Artykuły w czasopismach na temat „Acidosis”
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Areas, Jorge, Sevag Balian, Dianna Slemmer, Mario Belledonne i Harry G. Preuss. "Renal ammoniagenesis following glutamine loading in intact dogs during acute metabolic acid–base perturbations". Clinical Science 72, nr 1 (1.01.1987): 61–69. http://dx.doi.org/10.1042/cs0720061.
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1. Adaptation of renal ammoniagenesis during acute metabolic acidosis in intact dogs may be nonexistent or, at least, markedly less than in chronic acidosis. This contrasts to adaptation in acute respiratory acidosis, where levels similar to those attained in chronic acidosis occur within hours. 2. Accordingly, the inability to discern marked changes in acute metabolic acidosis compared with acute respiratory acidosis has been attributed to decreased glomerular filtration rate and renal blood flow seen frequently in the former. 3. In our studies, we found early changes in ammoniagenesis and glutamine metabolism during acute metabolic acidosis, but not of the magnitude seen in chronic acidosis, even considering the changes in renal blood flow (RBF) and glomerular filtration rate (GFR). Exogenous glutamine loading allowed us to discover that the qualitative changes in glutamine metabolism during acute metabolic acidosis differed from control but fell short of those seen in chronic metabolic a acidosis. 4. We also examined glutamine metabolism when renal ammoniagenic adaptation was acutely inhibited in chronically acidotic dogs. Infusing NaHCO3 into chronically acidotic dogs decreased renal ammonia production significantly (247 μmol min−1 100 ml−1 GFR vs 148 μmol min−1 100 ml−1 GFR: P < 0.001) and glutamine extraction (111.8 μmol min−1 100 ml−1 GFR vs 90.9 μmol min−1 100 ml−1 GFR: P < 0.02). 5. The qualitative changes in renal glutamine metabolism in both studies suggest that alterations in deamination of glutamate formed from glutamine are responsible, at least in part, for adaptation to acute acid–base perturbations. 6. Compared with respiratory acidosis, adaptation to metabolic acidosis is progressive and prolonged.
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Williams, Bryan, Ellis Layward i John Walls. "Skeletal muscle degradation and nitrogen wasting in rats with chronic metabolic acidosis". Clinical Science 80, nr 5 (1.05.1991): 457–62. http://dx.doi.org/10.1042/cs0800457.
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1. Chronic metabolic acidosis is associated with impaired growth and negative nitrogen balance, suggesting that it promotes endogenous protein catabolism. 2. Skeletal muscle is the major repository of body protein and is a potential target for stimuli of protein catabolism. 3. This study in vivo examines the effects of chronic metabolic acidosis on the relationship between growth, nitrogen disposal and skeletal muscle catabolism in the rat. 4. Growth, nitrogen utilization and acquisition of body mass were significantly impaired in acidotic animals compared with pair-fed controls. 5. Total nitrogen excretion was significantly increased in acidotic rats despite decreased urea production. The time course of this response to acidosis was synchronous with that of accelerated protein catabolism in skeletal muscle. 6. It is proposed that metabolic acidosis impairs growth by stimulating skeletal muscle protein catabolism. It is suggested that this forms part of a co-ordinated multi-organ homoeostatic response to acidosis, skeletal muscle and down-regulated urea production supplying the nitrogen required for renal ammoniagenesis.
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Challa, A., R. J. Krieg, M. A. Thabet, J. D. Veldhuis i J. C. Chan. "Metabolic acidosis inhibits growth hormone secretion in rats: mechanism of growth retardation". American Journal of Physiology-Endocrinology and Metabolism 265, nr 4 (1.10.1993): E547—E553. http://dx.doi.org/10.1152/ajpendo.1993.265.4.e547.
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To test the hypothesis that growth retardation in nonanion gap acidosis may be associated with impairment of growth hormone (GH) secretory patterns, we examined GH secretion in rats made acidotic with ammonium chloride ingestion. Considerable growth retardation was demonstrated in pair-fed and acidotic rats after 1 wk of ammonium chloride ingestion compared with control. With stable metabolic acidosis sustained on the 8th day of experiment, pulsatile secretion of GH was evaluated by blood samples drawn every 10 min for 6 h. Using deconvolution analysis to quantitate in vivo GH secretory rates, we found significant inhibition of pulsatile GH secretion in acidotic rats. Changes in amplitude of GH pulses and mean mass of GH pulses correlated with changes in body weight. These studies showed that chronic metabolic acidosis causes growth impairment, reduced food efficiency, and amplitude-specific inhibition of pulsatile secretion of GH. We propose that this GH axis suppression, whether mediated by decreased nutrients or not, contributes significantly to growth failure in children with renal tubular acidosis. Because a similar degree of inhibition of GH secretion was seen in pair-fed rats, we infer that insufficient calorie intake in metabolic acidosis may contribute to disruption of normal GH secretion patterns. These changes in GH secretion were specific, because acidotic rats were different from pair-fed controls in that they showed no change in either half-life of GH in circulation or in pulse frequency. Such observations offer a rationale for more detailed clinical investigations into the impact of metabolic acidosis on physiological regulation of pulsatile GH secretion in humans.
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Moody, Mikayla, Tannin A. Schmidt, Ruchir Trivedi i Alix Deymier. "Administration of alendronate exacerbates ammonium chloride-induced acidosis in mice". PLOS ONE 18, nr 9 (15.09.2023): e0291649. http://dx.doi.org/10.1371/journal.pone.0291649.
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Bone disease is highly prevalent in patients with chronic kidney disease (CKD), leading to an increased risk of bone fractures. This is due in part to metabolic acid-induced bone dissolution. Bisphosphonates (BPPs) are a potential treatment for inhibiting bone dissolution; however, there are limited studies observing the use of BPPs on acidotic patients. We aimed to determine efficacy of BPPs on maintaining bone health and pH regulation in acid-exposed mice. Using a diet-induced murine model of metabolic acidosis, we examined bone structure, composition, and mechanics as well as blood gases for three groups: control, acidosis, and acidosis + bisphosphonates (acidosis+BPP). Acidosis was induced for 14 days and alendronate was administered every 3 days for the acidosis+BPP group. The administration of BPP had little to no effect on bone structure, mechanics, and composition of the acidosis bones. However, administration of BPP did cause the mice to develop more severe acidosis than the acidosis only group. Overall, we discovered that BPPs may exacerbate acidosis symptoms by inhibiting the release of buffering ions from bone. Therefore, we propose that BPP administration should be carefully considered for those with CKD and that alkali supplementation could help minimize acidifying effects.
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Caso, Giuseppe, Barbara A. Garlick, George A. Casella, Dawn Sasvary i Peter J. Garlick. "Acute metabolic acidosis inhibits muscle protein synthesis in rats". American Journal of Physiology-Endocrinology and Metabolism 287, nr 1 (lipiec 2004): E90—E96. http://dx.doi.org/10.1152/ajpendo.00387.2003.
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In this study, we investigated the effect of acute metabolic acidosis on tissue protein synthesis. Groups of rats were made acidotic with intragastric administration of NH4Cl (20 mmol/kg body wt every 12 h for 24 h) or given equimolar amounts of NaCl (controls). Protein synthesis in skeletal muscle and a variety of different tissues, including lymphocytes, was measured after 24 h by injection of l-[2H5]phenylalanine (150 μmol/100 g body wt, 40 moles percent). Results show that acute acidosis inhibits protein synthesis in skeletal muscle (−29% in gastrocnemius, −23% in plantaris, and −17% in soleus muscles, P < 0.01) but does not affect protein synthesis in heart, liver, gut, kidney, and spleen. Protein synthesis in lymphocytes is also reduced by acidosis (−8%, P < 0.05). In a separate experiment, protein synthesis was also measured in acidotic and control rats by a constant infusion of l-[2H5]phenylalanine (1 μmol·100 g body wt−1·h−1). The results confirm the earlier findings showing an inhibition of protein synthesis in gastrocnemius (−28%, P < 0.01) and plantaris (−19%, P < 0.01) muscles but no effect on heart and liver by acidosis. Similar results were also observed using a different model of acute metabolic acidosis, in which rats were given a cation exchange resin in the H+ (acidotic) or the Na+ (controls) form. In conclusion, this study demonstrates that acute metabolic acidosis for 24 h depresses protein synthesis in skeletal muscle and lymphocytes but does not alter protein synthesis in visceral tissues. Inhibition of muscle protein synthesis might be another mechanism contributing to the loss of muscle tissue observed in acidosis.
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TETA, Daniel, Alan BEVINGTON, Jeremy BROWN, David THROSSELL, Kevin P. G. HARRIS i John WALLS. "Effects of acidosis on leptin secretion from 3T3-L1 adipocytes and on serum leptin in the uraemic rat". Clinical Science 97, nr 3 (6.08.1999): 363–68. http://dx.doi.org/10.1042/cs0970363.
