseases 24%). Also, when only patients in stages CKD 3-5 were compared, no significant differences in the prevalence of acidosis were found (glomerulonephritis 28%, hypertension 22%, diabetes 24%, and tubule-interstitial 21%). CONCLUSIONS: (1) MA is more frequent in patients with more advanced stages of CKD. (2) RRT reduces the prevalence of MA. (3) In PD patients, MA is rare. (4) Aetiology of CKD seems not to have a significant impact on MA prevalence.

A comparison of multifunctional donors of carbon monoxide: Their anticoagulant, antioxidant, anti-aggregatory and cytotoxicity activities in an in vitro model.

The study examines the effect of two water-soluble carbon monoxide (CO) donors, CORM-3 and CORM-A1, on selected parameters of oxidative stress and hemostasis in human plasma and blood platelets in vitro. It also compares their activity with that of the lipid-soluble CORM-2. The oxidation of amino acid residues in plasma proteins was evaluated by measuring the amounts of thiol and carbonyl groups. Plasma lipid peroxidation was measured as thiobarbituric acid reactive substance (TBARS) concentration. In addition, three haemostatic parameters of plasma were studied, viz. activated partial thromboplastin time (APTT), prothrombin time (PT) and thrombin time (TT), and one haemostatic parameter of platelets (platelet aggregation). Treatment with CORM-3 and CORM-A1 (all concentrations from 0.1 to 100 µM) decreased thiol group oxidation induced by H2O2/Fe. Incubation with CORM-3 and CORM-A1 also influenced plasma coagulation activity, e.g. CORM-3 and CORM-A1 significantly prolonged TT at the two highest tested concentrations (50 and 100 µM). Only CORM-2 at the highest tested concentration (100 µM) and CORM-3 (50 and 100 µM) reduced platelet aggregation induced by ADP. None of the tested CORMs caused platelet damage. The treatment of various diseases associated with oxidative stress, including cardiovascular diseases, may be enhanced by the administration of CO donors CORM-2 and CORM-3, these being modulators of oxidative stress and hemostasis.

Assessing the iron delivery efficacy of transferrin in clinical samples by native electrospray ionization mass spectrometry.

Serum transferrin is a key player in iron homeostasis, and its ability to deliver iron to cells via the endosomal pathway critically depends on the presence of carbonate that binds this protein synergistically with ferric ion. Oxalate is another ubiquitous anionic species that can act as a synergistic anion, and in fact its interaction with transferrin is notably stronger compared to carbonate, preventing the protein from releasing the metal in the endosomal environment. While this raises concerns that high oxalate levels in plasma may interfere with iron delivery to tissues, concentration of free oxalate in blood appears to be a poor predictor of impeded availability of iron, as previous studies showed that it cannot displace carbonate from ferro-transferrin on a physiologically relevant time scale under the conditions mimicing plasma. In this work we present a new method that allows different forms of ferro-transferrin (carbonate- vs. oxalate-bound) to be distinguished from each other by removing this protein from plasma without altering the composition of the protein/metal/synergistic anion complexes, and determining their accurate masses using native electrospray ionization mass spectrometry (ESI MS). The new method has been validated using a mixture of recombinant proteins, followed by its application to the analysis of clinical samples of human plasma, demonstrating that native ESI MS can be used in clinical analysis.

Copper-induced alterations in rat brain depends on route of overload and basal copper levels.

OBJECTIVES: Copper (Cu) is widely used in industry for the manufacture of a vast range of goods including Cu-intrauterine devices (IUDs), electronic products, agrochemicals, and many others. It is also one of the trace elements essential to human health in the right measure and is used as a parenteral supplement in patients unable to ingest food. Elevated Cu levels have been found in the plasma of women using Cu-IUDs and in farmers working with Cu-based pesticides. However, possible alterations due to Cu overload in the brain have been poorly studied. Therefore, the aim of this study was to investigate the effects of Cu administration on rat brain in Cu-sufficient and Cu-deficient animals fed on semi-synthetic diets with different doses of Cu (7 or 35 ppm). METHODS: We aimed to investigate the effects of Cu administration using two routes of administration: oral and intraperitoneal (IP). Male Wistar rats were feeding (one month) a complete (7 ppm) or a deficient (traces) Cu diets subdivided into three categories oral-, intraperitoneal- (or both) supplemented with copper carbonate (7 to 35 ppm). Cu content in plasma, brain zones (cortex and hippocampus), antioxidant enzyme activities, and protease systems involved in programmed cell death were determined. RESULTS: The results show that Cu levels and the concentration of Cu in plasma and brain were dose-dependent and administration route-dependent and demonstrated a prooxidative effect in plasma and brain homogenates. Oxidative stress biomarkers and antioxidative enzyme activity both increased under Cu overload, these effects being more noticeable when Cu was administered IP. Concomitantly, brain lipids from cortex and hippocampus were strongly modified, reflecting Cu-induced prooxidative damage. A significant increase in the activities of calpain (milli- and micro-) and caspase-3 activity also was observed as a function of dose and administration route. CONCLUSION: The findings of this study could be important in evaluating the role of Cu in brain metabolism and neuronal survival.