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Marked hyperleptinaemia and metabolic acidosis are common findings in patients with chronic renal failure. In animal models, both leptin administration and acidosis reduce food intake. However, leptin causes loss of body fat, while acidosis induces muscle wasting. Whether a low pH and leptin production are related has not been studied. Leptin secretion was measured in cultured 3T3-L1 adipocytes exposed to acid or control pH for up to 96 h. In addition, serum leptin was compared between acidotic and bicarbonate-treated uraemic Wistar rats using the remnant model. Leptin levels in the culture medium were decreased at an acid pH of 7.1 compared with a control pH of 7.5 at 96 h (562±78 and 831±103 pg·48 h-1·well-1 respectively; mean±S.E.M.; P = 0.037). Similarly, serum leptin in uraemic rats was found to be lower in the acidotic group than in the bicarbonate-treated group, although this observation fell just short of statistical significance (1273±171 compared with 2059±376 pg/ml; P = 0.07). In conclusion, acidosis decreases leptin secretion from cultured adipocytes. Accordingly, acidotic uraemic rats seem to exhibit lower serum leptin levels than their bicarbonate-supplemented counterparts. This study is the first report providing a link between acidosis and leptin levels.
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Türe, Hatice, Özgül Keskin, Ülkem Çakır, Canan Aykut Bingöl i Uğur Türe. "The frequency and severity of metabolic acidosis related to topiramate". Journal of International Medical Research 44, nr 6 (27.10.2016): 1376–80. http://dx.doi.org/10.1177/0300060516669897.
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Objective We planned a cross-sectional analysis to determine the frequency and severity of metabolic acidosis in patients taking topiramate while awaiting craniotomy. Methods Eighty patients (18 – 65 years) taking topiramate to control seizures while awaiting elective craniotomy were enrolled. Any signs of metabolic acidosis or topiramate-related side effects were investigated. Blood chemistry levels and arterial blood gases, including lactate, were obtained. The severity of metabolic acidosis was defined according to base excess levels as mild or moderate. Results Blood gas analysis showed that 71% ( n = 57) of patients had metabolic acidosis. The frequency of moderate metabolic acidosis was 56% ( n = 45), while that of mild metabolic acidosis was 15% ( n = 12). A high respiratory rate was reported in only 10% of moderately acidotic patients. Conclusions In patients receiving topiramate, baseline blood gas analysis should be performed preoperatively to determine the presence and severity of metabolic acidosis.
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Price, S. R., X. Wang i J. L. Bailey. "Tissue-specific responses of branched-chain alpha-ketoacid dehydrogenase activity in metabolic acidosis." Journal of the American Society of Nephrology 9, nr 10 (październik 1998): 1892–98. http://dx.doi.org/10.1681/asn.v9101892.
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In adrenalectomized rats, acidosis does not increase whole-body leucine oxidation unless a physiologic amount of glucocorticoids (dexamethasone) is also provided; an equivalent dose of dexamethasone without acidosis does not change leucine catabolism. Because the influences of acidification and glucocorticoids on branched-chain amino acid metabolism in specific organs are unknown, the function of branched-chain alpha-ketoacid dehydrogenase (BCKAD), the rate-limiting enzyme in branched-chain amino acid catabolism, in adrenalectomized rat skeletal muscle and liver, the two major tissues that degrade branched-chain amino acid was measured. In muscle of acidotic adrenalectomized rats receiving dexamethasone, basal and total BCKAD activities were increased 2.6- (P < 0.05) and 2.8-fold (P < 0.05), respectively. Neither acidosis nor dexamethasone alone increased these activities. BCKAD E1alpha subunit mRNA in muscle of acidotic rats given dexamethasone was increased 1.89-fold (P < 0.05) in parallel with the change in BCKAD activity; BCKAD E2 subunit mRNA was increased by acidosis, dexamethasone, or a combination of both stimuli. In contrast, basal BCKAD activity in liver of rats with acidosis or dexamethasone was nearly threefold lower (P < 0.05) and changes in enzyme activity reflected reduced subunit mRNA. Thus, there are reciprocal, tissue-specific changes in BCKAD function in response to acidosis.
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Karinch, Anne M., Cheng-Mao Lin, Christopher L. Wolfgang, Ming Pan i Wiley W. Souba. "Regulation of expression of the SN1 transporter during renal adaptation to chronic metabolic acidosis in rats". American Journal of Physiology-Renal Physiology 283, nr 5 (1.11.2002): F1011—F1019. http://dx.doi.org/10.1152/ajprenal.00106.2002.
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During chronic metabolic acidosis, renal glutamine utilization increases markedly. We studied the expression of the system N1 (SN1) amino acid transporter in the kidney during chronic ammonium chloride acidosis in rats. Acidosis caused a 10-fold increase in whole kidney SN1 mRNA level and a 100-fold increase in the cortex. Acidosis increased Na+-dependent glutamine uptake into basolateral and brush-border membrane vesicles (BLMV and BBMV, respectively) isolated from rat cortex (BLMV, 219 ± 66 control vs. 651 ± 180 pmol · mg−1 · min−1 acidosis; BBMV, 1,112 ± 189 control vs. 1,652 ± 148 pmol · mg−1 · min−1 acidosis, both P < 0.05). Na+-independent uptake was unchanged by acidosis in BLMV and BBMV. The acidosis-induced increase in Na+-dependent glutamine uptake was eliminated by histidine, confirming transport by system N. SN1 protein was detected only in BLMV and BBMV from acidotic rats. After recovery from acidosis, SN1 mRNA and protein and Na+-dependent glutamine uptake activity rapidly returned to control levels. These data provide evidence that regulation of expression of the SN1 amino acid transporter is part of the renal homeostatic response to acid-base imbalance.
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Lucioni, Alvaro, Christopher Womack, Mark W. Musch, Flavio L. Rocha, Cres Bookstein i Eugene B. Chang. "Metabolic acidosis in rats increases intestinal NHE2 and NHE3 expression and function". American Journal of Physiology-Gastrointestinal and Liver Physiology 283, nr 1 (1.07.2002): G51—G56. http://dx.doi.org/10.1152/ajpgi.00529.2001.
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Chronic metabolic acidosis increases intestinal Na absorption, although through undefined mechanisms. Whether this occurs through enhanced expression and/or function of the brush-border Na+/H+ exchangers (NHE)2 and NHE3 is unknown. Metabolic acidosis was induced in rats by feeding ammonium chloride through their drinking water. Intestinal NHE activities were measured using brush-border 22Na+ uptake. Western and Northern blots measured changes in protein and mRNA expression, respectively. Acidosis occurred within 2 days of ammonium chloride feedings but increased after 6 days. NHE2 and NHE3 activities, protein expression, and mRNA levels increased in acidotic rats compared with controls. In contrast, basolateral NHE1 expression was not affected. Brush-border alkaline phosphatase showed no effect of metabolic acidosis on cellular differentiation. This study demonstrated a direct effect of metabolic acidosis on NHE2 and NHE3 activity, expression, and gene transcription. Metabolic acidosis is one of the few circumstances shown to affect NHE2 function and expression, thus providing insights into the role of NHE2 on intestinal physiology.
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Boross, M., J. Kinsella, L. Cheng i B. Sacktor. "Glucocorticoids and metabolic acidosis-induced renal transports of inorganic phosphate, calcium, and NH4". American Journal of Physiology-Renal Physiology 250, nr 5 (1.05.1986): F827—F833. http://dx.doi.org/10.1152/ajprenal.1986.250.5.f827.
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The initial rate (5 s) of Na+-dependent inorganic phosphate (Pi) uptake in brush-border membrane vesicles isolated from rat proximal tubule was decreased in metabolic acidosis, 0.42 +/- 0.02 vs. 0.59 +/- 0.05 nmol/mg protein, in vesicles from control animals. Phosphate, ammonium, and Ca2+ excretions were increased 100, 600, and 56%, respectively. These changes in brush-border Pi transport and urinary excretion of ions were largely dependent on intact adrenal glands. After adrenalectomy there were no significant changes in brush-border Pi transport, Pi, and Ca2+ excretion, whereas ammonium excretion increased only 300% compared with controls. When the glucocorticoid dexamethasone was administered to adrenalectomized animals, it mimicked the effects of metabolic acidosis both in the presence and the absence of metabolic acidosis. The initial rate of brush-border Pi transport was decreased by dexamethasone administration to 0.37 +/- 0.04 nmol/mg protein in adrenalectomized acidotic animals and 0.39 +/- 0.03 nmol/mg protein in adrenalectomized animals. Dexamethasone administered to adrenalectomized acidotic animals increased Pi, ammonium, and Ca2+ excretion 190, 690, and 23%, respectively. Dexamethasone administered to nonacidotic adrenalectomized animals increased Pi ammonium and Ca2+ excretion 165, 240, and 31%, respectively. We conclude that changes in Pi, ammonium, and Ca2+ excretion observed during metabolic acidosis were dependent on intact adrenal glands and that glucocorticoids administered to adrenalectomized acidotic or nonacidotic animals mimicked the changes observed in acidotic animals with intact adrenal glands.
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Ogunade, Ibukun, Andres Pech-Cervantes i Hank Schweickart. "Metatranscriptomic Analysis of Sub-Acute Ruminal Acidosis in Beef Cattle". Animals 9, nr 5 (12.05.2019): 232. http://dx.doi.org/10.3390/ani9050232.
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Subacute ruminal acidosis (SARA) is a metabolic disease of ruminants characterized by low pH, with significant impacts on rumen microbial activity, and animal productivity and health. Microbial changes during subacute ruminal acidosis have previously been analyzed using quantitative PCR and 16S rRNA sequencing, which do not reveal the actual activity of the rumen microbial population. Here, we report the functional activity of the rumen microbiota during subacute ruminal acidosis. Eight rumen-cannulated Holstein steers were assigned randomly to acidosis-inducing or control diet. Rumen fluid samples were taken at 0, 3, 6, and 9 h relative to feeding from both treatments on the challenge day. A metatranscriptome library was prepared from RNA extracted from the samples and the sequencing of the metatranscriptome library was performed on Illumina HiSeq4000 following a 2 × 150 bp index run. Cellulolytic ruminal bacteria including Fibrobacter succinogenes, Ruminococcus albus, and R. bicirculans were reduced by an induced acidotic challenge. Up to 68 functional genes were differentially expressed between the two treatments. Genes mapped to carbohydrate, amino acid, energy, vitamin and co-factor metabolism pathways, and bacterial biofilm formation pathways were enriched in beef cattle challenged with sub-acute acidosis. This study reveals transcriptionally active taxa and metabolic pathways of rumen microbiota during induced acidotic challenge.
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Greiber, S., W. C. O'Neill i W. E. Mitch. "Impaired cation transport in thymocytes of rats with chronic uremia includes the Na+/H+ antiporter." Journal of the American Society of Nephrology 5, nr 9 (marzec 1995): 1689–96. http://dx.doi.org/10.1681/asn.v591689.
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To examine how uremia changes sodium, potassium, and proton transport, thymocytes from chronic renal failure (CRF) rats were studied. If alterations in cation transport associated with chronic uremia (CRF) extend to intracellular pH regulation, the susceptibility to the catabolic effects of acidosis might be increased. To evaluate the influence of acidosis, cation transport in thymocytes from normal rats with NH4Cl-induced acidosis was also studied. Ouabain-sensitive 86Rb influx in thymocytes from acidotic CRF rats was 32% lower than in control cells (P < 0.05), but intracellular sodium concentration was unchanged. This may be related to a 47 +/- 22% reduction in 22Na influx. In thymocytes from nonuremic, acidotic rats, ouabain-sensitive 86Rb influx was decreased 39% (P < 0.025), similar to the change in CRF. In CRF thymocytes, Na(+)-H+ antiporter activity in response to cell acidification (7.13 +/- 0.8 versus 9.42 +/- 0.8 mmol of H+/L per min; CRF versus control), or to osmotic shrinkage (0.43 +/- 0.09 versus 0.82 +/- 0.11 mmol of H+/L per min; CRF versus control), was significantly (P < 0.01) reduced. Buffering capacity at resting and acidic intracellular pH was unchanged by uremia, but Na+/H+ antiporter activity in response to acid loading or osmotic shrinkage was unchanged in thymocytes of nonuremic rats with metabolic acidosis. Thus, CRF reduces both Na/K-ATPase and Na+/H+ antiporter activities in rat thymocytes. The former may be secondary to reduced sodium influx. Impaired Na+/H+ antiporter activity is not caused by metabolic acidosis alone, whereas reduced Na/K-ATPase activity is found in both acidosis and uremia.
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Nissim, I., M. Yudkoff i S. Segal. "Metabolic fate of glutamate carbon in rat renal tubules. Studies with 13C nuclear magnetic resonance and gas chromatography-mass spectrometry". Biochemical Journal 241, nr 2 (15.01.1987): 361–70. http://dx.doi.org/10.1042/bj2410361.
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13C-n.m.r. spectroscopy and g.c.-m.s. were used to determine the metabolic fate of glutamate carbon in rat kidney. The main purpose was to characterize the effect of chronic metabolic acidosis on the utilization of glutamate carbon. Renal tubules obtained from normal and chronically acidotic rats were incubated in Krebs buffer, pH 7.4, in the presence of 2.5 mM-[3-13C]glutamate. During the course of incubation the concentrations of total glucose and NH3 were significantly (P less than 0.05) higher in tissue from acidotic rats. The levels of some tricarboxylic-acid-cycle intermediates were higher (P less than 0.05) in control tissue. In control tissue, 13C-n.m.r. spectra demonstrated a significantly higher rate of 13C appearance of aspartate, glutamine and [2,4-13C]glutamate. However, in acidosis the resonances of [13C]glucose carbon atoms were significantly higher. In the control, approx. 15% of glutamate carbon was accounted for by [13C]glucose formation as against 30% in chronic acidosis. However, in control tissue, 44% of glutamate carbon utilization was accounted for by recycling to glutamate and formation of aspartate, glutamine and GABA. In acidosis, only 11% was so recovered. Analysis of 15NH3 formation during the course of incubation with 2.5 mM-[15N]glutamate demonstrated a positive association between the appearance of [13C]glucose and 15NH3 both in the control and in acidosis. The data suggest that the control of gluconeogenesis and ammoniagenesis in acidosis is, in part, referable to a diminution in the rate of the reductive amination of alpha-oxoglutarate, that of the transamination reaction and that of glutamine synthesis.
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Throssell, D., J. Brown, K. P. G. Harris i J. Walls. "Metabolic Acidosis Does Not Contribute to Chronic Renal Injury in the Rat". Clinical Science 89, nr 6 (1.12.1995): 643–50. http://dx.doi.org/10.1042/cs0890643.
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1. Metabolic acidosis invariably accompanies chronic renal failure, and short periods of metabolic acidosis cause renal growth and proteinuria in normal rats. Rates of ammoniagenesis are increased in chronic renal failure, and it has been suggested that this contributes to disease progression. This study assessed (i) whether prolonged acidosis causes chronic renal injury in the normal kidney and (ii) whether abrogation of acidosis slows disease progression in the remnant kidney. 2. Metabolic acidosis was induced in normal rats by dietary hydrochloric acid. Urinary excretion of total protein, lysozyme and albumin increased, peaking at week 8 but returning to baseline by week 14. At killing after 14 weeks, kidney weights, glomerular filtration rates and serum creatinine were the same in both groups, but kidney/body weight and kidney/heart weight ratios were greater in the acidotic group. All kidneys were normal by light microscopy. 3. Rats subjected to five-sixths nephrectomy were given sufficient dietary bicarbonate to abolish uraemic acidosis, and their outcome was compared with that of non-alkalinized remnants (controls). Proteinuria, glomerular filtration rates, blood pressure, histological injury and time to the development of terminal uraemia were no better in bicarbonate-supplemented animals than in controls. 4. These data demonstrate that metabolic acidosis neither causes nor exacerbates chronic renal injury. We conclude that the treatment of uraemic acidosis is unlikely to influence disease progression in patients with chronic renal failure.
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Dhelaria, Anshoo, Raghuram Commondoor, Ananya Kar i Michael Eisenhut. "Characteristics of metabolic acidosis and management of rotavirus gastro-enteritis". Journal of Pediatric Biochemistry 01, nr 04 (grudzień 2010): 297–301. http://dx.doi.org/10.1055/s-0036-1586387.
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AbstractObjectives of this study were to investigate the characteristics of metabolic acidosis associated with rotavirus gastroenteritis and to explore them as a tool in the management of dehydration. The study was retrospective, case record based and conducted in a secondary level District General Hospital. Included study population were 133 children who were admitted to the Paediatric Unit with rotavirus gastroenteritis. Degree of dehydration, result of blood gas analysis, C-reactive protein level, urinary ketones, renal function tests, fluid management and duration of hospitalization were recorded and results compared between patients with and without severe metabolic acidosis (serum bicarbonate < 17 mmol/L). Out of 133 patients, blood gas analysis was obtained in 78 (59%) and 73 (94%) of those showed metabolic acidosis (bicarbonate < 22 mmol/L). Thirty five patients developed severe metabolic acidosis. Patients with severe metabolic acidosis showed signs of dehydration more commonly (97% vs. 74%, p < 0.05) and required intravenous rehydration more frequently (94% vs. 63%, p < 0.05) than those who were not severely acidotic. With respect to gender ratio, initial temperature, serum levels of C-reactive protein, chloride, anion-gap, lactate and ketonuria, there were no significant differences between the severely acidotic patients and those who were not. Urea and creatinine levels were higher (46.6 (11.7) versus 37.8 (11.9) micromole/L for creatinine and 5.5 (1.9) versus 4.2 (2.1) mmol/L for urea, p < 0.05) in patients with severe metabolic acidosis and correlated significantly negatively (for both: r = − 0.29, p = 0.02) with serum bicarbonate levels. We concluded that the majority of children attending hospital with rotavirus gastroenteritis had a metabolic acidosis. Severe metabolic acidosis was associated with more severe dehydration and higher urea and creatinine levels and increased requirement for intravenous fluid boluses and intravenous rehydration. A bicarbonate level of > 17 mmol/L excluded severe clinical dehydration and below this level a degree of dehydration was very likely.
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Berger, David S., Susan K. Fellner, Kimberly A. Robinson, Katherine Vlasica, Ivan E. Godoy i Sanjeev G. Shroff. "Disparate effects of three types of extracellular acidosis on left ventricular function". American Journal of Physiology-Heart and Circulatory Physiology 276, nr 2 (1.02.1999): H582—H594. http://dx.doi.org/10.1152/ajpheart.1999.276.2.h582.