Splanchnic net balance of oxygen and metabolites in response to a discontinuous mesenteric vein infusion of ammonium in sheep.

To simulate daily episodes of high absorption associated with the intake of diets with high N content, four wethers (42 ± 3.4 kg body weight), fitted with permanent catheters in the femoral artery and splanchnic vessels, were infused with 340 µmol into the mesenteric vein for 3 h, during the morning meal, over seven consecutive days. On the 7th day, mass transfers of , urea, glucose, lactate, ß-OH-butyrate and O2 were measured across portal-drained viscera (PDV), liver and splanchnic tissues during the last 90 min of the infusion. Measurements were repeated on the following day, at the same time, without the infusion. Plasma concentration in the portal vein (+332 µm; p = 0.006), portal absorption (+424 µmol/min; p < 0.001), liver uptake (+375 µmol/min; p = 0.003) and urea N production (+338 µmol/min; p = 0.059) were higher during infusion. Mass transfers of urea, glucose, lactate, ß-OH-butyrate and O2 across the PDV, and glucose, lactate, ß-OH-butyrate and O2 across the liver, were not altered by the infusion. Results suggest that a daily, discontinuous increase in portal flow during a meal stimulates liver removal and urea N production but does not significantly affect liver glucose production and O2 consumption in sheep.

Involvement of placental/umbilical cord blood acid-base status and gas values on the radiosensitivity of human fetal/neonatal hematopoietic stem/progenitor cells.

Arterial cord blood (CB) acid-base status and gas values, such as pH, PCO2, PO2, HCO3(-)and base excess, provide useful information on the fetal and neonatal condition. However, it remains unknown whether these values affect the radiosensitivity of fetal/neonatal hematopoiesis. The present study evaluated the relationship between arterial CB acid-base status, gas values, and the radiosensitivity of CB hematopoietic stem/progenitor cells (HSPCs). A total of 25 CB units were collected. The arterial CB acid-base status and gas values were measured within 30 min of delivery. The CD34(+)HSPCs obtained from CB were exposed to 2 Gy X-irradiation, and then assayed for colony-forming unit-granulocyte-macrophage, burst-forming unit-erythroid (BFU-E), and colony-forming unit-granulocyte erythroid, macrophage and megakaryocyte cells. Acid-base status and gas values for PCO2and HCO3(-)showed a statistically significant negative correlation with the surviving fraction of BFU-E. In addition, a significant positive correlation was observed between gestational age and PCO2. Moreover, the surviving fraction of BFU-E showed a significant negative correlation with gestational age. Thus, HSPCs obtained from CB with high PCO2/HCO3(-)levels were sensitive to X-irradiation, which suggests that the status of arterial PCO2/HCO3(-)influences the radiosensitivity of fetal/neonatal hematopoiesis, especially erythropoiesis.

Successful application of lead isotopes in source apportionment, legal proceedings, remediation and monitoring.

In late 2006, the seaside community in Esperance Western Australia was alerted to thousands of native bird species dying. The source of the lead (Pb) was determined by Pb isotopes to derive from the handling of Pb carbonate concentrate through the Port, which began in July 2005. Concern was expressed for the impact of this on the community. Our objectives were to employ Pb isotope ratios to evaluate the source of Pb in environmental samples for use in legal proceedings, and for use in remediation and monitoring. Isotope measurements were undertaken of bird livers, plants, drinking water, soil, harbour sediments, air, bulk ceiling dust, gutter sludge, surface swabs and blood. The unique lead isotopic signature of the contaminating Pb carbonate enabled diagnostic apportionment of lead in samples. Apart from some soil and water samples, the proportion of contaminating Pb was >95% in the environmental samples. Lead isotopes were critical in resolving legal proceedings, are being used in the remediation of premises, were used in monitoring of workers involved in the decontamination of the storage facility, and monitoring transport of the concentrate through another port facility. Air samples show the continued presence of contaminant Pb, more than one year after shipping of concentrate ceased, probably arising from dust resuspension. Brief details of the comprehensive testing and cleanup of the Esperance community are provided along with the role of the Community. Lead isotopic analyses can provide significant benefits to regulatory agencies, interested parties, and the community where the signature is able to be characterised with a high degree of certainty.