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Effects of acidosis on muscle contractile function have been studied extensively. However, the relative effects of different types of extracellular acidosis on left ventricular (LV) contractile function, especially the temporal features of contraction, have not been investigated in a single model. We constituted perfusion buffers of identical ionic composition, including Ca2+concentration ([Ca2+]), to mimic physiological control condition (pH 7.40) and three types of acidosis with pH of 7.03: inorganic (IA), respiratory (RA), and lactic (LA). Isolated rabbit hearts ( n = 9) were perfused with acidotic buffers chosen at random, each preceded by the control buffer. Under steady-state conditions, instantaneous LV pressure (Pv) and volume (Vv) were recorded for a range of Vv. The results were as follows. 1) LV passive (end-diastolic) elastance increased with IA and RA. However, this increase may not be a direct effect of acidosis; it can be explained on the basis of myocardial turgor. 2) Although LV inotropic state (peak active Pv and elastance) was depressed by all three acidotic buffers, the magnitude of inotropic depression was significantly less for LA. 3) Temporal features of Pv were altered differently. Whereas IA and RA reduced time to peak Pv( t max) and hastened isovolumic relaxation at a common level of LV wall stress, LA significantly increased t max and retarded relaxation. These results and a model-based interpretation suggest that cooperative feedback (i.e., force-activation interaction) plays an important role in acidosis-induced changes in LV contractile function. Furthermore, it is proposed that LA-induced responses comprise two components, one due to intracellular acidosis and the other due to pH-independent effects of lactate ions.
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López-Flores, Inmaculada, Juan Peragón, Raquel Valderrama, Francisco J. Esteban, Francisco Luque, M. Ángeles Peinado, Fermín Aranda, José A. Lupiáñez i Juan B. Barroso. "Downregulation in the expression of the serine dehydratase in the rat liver during chronic metabolic acidosis". American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 291, nr 5 (listopad 2006): R1295—R1302. http://dx.doi.org/10.1152/ajpregu.00095.2006.
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Blood pH controls the activity of important regulatory enzymes in the metabolism. Serine dehydratase (SerDH) transforms l-serine into pyruvate and ammonium and is involved in the regulation of gluconeogenesis from serine in the rat liver. In this work, we investigate the effect of chronic metabolic acidosis on the kinetics, specific protein level, tissue location, and mRNA levels of rat liver SerDH. Experimental acidosis was induced in rats by ingestion of 0.28 M ammonium chloride solution for 10 days. Acidosis significantly ( P < 0.05) decreased SerDH activity at all substrate concentrations assayed. Moreover, the Vmaxvalue was 38.50 ± 3.51 mU/mg ( n = 7) of mitochondrial protein in the acidotic rats and 92.49 ± 6.79 mU/mg ( n = 7) in the control rats. Western blot analysis revealed a significant reduction (14%) in the level of SerDH protein content in the rat liver during acidosis. Immunohistochemical analysis showed that SerDH location did not change in response to chronic metabolic acidosis and confirmed previous results on SerDH protein levels. Moreover, the SerDH mRNA level, estimated by RT-PCR, was also significantly 33.8% lower than in control. These results suggest that during experimental acidosis a specific repression of rat-liver SerDH gene transcription could result, lowering the amount and activity of this enzyme. The changes found in SerDH expression are part of an overall metabolic response of liver to maintain acid-base homeostasis during acidosis.
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Wang, Tao, Guokun Zhou, Mindi He, Yuanyuan Xu, W. G. Rusyniak, Yan Xu, Yonghua Ji, Roger P. Simon, Zhi-Gang Xiong i Xiang-ming Zha. "GPR68 Is a Neuroprotective Proton Receptor in Brain Ischemia". Stroke 51, nr 12 (grudzień 2020): 3690–700. http://dx.doi.org/10.1161/strokeaha.120.031479.
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Background and Purpose: Brain acidosis is prevalent in stroke and other neurological diseases. Acidosis can have paradoxical injurious and protective effects. The purpose of this study is to determine whether a proton receptor exists in neurons to counteract acidosis-induced injury. Methods: We analyzed the expression of proton-sensitive GPCRs (G protein-coupled receptors) in the brain, examined acidosis-induced signaling in vitro, and studied neuronal injury using in vitro and in vivo mouse models. Results: GPR68, a proton-sensitive GPCR, was present in both mouse and human brain, and elicited neuroprotection in acidotic and ischemic conditions. GPR68 exhibited wide expression in brain neurons and mediated acidosis-induced PKC (protein kinase C) activation. PKC inhibition exacerbated pH 6-induced neuronal injury in a GPR68-dependent manner. Consistent with its neuroprotective function, GPR68 overexpression alleviated middle cerebral artery occlusion–induced brain injury. Conclusions: These data expand our knowledge on neuronal acid signaling to include a neuroprotective metabotropic dimension and offer GPR68 as a novel therapeutic target to alleviate neuronal injuries in ischemia and multiple other neurological diseases.
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Zhou, H. Z., D. Malhotra i J. I. Shapiro. "Contractile dysfunction during metabolic acidosis: role of impaired energy metabolism". American Journal of Physiology-Heart and Circulatory Physiology 261, nr 5 (1.11.1991): H1481—H1486. http://dx.doi.org/10.1152/ajpheart.1991.261.5.h1481.
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To investigate the mechanisms by which acidosis depresses cardiac function, a Langendorff isolated perfused rat heart preparation was studied using 31P magnetic resonance spectroscopy. Isolated hearts were subjected to normal perfusion conditions or experimental manipulations simulating severe metabolic acidosis, substrate depletion, impairment of oxidative metabolism, or low perfusate calcium concentrations. All maneuvers resulted in marked reductions in oxygen consumption and the force of myocardial contraction (dP/dt). Metabolic acidosis had bioenergetic changes suggestive of impaired energy production, specifically, increases in Pi and decreases in phosphocreatine concentrations, which did not occur in hearts subjected to low perfusate calcium concentrations. In acidotic perfusions as well as substrate depletion and impairment of oxidative metabolism, the change in dP/dt correlated best with the change in the intracellular concentration of monovalent Pi (P(im)) (r = 0.70, P less than 0.01), whereas in hearts subjected to a low perfusate calcium concentration, there was no relationship between dP/dt and the change in Pim concentrations. More detailed analysis of the time course of the metabolic and physiological changes with metabolic acidosis revealed a discordance between changes in Pim and the decreases in dP/dt during the first 20 min of the induction of acidosis and the first 10 min of recovery from acidosis. These data suggest that metabolic acidosis has a major direct effect on energy metabolism in this model. Moreover, impairment of oxidative metabolism in concert with decreases in intracellular pH may be important in the contractile failure associated with prolonged metabolic acidosis.
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Nakanishi, T., H. Okuda, K. Kamata, M. Seguchi, M. Nakazawa i A. Takao. "Influence of acidosis on inotropic effect of catecholamines in newborn rabbit hearts". American Journal of Physiology-Heart and Circulatory Physiology 253, nr 6 (1.12.1987): H1441—H1448. http://dx.doi.org/10.1152/ajpheart.1987.253.6.h1441.
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The influence of acidosis on the inotropic effect of isoproterenol was studied in the isolated arterially perfused heart of the newborn rabbits. Baseline mechanical function during acidosis (pH 6.8) was not different from control (pH 7.4). However, the inotropic effect of isoproterenol was significantly suppressed in the acidotic muscles. The increment of myocardial adenosine 3',5'-cyclic monophosphate (cAMP) content during isoproterenol infusion was also reduced in acidosis. Inotropic effects of Ca and dibutyryl cAMP in the acidotic muscles were not significantly different from those in the control muscles. beta-Receptor number and affinity in the respiratory acidotic muscle was similar to those in the control muscle. Effects of pH on myocardial beta-receptor and adenylate cyclase activity were further determined in the membrane fraction by changing the pH of the reaction medium from 7.4 (control) to 6.8 or 6.0. beta-Receptor numbers were significantly decreased at pH 6.0 but not at pH 6.8. Adenylate cyclase activity was depressed at pH 6.8 and 6.0. These data suggest that the inotropic effect of isoproterenol is diminished in the acidotic muscle. This may be due to the decreased activation of cAMP production, which in turn most likely results from depressed adenylate cyclase activity.
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Freund, Dana M., Jessica E. Prenni i Norman P. Curthoys. "Response of the mitochondrial proteome of rat renal proximal convoluted tubules to chronic metabolic acidosis". American Journal of Physiology-Renal Physiology 304, nr 2 (15.01.2013): F145—F155. http://dx.doi.org/10.1152/ajprenal.00526.2012.
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Metabolic acidosis is a common clinical condition that is caused by a decrease in blood pH and bicarbonate concentration. Increased extraction and mitochondrial catabolism of plasma glutamine within the renal proximal convoluted tubule generates ammonium and bicarbonate ions that facilitate the excretion of acid and partially restore acid-base balance. Previous studies identified only a few mitochondrial proteins, including two key enzymes of glutamine metabolism, which are increased during chronic acidosis. A workflow was developed to characterize the mitochondrial proteome of the proximal convoluted tubule. Based upon the increase in specific activity of cytochrome c oxidase, the isolated mitochondria were enriched eightfold. Two-dimensional liquid chromatography coupled with mass spectrometry was utilized to compare mitochondrial-enriched samples from control and chronic acidotic rats. Proteomic analysis identified 901 proteins in the control and acidotic samples. Further analysis identified 37 peptides that contain an N-ε-acetyl-lysine; of these, 22 are novel sites. Spectral counting analysis revealed 33 proteins that are significantly altered in abundance in response to chronic metabolic acidosis. Western blot analysis was performed to validate the calculated changes in abundance. Thus the current study represents the first comprehensive analysis of the mitochondrial proteome of the rat renal proximal convoluted tubule and its response to metabolic acidosis.