Imbalance of arginine and asymmetric dimethylarginine is associated with markers of circulatory failure, organ failure and mortality in shock patients.

In shock, organ perfusion is of vital importance because organ oxygenation is at risk. NO, the main endothelial-derived vasodilator, is crucial for organ perfusion and coronary patency. The availability of NO might depend on the balance between a substrate (arginine) and an inhibitor (asymmetric dimethylarginine; ADMA) of NO synthase. Therefore, we investigated the relationship of arginine, ADMA and their ratio with circulatory markers, disease severity, organ failure and mortality in shock patients. In forty-four patients with shock (cardiogenic n 17, septic n 27), we prospectively measured plasma arginine and ADMA at intensive care unit admission, Acute Physiology and Chronic Health Evaluation (APACHE) II-(predicted mortality) and Sequential Organ Failure Assessment (SOFA) score, and circulatory markers to investigate their relationship. Arginine concentration was decreased (34·6 (SD 17·9) µmol/l) while ADMA concentration was within the normal range (0·46 (SD 0·18) µmol/l), resulting in a decrease in the arginine:ADMA ratio. The ratio correlated with several circulatory markers (cardiac index, disseminated intravascular coagulation, bicarbonate, lactate and pH), APACHE II and SOFA score, creatine kinase and glucose. The arginine:ADMA ratio showed an association (OR 0·976, 95 % CI 0·963, 0·997, P = 0·025) and a diagnostic accuracy (area under the curve 0·721, 95 % CI 0·560, 0·882, P = 0·016) for hospital mortality, whereas the arginine or ADMA concentration alone or APACHE II-predicted mortality failed to do so. In conclusion, in shock patients, the imbalance of arginine and ADMA is related to circulatory failure, organ failure and disease severity, and predicts mortality. We propose a pathophysiological mechanism in shock: the imbalance of arginine and ADMA contributes to endothelial and cardiac dysfunction resulting in poor organ perfusion and organ failure, thereby increasing the risk of death.

Sample evaporation from pierceable cups: still an important source of analytical error.

BACKGROUND: We illustrate the impact of sample evaporation on analytical results in laboratory practice and highlight preventive measures. METHODS: Plasma (n=10) was analysed for glucose, Na(+), HCO(3)(-) and calcium on six different sample configurations at 5 time points within 2h. RESULTS: With time glucose, Na(+) and calcium values increased and HCO(3)(-) values decreased in a clinically significant way. CONCLUSIONS: Analytical error due to evaporation may be significant, but can be reduced with optimal sample handling. A pierceable cover does not prevent loss of HCO(3)(-).

Quantification of carbonate by gas chromatography-mass spectrometry.

Carbon dioxide and carbonates are widely distributed in nature, are constituents of inorganic and organic matter, and are essential in vegetable and animal organisms. CO(2) is the principal greenhouse gas in the atmosphere. In human blood, CO(2)/HCO(3)(-) is an important buffering system. Quantification of bicarbonate and carbonate in inorganic and organic matter and in biological fluids such as blood or blood plasma by means of the GC-MS technology has been impossible so far, presumably because of the lack of suitable derivatization reactions to produce volatile and thermally stable derivatives. Here, a novel derivatization reaction is described for carbonate that allows for its quantification in aqueous alkaline solutions and alkalinized plasma and urine. Carbonate in acetonic solutions of these matrices (1:4 v/v) and added (13)C-labeled carbonate for use as the internal standard were heated in the presence of the derivatization agent pentafluorobenzyl (PFB) bromide for 60 min and 50 °C. Investigations with (12)CO(3)(2-), (13)CO(3)(2-), (CH(3))(2)CO, and (CD(3))(2)CO in alkaline solutions and GC-MS and GC-MS/MS analyses under negative-ion chemical ionization (NICI) or electron ionization (EI) conditions of toluene extracts of the reactants revealed formation of two minor [i.e., PFB-OCOOH and O=CO(2)-(PFB)(2)] and two major [i.e., CH(3)COCH(2)-C(OH)(OPFB)(2) and CH(3)COCH=C(OPFB)(2)] carbonate derivatives. The latter have different retention times (7.9 and 7.5 min, respectively) but virtually identical EI and NICI mass spectra. It is assumed that CH(3)COCH(2)-C(OH)(OPFB)(2) is formed from the reaction of the carbonate dianion with two molecules of PFB bromide to form the diPFB ester of carbonic acid, which further reacts with one molecule of acetone. Subsequent loss of water finally generates the major derivative CH(3)COCH=C(OPFB)(2). This derivatization reaction was utilized to quantify total CO(2)/HCO(3)(-)/CO(3)(2-) (tCO(2)) in human plasma and urine by GC-MS in the NICI mode by selected ion monitoring of the anions [M-H](-) of CH(3)COCH=C(OPFB)(2) at m/z 461 for the endogenous species and m/z 462 for the internal standard (13)CO(3)(2-). Oral intake of the carboanhydrase inhibitor drug acetazolamide by two healthy volunteers resulted in temporary increased excretion of tCO(2) in the urine. The method is specific for carbonate, accurate, sensitive and should be applicable to various matrices including human fluids and environmental samples.

Regulation of protein kinases and coregulatory interplay of S-100beta and serotonin transporter on serotonin levels in diabetic rat brain.

Protein kinases are critical component in the regulation of signal transduction pathways, including neurotransmitters. Our previous studies have shown that serotonin (5-HT) altered under diabetic condition was accompanied by alterations of protein kinase C-alpha (PKC-alpha) and CaMKII, and those alterations were reversed after insulin administration. The current study showed that alloxan-induced diabetic animals revealed hyperglycemia and was associated with an increase in the content of 5-HT, PKC-alpha expression and PKC activity (P < 0.05) simultaneously in striatum (ST), midbrain (MB), pons medulla (PM), cerebellum (CB), and cerebral cortex (CCX) from 7 days to 60 days. Although the 5-HT levels in hippocampus (HC) and hypothalamus (HT) were not altered, the PKC-alpha expression and PKC activity showed increases (P < 0.05) in level in HC. Insulin administration reversed all these changes to a normal level. In contrast, the in vitro study has shown that the 5-HT levels correlated with PKC-alpha expressions as well as PKC activity (P < 0.05) only in ST, MB, and CB either after induction with phorbol 12-myristate 13-acetate (PMA) or blocking with chelerythrine, whereas PM and CCX remained elevated (P < 0.05), implying a regulatory role for PKC-alpha only in ST, MB, and CB. However, our consecutive studies have shown that the 5-HT level in PM was regulated by p38-mitogen-activated protein kinase (p38-MAPK) both in vivo and in vitro, whereas the 5-HT level in CCX was coregulated by S-100beta by protein-protein interaction with serotonin transporter (SERT) via 8-bromoadenosine 3',5'-cyclic monophosphate sodium salt (8-Br-cAMP)-induced cAMP/PKAII pathway(s).

Respiratory acidosis: a quick reference.

This article serves as a quick reference for respiratory acidosis. Guidelines for analysis and causes, signs, and a stepwise approach are presented.

Metabolic alkalosis: a quick reference.

This article serves as a quick reference for metabolic alkalosis. Guidelines for analysis and causes, signs, and a stepwise approach are presented.

Metabolic acidosis: a quick reference.

This article serves as a quick reference for metabolic acidosis. Guidelines for analysis and causes, signs, and a stepwise approach are presented.

Zinc en sangre durante la gestación y su relación con la ingesta de calcio / No disponible

Fundamentos: estudiar los niveles de Zn en sangre (ZnSE)durante la gestación y la influencia de la ingesta de calcio.Métodos: 85 gestantes, clínicamente sanas (22,0 ± 6,0años), atendidas en un Hospital del Gran Buenos Airesdesde la edad gestacional de 19,6 ± 6,6 semanas (To).Se calculó la ingesta de calcio (ICa) y de Zinc (IZn) y sedividieron en grupos que recibieron diariamente 600 mgde calcio de : leche en polvo (GL, n=20); citrato de calcio(GCit, n=12) ó carbonato de calcio (GCar, n=27). Ungrupo no aceptó tratamiento (GNs, n=26). A To, al finaldel segundo trimestre (T1) y a Tf (34,7 ± 2,8 semanas)se determinó en sangre entera: hemoglobina (Hb) y Zn.Resultados: promedio ± DE (mg/d): To: ICa: 579 ± 382;IZn: 6,5 ± 2,8.ZnSE (μg/mL), a To y T1, no presentó diferencias significativasentre los cuatro grupos. Sin embargo, a Tf, GL disminuyósignificativamente (4,06 ± 1,08) (p<0,0001) en relación aGNs (5,64 ± 0,63), GCit (6,58 ± 0,98) y GCar (6,47 ± 0,60).Conclusiones: el calcio lácteo disminuyó los valores de ZnSEdurante la gestación, sugiriendo interacción Zn-Ca, mientrasque el del citrato y carbonato no presentaron ese efecto(AU)