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Bellorin-Font, E., R. Starosta, C. L. Milanes, C. Lopez, N. Pernalete, J. Weisinger i V. Paz-Martinez. "Effect of acidosis on PTH-dependent renal adenylate cyclase in phosphorus deprivation: role of G proteins". American Journal of Physiology-Renal Physiology 258, nr 6 (1.06.1990): F1640—F1649. http://dx.doi.org/10.1152/ajprenal.1990.258.6.f1640.
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These studies examine the regulation of adenylate cyclase in renal cortical membranes from phosphate-deprived and phosphate-deprived acidotic dogs. Enzyme stimulation by parathyroid hormone (PTH) was decreased in phosphate deprivation [Vmax 1,578 +/- 169 vs. 2,581 +/- 219 pmol adenosine 3',5'-cyclic monophosphate (cAMP).mg protein-1 x 30 min-1 in controls, P less than 0.01]. Metabolic acidosis further decreased PTH-stimulated activity. Membranes from phosphate-deprived dogs showed a decrease in Gs alpha-content by cholera toxin-dependent ADP-ribosylation (174 +/- 18 arbitrary units vs. 266.4 +/- 13.6 in controls, P less than 0.01). Metabolic acidosis further decreased Gs alpha-content, P less than 0.01. Gi content by pertussis-dependent ADP-ribosylation was also lower in phosphate-deprived and phosphate-deprived acidotic animals. Gs function was examined by its property to protect the catalytic unit from inactivation by N-ethylmaleimide when preincubated with GTP gamma S. In controls, protection of inactivation was 80% of the maximal activity, whereas in phosphate deprivation protection was less than 50%. In conclusion, metabolic acidosis enhances adenylate cyclase resistance to PTH in phosphate deprivation. These alterations are associated with a decrease in the content and function of Gs alpha, suggesting a role of Gs in the renal adaptation to phosphate depletion and acidosis.
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Porras, Miguel C., José N. Lecumberri i José Luis P. Castrillón. "Trimethoprim/Sulfamethoxazole and Metabolic Acidosis in HIV-Infected Patients". Annals of Pharmacotherapy 32, nr 2 (luty 1998): 185–89. http://dx.doi.org/10.1345/aph.17042.
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OBJECTIVE: To describe a retrospective study of six HIV-positive individuals with compensated metabolic acidosis while receiving intravenous trimethoprim/sulfamethoxazole (TMP/SMX). CASE SUMMARY: Six HIV-infected patients were treated for Pneumocystis carinii pneumonia (PCP) with high-dose intravenous TMP/SMX. In spite of a favorable clinical and radiologic course, all six patients developed compensated metabolic acidosis 3–5 days after the start of treatment. This potential complication of TMP/SMX use was successfully managed with conservative treatment (cessation of therapy with or without additional administration of intravenous bicarbonate). DISCUSSION: TMP/SMX is first-line therapy for PCP in HIV-positive individuals, despite a high frequency of toxic effects in these patients. In addition to the cases reported here, only two other reports of metabolic acidosis secondary to TMP/SMX use in HIV-infected patients have been published in the literature. The precise mechanism of this untoward effect is not fully understood, although renal tubular acidosis induced by TMP/SMX could be implicated. CONCLUSIONS: TMP/SMX toxicity should be considered in the differential diagnosis of HIV-infected patients with acute metabolic acidosis. Metabolic acidosis can be expected to resolve shortly after discontinuation of the drug. OBJETIVO: Describir una serie retrospectiva de seis pacientes infectados por VIH-positivos que desarrollaron acidosis metabólica durante la administración de trimetoprima/sulfametoxazol (TMP/SMX). RESUMEN DEL CASO: Seis pacientes con infección por VIH y neumonía por Pneumocystis carinii (NPC) recibieron altas dosis de TMP/SMX vía intravenosa. A pesar de un curso clínico-radiológico favorable, se objetivó acidosis metabólica compensada en los seis enfermos entre los 3–5 días posteriores al inicio del tratamiento. Esta potencial complicación del TMP/SMX fue manejada satisfactoriamente con medidas conservadoras (suspensión del fármaco, con o sin la administración adicional de bicarbonato intravenoso). DISCUSIÓN: TMP/SMX es el tratamiento de elección para la NPC en individuos VIH-positivos, a pesar de la elevada frecuencia de efectos adversos en estos enfermos. Además de los casos comunicados aquí, únicamente se han publicado otros dos trabajos en la literatura mundial relativos a la acidosis metabólica como potencial efecto indeseable del TMP/SMX en pacientes VIH-positivos. El mecanismo exacto de este efecto adverso no está totalmente aclarado, aunque una acidosis renal tubular inducida por el TMP/SMX pudiera estar implicada. CONCLUSIONES: Sugerimos que se incluya la posible toxicidad del TMP/SMX en el diagnóstico diferencial de la acidosis metabólica aguda en pacientes VIH-positivos. Si se detectara acidosis metabólica aguda previsiblemente relacionada con TMP/SMX, la suspensión del fármaco determinaría una rápida normalización del equilibrio ácido-base. OBJECTIF: Décrire une série rétrospective de six individus séropositifs pour le VIH qui ont développé une acidose métabolique compensée alors qu'ils recevaient du triméthoprim/sulfaméthoxazole (TMP/SMX) par voie intraveineuse. DU CAS: Six patients infectés par le VIH ont été traités pour une pneumonie à Pneumocystis carinii (PPC) avec des doses élevées de TMP/SMX. Malgré une évolution clinique et radiologique favorable, les six patients ont développé une acidose métabolique compensée 3–5 jours après le début du traitement. Cette complication potentiellement associée à l'utilisation du TMP/SMX a été corrigée avec succès à l'aide d'un traitement conservateur (l'arrêt du traitement avec l'ajout ou non de bicarbonate par voie intraveineuse). DISCUSSION: Le TMP/SMX demeure la thérapie de première intention chez les patients infectés par le VIH et souffrant de PPC, malgré une fréquence élevée d'effets toxiques chez ces patients. En plus des cas signalés dans cet article, seuls deux autres cas d'acidose métabolique associée à l'utilisation du TMP/SMX ont été publiés dans la documentation scientifique. Le mécanisme précis de cet effet indésirable n'est pas entièrement compris, bien qu'on pense qu'une acidose tubulaire rénale induite par le TMP/SMX puisse être en cause. CONCLUSIONS: Les auteurs suggèrent qu'une toxicité associée au TMP/SMX devrait être considérée lors du diagnostic différentiel chez les patients infectés par le VIH qui présentent une acidose métabolique aigue. Quand une acidose métabolique se développe, on peut s'attendre à sa correction peu de temps après l'arrêt du médicament.
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Petrovic, Snezana, Zhaohui Wang, Liyun Ma i Manoocher Soleimani. "Regulation of the apical Cl−/HCO 3 − exchanger pendrin in rat cortical collecting duct in metabolic acidosis". American Journal of Physiology-Renal Physiology 284, nr 1 (1.01.2003): F103—F112. http://dx.doi.org/10.1152/ajprenal.00205.2002.
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Pendrin is an apical Cl−/OH−/HCO[Formula: see text] exchanger in β-intercalated cells (β-ICs) of rat and mouse cortical collecting duct (CCD). However, little is known about its regulation in acid-base disorders. Here, we examined the regulation of pendrin in metabolic acidosis, a condition known to decrease HCO[Formula: see text]secretion in CCD. Rats were subjected to NH4Cl loading for 4 days, which resulted in metabolic acidosis. Apical Cl−/HCO[Formula: see text] exchanger activity in β-ICs was determined as amplitude and rate of intracellular pH change when Cl was removed in isolated, microperfused CCDs. Intracellular pH was measured by single-cell digital ratiometric imaging using fluorescent pH-sensitive dye 2′,7′-bis-(3-carboxypropyl)-5-(and-6)-carboxyfluorescein-AM. Pendrin mRNA expression in kidney cortex was examined by Northern blot hybridizations. Expression of pendrin protein was assessed by indirect immunofluorescence. Microperfused CCDs isolated from acidotic rats demonstrated ∼60% reduction in apical Cl−/HCO[Formula: see text] exchanger activity in β-ICs ( P < 0.001 vs. control). Northern blot hybridizations indicated that the mRNA expression of pendrin in kidney cortex decreased by 68% in acidotic animals ( P < 0.02 vs. control). Immunofluorescence labeling demonstrated significant reduction in pendrin expression in CCDs of acidotic rats. We conclude that metabolic acidosis decreases the activity of the apical Cl−/HCO[Formula: see text] exchanger in β-ICs of the rat CCD by reducing the expression of pendrin. Adaptive downregulation of pendrin in metabolic acidosis indicates the important role of this exchanger in acid-base regulation in the CCD.
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Peng, Hu, Jeffrey M. Purkerson, Andy L. Schwaderer i George J. Schwartz. "Metabolic acidosis stimulates the production of the antimicrobial peptide cathelicidin in rabbit urine". American Journal of Physiology-Renal Physiology 313, nr 5 (1.11.2017): F1061—F1067. http://dx.doi.org/10.1152/ajprenal.00701.2016.
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Intercalated cells of the collecting duct (CD) are critical for acid-base homeostasis and innate immune defense of the kidney. Little is known about the impact of acidosis on innate immune defense in the distal nephron. Urinary tract infections are mainly due to Escherichia coli and are an important risk factor for development of chronic kidney disease. While the effect of urinary pH on growth of E. coli is well established, in this study, we demonstrate that acidosis increases urine antimicrobial activity due, at least in part, to induction of cathelicidin expression within the CD. Acidosis was induced in rabbits by adding NH4Cl to the drinking water and reducing food intake over 3 days or by casein supplementation. Microdissected CDs were examined for cathelicidin mRNA expression and antimicrobial activity, and cathelicidin protein levels in rabbit urine were measured. Cathelicidin expression in CD cells was detected in kidney sections. CDs from acidotic rabbits expressed three times more cathelicidin mRNA than those isolated from normal rabbits. Urine from acidotic rabbits had significantly more antimicrobial activity (vs. E. coli) than normal urine, and most of this increased activity was blocked by cathelicidin antibody. The antibody had little effect on antimicrobial activity of normal urine. Urine from acidotic rabbits had at least twice the amount of cathelicidin protein as did normal urine. We conclude that metabolic acidosis not only stimulates CD acid secretion but also induces expression of cathelicidin and, thereby, enhances innate immune defense against urinary tract infections via induction of antimicrobial peptide expression.
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Stecyk, Jonathan A. W., Bent C. Larsen i Göran E. Nilsson. "Intrinsic contractile properties of the crucian carp (Carassius carassius) heart during anoxic and acidotic stress". American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 301, nr 4 (październik 2011): R1132—R1142. http://dx.doi.org/10.1152/ajpregu.00372.2010.
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The crucian carp ( Carassius carassius ) seems unique among vertebrates in its ability to maintain cardiac performance during prolonged anoxia. We investigated whether this phenomenon arises in part from a myocardium tolerant to severe acidosis or because the anoxic crucian carp heart may not experience a severe extracellular acidosis due to the fish's ability to convert lactate to ethanol. Spontaneously contracting heart preparations from cold-acclimated (6–8°C) carp were exposed (at 6.5°C) to graded or ungraded levels of acidosis under normoxic or anoxic conditions and intrinsic contractile performance was assessed. Our results clearly show that the carp heart is tolerant of acidosis as long as oxygen is available. However, heart rate and contraction kinetics of anoxic hearts were severely impaired when extracellular pH was decreased below 7.4. Nevertheless, the crucian carp heart was capable of recovering intrinsic contractile performance upon reoxygenation regardless of the severity of the anoxic + acidotic insult. Finally, we show that increased adrenergic stimulation can ameliorate, to a degree, the negative effects of severe acidosis on the intrinsic contractile properties of the anoxic crucian carp heart. Combined, these findings indicate an avoidance of severe extracellular acidosis and adrenergic stimulation are two important factors protecting the intrinsic contractile properties of the crucian carp heart during prolonged anoxia, and thus likely facilitate the ability of the anoxic crucian carp to maintain cardiac pumping.
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Riemann, Anne, Mandy Rauschner, Sarah Reime i Oliver Thews. "The Role of microRNAs in Gene Expression and Signaling Response of Tumor Cells to an Acidic Environment". International Journal of Molecular Sciences 24, nr 23 (29.11.2023): 16919. http://dx.doi.org/10.3390/ijms242316919.
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Many tumors are characterized by marked extracellular acidosis due to increased glycolytic metabolism, which affects gene expression and thereby tumor biological behavior. At the same time, acidosis leads to altered expression of several microRNAs (Mir7, Mir183, Mir203, Mir215). The aim of this study was to analyze whether the acidosis-induced changes in cytokines and tumor-related genes are mediated via pH-sensitive microRNAs. Therefore, the expression of Il6, Nos2, Ccl2, Spp1, Tnf, Acat2, Aox1, Crem, Gls2, Per3, Pink1, Txnip, and Ypel3 was examined in acidosis upon simultaneous transfection with microRNA mimics or antagomirs in two tumor lines in vitro and in vivo. In addition, it was investigated whether microRNA expression in acidosis is affected via known pH-sensitive signaling pathways (MAPK, PKC, PI3K), via ROS, or via altered intracellular Ca2+ concentration. pH-dependent microRNAs were shown to play only a minor role in modulating gene expression. Individual genes (e.g., Ccl2, Txnip, Ypel3) appear to be affected by Mir183, Mir203, or Mir215 in acidosis, but these effects are cell line-specific. When examining whether acid-dependent signaling affects microRNA expression, it was found that Mir203 was modulated by MAPK and ROS, Mir7 was affected by PKC, and Mir215 was dependent on the intracellular Ca2+ concentration. Mir183 could be increased by ROS scavenging. These correlations could possibly result in new therapeutic approaches for acidotic tumors.
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Krieger, Nancy S., i David A. Bushinsky. "Metabolic acidosis regulates RGS16 and G protein signaling in osteoblasts". American Journal of Physiology-Renal Physiology 321, nr 4 (1.10.2021): F424—F430. http://dx.doi.org/10.1152/ajprenal.00166.2021.
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The results presented in this study indicate that regulation of regulator of G protein signaling 16 and G protein signaling in the osteoblast plays an important role in modulating the response of osteoblastic ovarian cancer G protein-coupled receptor 1 (OGR1) to metabolic acidosis and the subsequent stimulation of osteoclastic bone resorption. Further characterization of the regulation of OGR1 in metabolic acidosis-induced bone resorption will help in understanding bone loss in acidotic patients with chronic kidney disease.
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Klein, Janet D., Patricia Rouillard, Brian R. Roberts i Jeff M. Sands. "Acidosis Mediates the Upregulation of UT-A Protein in Livers from Uremic Rats". Journal of the American Society of Nephrology 13, nr 3 (marzec 2002): 581–87. http://dx.doi.org/10.1681/asn.v133581.
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ABSTRACT. Liver expresses a 49-kD UT-A protein whose abundance is increased by uremia. Chronic renal failure causes acidosis; therefore, the role of acidosis in increasing UT-A abundance was tested. Rats underwent 5/6 nephrectomy, and half were given bicarbonate mixed in their food. Bicarbonate administration significantly increased blood pH. Compared with sham-operated rats, UT-A protein abundance was significantly increased by 50% in livers from uremic, acidotic rats; bicarbonate administration prevented the increase in UT-A protein. To determine whether acidosis alone would increase UT-A protein in liver, rats were made acidotic, but not uremic, by feeding them HCl. HCl-feeding significantly lowered blood pH, increased urea excretion, and increased the abundance of the 49-kD liver UT-A protein by 36% compared with pair-fed nonacidotic rats. HCl-feeding significantly increased the abundance of the 117-kD UT-A1 protein in kidney inner medulla but did not change aquaporin-2 protein. Next, rats were fed urea to determine whether elevated blood urea would increase UT-A protein. However, urea feeding had no effect on UT-A in liver or kidney inner medulla. It was, therefore, concluded that acidosis, either directly or through a change in ammonium concentration, rather than other dietary components, stimulates the upregulation of UT-A protein in liver and kidney inner medulla.
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Ramakrishnan, R., M. Y. Nazer, N. Suthanthirarajan i A. Namasivayam. "An Experimental Analysis of the Catecholamines in Hyperglycemia and Acidosis-Induced Rat Brain". International Journal of Immunopathology and Pharmacology 16, nr 3 (wrzesień 2003): 233–39. http://dx.doi.org/10.1177/039463200301600308.
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Hyperglycemia and acidosis are the hallmarks of diabetes. Since these factors play an important role in diabetic complications, we have studied the brain catecholamine levels in hyperglycemic and acidotic conditions per se. Experimentally induced hyperglycemia and acidosis are accompanied by significant alterations in the catecholamine levels in discrete areas of the brain. We and others have shown that chronic or acute diabetes in animals, as well as in humans results in altered neurotransmitter levels. In the present study, hyperglycemia maintained by daily external administration of glucose for thirty days showed increased level of dopamine in striatum and hippocampus, elevation of norepinephrine in hippocampus, and increased level of epinephrine in hypothalamus, midbrain and pons medulla. The ammonium chloride induced acidosis demonstrated significant elevation of dopamine in midbrain and significant increase of norepinephrine in hypothalamus and midbrain, and increased level of epinephrine in hypothalamus, pons medulla and cerebral cortex. On the other hand, sodium acetoacetate induced acidosis did not show any significant change in the level of catecholamines in any of the areas studied. In conclusion, the changes in catecholamine levels observed in experimentally induced hyperglycemic as well as in acidotic conditions are closely related to the changes observed in spontaneous or alloxan or streptozotocin diabetic animals, thereby suggesting that these conditions may be responsible for the changes observed in diabetic animals.
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Harlin, Cindy A., James M. Tucker, Cary L. Winkler, Brenda Henson i Charles R. Parker. "Altered adrenal steroid production in term infants having respiratory acidosis". Acta Endocrinologica 128, nr 2 (luty 1993): 136–39. http://dx.doi.org/10.1530/acta.0.1280136.
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Prior studies have provided evidence for reduced fetal adrenal production of dehydroepiandrosterone sulfate and normal or increased production of cortisol in association with pregnancy complications believed to result in fetal stress. In the present study, we sought to determine the status of adrenal steroidogenesis in 36 term infants having respiratory acidosis and to compare acidotic infants to (i) non-acidotic infants matched for pregnancy complications, gestational age, and method and indications for delivery (control infants), and (ii) non-acidotic infants of non-complicated pregnancies who were also matched for gestational age and delivery method (normal infants). Umbilical cord serum levels of dehydroepiandrosterone sulfate were lowest in acidotic infants, intermediate in the condition matched control infants and highest in the non-acidotic infants of normal pregnancies. On the other hand, cortisol levels were highest in acidotic infants, intermediate in control infants and lowest in the normal infants. These data suggest that various pregnancy complications give rise to significant alterations in adrenal steroidogenesis (decreased dehydroepiandrosterone sulfate and increased cortisol). Intrauterine deterioration during labor with resultant respiratory acidosis has an additional effect on fetal adrenal function.