Objective: The aim of this study was to analyse the inluenceof dietary calcium during pregnancy on Zn levels in maternalwhole blood (ZnWB).Methods: A group of 85 healthy pregnant women (meanage: 22,0 ± 6,0 years) were evaluated at “Diego Paroissien”Hospital since gestational age of: 19,6 ± 6,6 weeks (To) to,34,7 ± 2,8 weeks (Tf). At To mean daily dietary intake ofcalcium (CaI) and zinc (ZnI) was calculated. Women weredivided into three groups consuming daily a supplementof 600 mg of calcium as dried whole milk (GM, n=20);calcium citrate (GCit, n=12) or calcium carbonate (GCar,n=27). A group didn’t accepted any treatment (GNt n=26).At To, T1 (end of 2º trimester) and Tf, hemoglobin andZnWB was determined.Results: Mean ± SD (mg/d): To: CaI: 579 ± 382; ZnI:6,5 ± 2,8. At To and T1 there were no significant differencesin ZWB; however, at Tf, GM decreased significantlyregarding the GNt, GCit and GCar groups (4,06 ± 1,08 vs5,64 ± 0,63; 6,58 ± 0,98; 6,47 ± 0,60, respectively;p< 0.0001).Conclusions: This study shows that milk calcium intake, butnot calcium citrate and calcium carbonate, decreased ZnWBduring pregnancy, suggesting Zn-Ca interaction(AU)

Endotoxin augments hemodynamic and metabolic effects of formyl-methionyl-leucyl-phenylalanine (FMLP) in rabbits.

The chemotactic factor formyl-methionyl-leucyl-phenylalanine (FMLP) when injected in rabbits causes dose-dependent transient hypotension, as well as neutropenia, thrombocytopenia and a decrease in systemic vascular resistance, as previously shown. Since both FMLP and endotoxin are elaborated at sites of infection by certain bacteria, whether they act in concert to produce shock was examined. Animals were pretreated with 380 microg/kg of E. coli endotoxin, 24 hours before the infusion of 10(-9) moles FMLP and were compared with animals pretreated only with saline and administered FMLP. Within 3 min after FMLP, endotoxin-pretreated animals developed a significant fall in MAP (p < 0.001) and neutrophils (p < 0.001) compared to controls. Statistically significant lactic acidemia, with reduced HCO(-)3 levels also developed in the endotoxin-pretreated group after FMLP injection. These results indicate that endotoxin apparently induces a prepared state, thus facilitating the hemodynamic and cellular effects of FMLP in this model.

Isoflurane-induced acidosis depresses basal and PGE(2)-stimulated duodenal bicarbonate secretion in mice.

When running in vivo experiments, it is imperative to keep arterial blood pressure and acid-base parameters within the normal physiological range. The aim of this investigation was to explore the consequences of anesthesia-induced acidosis on basal and PGE(2)-stimulated duodenal bicarbonate secretion. Mice (strain C57bl/6J) were kept anesthetized by a spontaneous inhalation of isoflurane. Mean arterial blood pressure (MAP), arterial acid-base balance, and duodenal mucosal bicarbonate secretion (DMBS) were studied. Two intra-arterial fluid support strategies were used: a standard Ringer solution and an isotonic Na(2)CO(3) solution. Duodenal single perfusion was used, and DMBS was assessed by back titration of the effluent. PGE(2) was used to stimulate DMBS. In Ringer solution-infused mice, isoflurane-induced acidosis became worse with time. The blood pH was 7.15-7.21 and the base excess was about -8 mM at the end of experiments. The continuous infusion of Na(2)CO(3) solution completely compensated for the acidosis. The blood pH was 7.36-7.37 and base excess was about 1 mM at the end of the experiment. Basal and PGE(2)-stimulated DMBS were markedly greater in animals treated with Na(2)CO(3) solution than in those treated with Ringer solution. MAP was slightly higher after Na(2)CO(3) solution infusion than after Ringer solution infusion. We concluded that isoflurane-induced acidosis markedly depresses basal and PGE(2)-stimulated DMBS as well as the responsiveness to PGE(2), effects prevented by a continuous infusion of Na(2)CO(3). When performing in vivo experiments in isoflurane-anesthetized mice, it is recommended to supplement with a Na(2)CO(3) infusion to maintain a normal acid-base balance.