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Johnson, David. "Acidosis". Nephrology 11 (kwiecień 2006): S33. http://dx.doi.org/10.1111/j.1440-1797.2006.00606.x.
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May, R. C., Y. Hara, R. A. Kelly, K. P. Block, M. G. Buse i W. E. Mitch. "Branched-chain amino acid metabolism in rat muscle: abnormal regulation in acidosis". American Journal of Physiology-Endocrinology and Metabolism 252, nr 6 (1.06.1987): E712—E718. http://dx.doi.org/10.1152/ajpendo.1987.252.6.e712.
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Branched-chain amino acid (BCAA) metabolism is frequently abnormal in pathological conditions accompanied by chronic metabolic acidosis. To study how metabolic acidosis affects BCAA metabolism in muscle, rats were gavage fed a 14% protein diet with or without 4 mmol NH4Cl X 100 g body wt-1 X day-1. Epitrochlearis muscles were incubated with L-[1-14C]-valine and L-[1-14C]leucine, and rates of decarboxylation, net transamination, and incorporation into muscle protein were measured. Plasma and muscle BCAA levels were lower (P less than 0.05) in acidotic rats. Rates of valine and leucine decarboxylation and net transamination were higher (P less than 0.05) in muscles from acidotic rats; these differences were associated with a 79% increase in the total activity of branched-chain alpha-keto acid dehydrogenase and a 146% increase in the activated form of the enzyme. We conclude that acidosis affects the regulation of BCAA metabolism by enhancing flux through the transaminase and by directly stimulating oxidative catabolism through activation of branched-chain alpha-keto acid dehydrogenase.
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Nissim, I., C. Cattano, Z. Lin i I. Nissim. "Acid-base regulation of hepatic glutamine metabolism and ureagenesis: study with 15N." Journal of the American Society of Nephrology 3, nr 7 (styczeń 1993): 1416–27. http://dx.doi.org/10.1681/asn.v371416.
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The metabolism of (5-15N)glutamine and (2-15N) glutamine has been studied by isolated hepatocytes obtained from either control, chronically acidotic, or alkalotic rats. The main goal was to elucidate the mechanism(s) by which altered acid-base state affects hepatic ureagenesis from glutamine. Isolated hepatocytes were incubated in Krebs buffer (pH 7.4) supplemented with 0.1 mM ornithine plus either 1 mM (5-15N)glutamine or (2-15N)glutamine. To elucidate the role of glutamine cycling in net ammonia metabolism, a separate series of experiments were performed with 1 mM unlabeled glutamine plus 1 mM (15N)H4Cl. Net glutamine utilization was significantly lower in hepatocytes obtained from chronically acidotic rats compared with control or alkalotic rats. The sum of the rates of 15NH3 and (15N)urea production from (5-15N)glutamine was decreased in acidosis compared with alkalosis. After incubations of 50 min, approximately 75, 65, or 90% of the N in carbamoyl-phosphate was derived from the 5-N of glutamine in control, acidosis, or alkalosis respectively. In experiments with (2-15N)glutamine, the production of singly and doubly labeled (15N)urea as well as (15N)aspartate and (15N)H3 was significantly smaller in acidosis compared with alkalosis. Furthermore, a correlation was observed between production rates of (15N)aspartate and (15N)urea, suggesting that alterations in urea production may depend on aspartate formed from glutamine. However, the production of (15N)alanine was higher in acidosis compared with alkalosis with apparent correlation between the production of (15N)alanine and 2-oxoglutaramate, a product of the glutamine aminotransferase pathway. In addition, the rate of glutamine recycling was significantly higher in acidosis compared with control or alkalosis, indicating that both flux through glutamine aminotransferase and flux through glutamine synthetase were elevated in acidosis compared with alkalosis. These data suggest that decreased formation of aspartate from glutamine may limit ureagenesis in chronic metabolic acidosis. The formation of aspartate may depend on the availability of oxaloacetate rather than diminished flux through transaminase reaction. The enhancement of alanine production and glutamine synthesis may provide an alternate route of N disposal in cases of diminished urea formation.
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Almond, M. K., A. Smith, R. D. Cohen, R. A. Iles i G. Flynn. "Substrate and pH effects on glutamine synthesis in rat liver. Consequences for acid-base regulation". Biochemical Journal 278, nr 3 (15.09.1991): 709–14. http://dx.doi.org/10.1042/bj2780709.
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Switching in acidosis of hepatic nitrogen disposal from urea synthesis to NH4+ and net glutamine production was demonstrated in the isolated perfused livers of starved male Wistar rats. Lactate was preferred to glucose as the substrate for the carbon skeleton of glutamine synthesized over the pH range 6.9-7.5. This is necessary if the switch away from a proton-producing process (ureagenesis) in acidosis is to constitute an acid-base regulating system intrinsic to the liver. Glutamine balance shifted with pH from marked net uptake to small net output under acidotic conditions (pH 7.5-6.9), an effect due solely to a decrease in glutamine uptake. NH4+ uptake by the liver had a linear relationship with pH, being markedly decreased in acidosis because glutamine synthesis was insufficient to compensate for the decreased incorporation into urea. Animals rendered chronically acidotic showed a lower central venous plasma urea concentration and a raised NH4+ concentration, but their livers synthesized no more glutamine when perfused at an acidotic pH than did normal livers. We conclude that perivenous hepatocytes may not be efficient scavengers of NH4+ ions, which must be partly disposed of elsewhere by non-proton-generating pathways if inhibition of ureagenesis is to represent a hepatic acid-base regulating system.
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Barclay, J. K., T. E. Graham, B. R. Wolfe, J. Van Duk i B. A. Wilson. "Effect of acidosis on skeletal muscle metabolism with and without propranolol". Canadian Journal of Physiology and Pharmacology 68, nr 7 (1.07.1990): 870–76. http://dx.doi.org/10.1139/y90-132.
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Does the stimulatory effect of circulating catecholamines counteract the inhibitory effect of acidosis on skeletal muscle metabolism? To investigate this possibility, we studied gastrocnemii in dogs breathing either air (n = 10) or 4% carbon dioxide in air (n = 10) at rest and during contractions. In five dogs from each group, we infused propranolol into the arterial supply of the right and left muscles for 40 min. After 30 min of infusion, the left muscle was stimulated at 3 Hz for 10 min. During the 10th min of contractions, we removed and froze both muscles in liquid nitrogen. Oxygen uptake and blood flow to the left muscle prior to or during stimulation was not affected by acidosis either with or without propranolol. Glycogen concentration in resting muscle was unaffected by acidosis with or without propranolol. There was an acidosis related decrease of approximately 50% in the glycolytic intermediates (glucose 6-phosphate, fructose 1,6-diphosphate, α-glycerol phosphate, and dihydroxyacetone phosphate) in unstimulated muscles without β-blockade. At rest, acidosis decreased muscle lactate by 50% with and 64% without propranolol, but lactate release was decreased only with acidosis without propranolol (1.4–0.1 μmol/kg∙s). Acidosis without propranolol had no effect on the changes in glycogen concentration or the change in the concentration of glycolytic intermediates resulting from contractions. In β-blocked muscle, the difference between stimulated and unstimulated concentrations of glycogen and glycolytic intermediates including lactate was 20–50% smaller with acidosis. Thus, with β-blockade, the acidotic effects at rest disappeared and an inhibition of the metabolic adjustment to contractions appeared, indicating that circulating catecholamines do modify some metabolic effects of acidosis.Key words: oxidative muscle, glycogen, lactate efflux, glycolytic intermediates, β-blockade.
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Hall, K., P. Forrest i C. Sawyer. "The Effects of Acidosis and Hypothermia on Blood Transfusion Requirements following Factor VII Administration". Anaesthesia and Intensive Care 35, nr 4 (sierpień 2007): 494–97. http://dx.doi.org/10.1177/0310057x0703500405.
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While there is laboratory evidence that the activity of recombinant activated factor VII (rFVIIa) is reduced by the presence of acidosis and hypothermia, there is limited clinical data to support this observation. Recombinant FVIIa may be used as rescue therapy in surgical patients who have bleeding that is refractory to conventional therapy. However, these patients are also frequently acidotic and hypothermic at the time the drug is administered. In this retrospective study, the records of 38 adult surgical patients who received rFVIIa intraoperatively or within six hours postoperatively were reviewed. The requirements for red cell transfusion in the two hours following the administration of rFVIIa and the need for repeated doses of rFVIIa were recorded. The relationship between red cell transfusion and pH and temperature of the patient at the time of rFVIIa administration was assessed by multiple regression analysis. The major finding was an inverse relationship between the degree of acidosis at the time of rFVIIa administration and the requirement for either subsequent blood transfusion or repeat dosing of rFVIIa (P=0.003 and P <0.001 respectively). For patients with apH <7.2 vs. pH >7.2, the odds ratio for receiving two or more packs of red blood cells within two hours of rFVIIa administration was 15:1. This effect was not observed for hypothermia. The implication of this study is that rFVIIa may be less effective when administered to severely acidotic patients. Further studies are required to examine whether this is related to the acidosis directly, or is secondary to other intraoperative variables affecting acidosis. The clinical utility of rFVIIa in acidotic patients also requires further investigation.