Detoxification of formate by formate dehydrogenase-loaded erythrocytes and carbicarb in folate-deficient methanol-intoxicated rats.

BACKGROUND: Formic acid is a toxic metabolite responsible for the metabolic acidosis in methanol poisoning. Formate dehydrogenase (EC 1.2.1.2) converts formate into CO2 in the presence of NAD. We examined the in vitro and in vivo efficiency of formate dehydrogenase-loaded carrier erythrocytes along with carbicarb in eliminating the formate in methanol-intoxicated folate-deficient rats. METHOD: Formate dehydrogenase-loaded erythrocytes were prepared by hypotonic dialysis method. Carbicarb (carb) (equimolar solution of sodium carbonate and sodium bicarbonate) was used to treat metabolic acidosis. Folate depletion was induced by methotrexate (MTX) treatment. Experimental design consisted of 8 groups: saline control, methanol control, MTX control, ELE control, MTX-methanol control, MTX-methanol-carb, MTX-methanol-carb-ELE, and MTX-MeOH-ELE group. Male Wistar rats treated with MTX (0.3 mg/kg) for a week were injected (i.p.) with methanol (4 g/kg). Twelve hours later, the carbicarb solution was infused, and then a formate dehydrogenase-loaded erythrocytes suspension (40% hematocrit) was infused (i.v.) in bolus. Blood samples were collected every hour for 4 h from the cannulated left jugular vein. Blood methanol and formate were estimated respectively with HPLC and fluorimetric assay. Blood pH, blood pO2, pCO2 and bicarbonate were also measured. RESULTS: There was marked elimination of formate in selected groups. CONCLUSION: Formate dehydrogenase-loaded erythrocytes, along with carbicarb, facilitates removal of formate, in methanol poisoning.

A method for evaluating the fluctuations in the intensity of substance transport between blood and bones in the predominant direction.

The dynamics of fluctuations in the intensity of the blood-bone flow of substances in the predominant and opposite directions was evaluated using the percent radioactivity difference coefficient and its graphic presentation. The technology of calculating this coefficient is described.

Neutralization of Western diet inhibits bone resorption independently of K intake and reduces cortisol secretion in humans.

A Western-type diet is associated with osteoporosis and calcium nephrolithiasis. On the basis of observations that calcium retention and inhibition of bone resorption result from alkali administration, it is assumed that the acid load inherent in this diet is responsible for increased bone resorption and calcium loss from bone. However, it is not known whether the dietary acid load acts directly or indirectly (i.e., via endocrine changes) on bone metabolism. It is also unclear whether alkali administration affects bone resorption/calcium balance directly or whether alkali-induced calcium retention is dependent on the cation (i.e., potassium) supplied with administered base. The effects of neutralization of dietary acid load (equimolar amounts of NaHCO(3) and KHCO(3) substituted for NaCl and KCl) in nine healthy subjects (6 men, 3 women) under metabolic balance conditions on calcium balance, bone markers, and endocrine systems relevant to bone [glucocorticoid secretion, IGF-1, parathyroid hormone (PTH)/1,25(OH)(2) vitamin D and thyroid hormones] were studied. Neutralization for 7 days induced a significant cumulative calcium retention (10.7 +/- 0.4 mmol) and significantly reduced the urinary excretion of deoxypyridinoline, pyridinoline, and n-telopeptide. Mean daily plasma cortisol decreased from 264 +/- 45 to 232 +/- 43 nmol/l (P = 0.032), and urinary excretion of tetrahydrocortisol (THF) decreased from 2,410 +/- 210 to 2,098 +/- 190 microg/24 h (P = 0.027). No significant effect was found on free IGF-1, PTH/1,25(OH)(2) vitamin D, or thyroid hormones. An acidogenic Western diet results in mild metabolic acidosis in association with a state of cortisol excess, altered divalent ion metabolism, and increased bone resorptive indices. Acidosis-induced increases in cortisol secretion and plasma concentration may play a role in mild acidosis-induced alterations in bone metabolism and possibly in osteoporosis associated with an acidogenic Western diet.