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Sikter, Andras, Ede Frecska, Ivan Mario Braun, Xenia Gonda i Zoltan Rihmer. "The role of hyperventilation: hypocapnia in the pathomechanism of panic disorder". Revista Brasileira de Psiquiatria 29, nr 4 (27.06.2007): 375–79. http://dx.doi.org/10.1590/s1516-44462006005000048.
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OBJECTIVE: The authors present a profile of panic disorder based on and generalized from the effects of acute and chronic hyperventilation that are characteristic of the respiratory panic disorder subtype. The review presented attempts to integrate three premises: hyperventilation is a physiological response to hypercapnia; hyperventilation can induce panic attacks; chronic hyperventilation is a protective mechanism against panic attacks. METHOD: A selective review of the literature was made using the Medline database. Reports of the interrelationships among panic disorder, hyperventilation, acidosis, and alkalosis, as well as catecholamine release and sensitivity, were selected. The findings were structured into an integrated model. DISCUSSION: The panic attacks experienced by individuals with panic disorder develop on the basis of metabolic acidosis, which is a compensatory response to chronic hyperventilation. The attacks are triggered by a sudden increase in (pCO2) when the latent (metabolic) acidosis manifests as hypercapnic acidosis. The acidotic condition induces catecholamine release. Sympathicotonia cannot arise during the hypercapnic phase, since low pH decreases catecholamine sensitivity. Catecholamines can provoke panic when hyperventilation causes the hypercapnia to switch to hypocapnic alkalosis (overcompensation) and catecholamine sensitivity begins to increase. CONCLUSION: Therapeutic approaches should address long-term regulation of the respiratory pattern and elimination of metabolic acidosis.
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Sundset, Rune, Geir Bertelsen i Kirsti Ytrehus. "Role of the Na+H+ exchanger (NHE1) in heart muscle function during transient acidosis. A study in papillary muscles from rat and guinea pig hearts". Canadian Journal of Physiology and Pharmacology 81, nr 10 (1.10.2003): 937–43. http://dx.doi.org/10.1139/y03-091.
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The sodiumhydrogen exchanger (NHE) helps the cell to recover from intracellular acidosis. In this study, we have investigated the effect of HOE 642 (a specific NHE1 blocker) on papillary muscles from rats and guinea pigs during transient acidosis and PKC activation by recording developed force (DF), action potential characteristics, and electrical conductance (stimulusresponse interval). Two protocols were used, with or without HOE 642 (105 mol/L): papillary muscle was exposed (i) for 15 min to a glucose-free, nonoxygenated HEPES buffer containing lactate (20 mmol/L) (pH 6.8) followed by 15 min recovery or (ii) to a PKC activator (phorbolmyristate acetate (PMA) (109 mol/L)) for 30 min. The DF after acidification remained significantly decreased in the NHE-blocked papillary muscles. During recovery from acidosis, papillary muscles exposed to HOE 642 remained at a higher electrical resistance. The present study shows that post-acidotic continued depression of DF and change in tissue electrophysiological properties might occur as a result of blocking the NHE. During infarct development, the tissue-protecting effect of NHE blockade has been well documented. When acidosis or reduced contractile function is present, however, blocking NHE by HOE 642 might not improve the situation.Key words: sodiumhydrogen exchange (NHE), HOE 642 (cariporide), gap junction, PKC, acidosis.
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Robergs, Robert, Keith Hutchinson, Shonn Hendee, Sean Madden i Jason Siegler. "Influence of Pre-Exercise Acidosis and Alkalosis on the Kinetics of Acid-Base Recovery Following Intense Exercise". International Journal of Sport Nutrition and Exercise Metabolism 15, nr 1 (luty 2005): 59–74. http://dx.doi.org/10.1123/ijsnem.15.1.59.
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The purpose of this study was to measure the recovery kinetics of pH and lactate for the conditions of pre-exercise acidosis, alkalosis, and placebo states. Twelve trained male cyclists completed 3 exercise trials (110% workload at VO2max), ingesting either 0.3 g/kg of NH4Cl (ACD), 0.2 g/kg of Na+HCO3- and 0.2 g/kg of sodium citrate (ALK), or a placebo (calcium carbonate) (PLAC). Blood samples (heated dorsal hand vein) were drawn before, during, and after exercise. Exercise-induced acidosis was more severe in the ACD and PLAC trials (7.15 ± 0.06, 7.21 ± 0.07, 7.16 ± 0.06, P < 0.05, for ACD, ALK, PLAC, respectively). Recovery kinetics for blood pH and lactate, as assessed by the monoexponential slope constant, were not different between trials (0.057 ± 0.01, 0.050 ± 0.01, 0.080 ± 0.02, for ACD, ALK, PLAC, respectively). Complete recovery of blood pH from metabolic acidosis can take longer than 45 min. Such a recovery profile is nonlinear, with 50% recovery occurring in approximately 12 min. Complete recovery of blood lactate can take longer than 60 min, with 50% recovery occurring in approximately 30 min. Induced alkalosis decreases metabolic acidosis and improves pH recovery compared to acidodic and placebo conditions. Although blood pH and lactate are highly correlated during recovery from acidosis, they recover at significantly different rates.
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Lemieux, G., C. Lemieux, S. Duplessis i J. Berkofsky. "Metabolic characteristics of cat kidney: failure to adapt to metabolic acidosis". American Journal of Physiology-Regulatory, Integrative and Comparative Physiology 259, nr 2 (1.08.1990): R277—R281. http://dx.doi.org/10.1152/ajpregu.1990.259.2.r277.
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During studies performed on domestic cats made acidotic with ammonium chloride, it was found that the cat kidney is unable to adapt to metabolic acidosis. Renal proximal tubules do not increase their production of ammonia or glucose from glutamine during acidosis. During in vivo studies, the renal excretion of ammonia did not change much during acidosis. Other metabolic parameters in the cat were not very different from those found in other animals such as rat or dog. However, it was found that cats may show a relatively high plasma glucose concentration compared with other animals. Plasma insulin concentration was normal, and the animals showed no evidence of diabetes mellitus. It is not known whether limitation of ammoniagenesis and elevated plasma glucose concentration also characterize larger felidae such as panthers and cougars.
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Reaich, D., S. M. Channon, C. M. Scrimgeour i T. H. Goodship. "Ammonium chloride-induced acidosis increases protein breakdown and amino acid oxidation in humans". American Journal of Physiology-Endocrinology and Metabolism 263, nr 4 (1.10.1992): E735—E739. http://dx.doi.org/10.1152/ajpendo.1992.263.4.e735.
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The effect of acidosis on whole body protein turnover was determined from the kinetics of infused L-[1-13C]leucine. Seven healthy subjects were studied before (basal) and after (acid) the induction of acidosis with 5 days oral ammonium chloride (basal pH 7.42 +/- 0.01, acid pH 7.35 +/- 0.03). Bicarbonate recovery, measured from the kinetics of infused NaH13CO3, was increased in the acidotic state (basal 72.9 +/- 1.2 vs. acid 77.6 +/- 1.6%; P = 0.06). Leucine appearance from body protein (PD), leucine disappearance into body protein (PS), and leucine oxidation (O) increased significantly (PD: basal 120.5 +/- 5.6 vs. acid 153.9 +/- 6.2, P < 0.01; PS: basal 98.8 +/- 5.6 vs. acid 127.0 +/- 4.7, P < 0.01; O: basal 21.6 +/- 1.1 vs. acid 26.9 +/- 2.3 mumol.kg-1.h-1, P < 0.01). Plasma levels of the amino acids threonine, serine, asparagine, citrulline, valine, leucine, ornithine, lysine, histidine, arginine, and hydroxyproline increased significantly with the induction of acidosis. These results confirm that acidosis in humans is a catabolic factor stimulating protein degradation and amino acid oxidation.
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Merle, Evan, Saad Zaatari, Rory Spiegel i Mabrouk Bahloul. "Is It the pH That Matters? Challenging the Pathophysiology of Acidemia in a Case of Severe Hypercapnia Secondary to Intraoperative CO2 Insufflation". Case Reports in Critical Care 2020 (27.09.2020): 1–4. http://dx.doi.org/10.1155/2020/1898759.
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Background. Acidemia has been long thought to lead to hemodynamic compromise. While some literature to date challenges this idea, there is no consensus on this topic. Case Summary. To our knowledge, this is the most severe case of hypercapnia and acidosis due to carbon dioxide (CO2) insufflation during laparoscopy reported in the literature. Remarkably, this patient remained hemodynamically normal despite having a blood pH below 6.81. This prompts a wider discussion about the effects of blood pH on human physiology. Most patients who present acidotic are critically ill and have confounding underlying metabolic or respiratory pathophysiology driving their illness. In this case, the patient experienced no respiratory insult leading to an increase in blood CO2 but rather had CO2 iatrogenically introduced into the circulatory system, effectively detaching the deleterious effects of CO2 from the respiratory pathologies that so often cause its accumulation. Conclusion. This raises the question, in patients with severe acidosis and hemodynamic compromise, is acidosis a symptom of the underlying process, or is the acidosis itself causing harm?
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Wang, Tong, Allan L. Egbert, Peter S. Aronson i Gerhard Giebisch. "Effect of metabolic acidosis on NaCl transport in the proximal tubule". American Journal of Physiology-Renal Physiology 274, nr 6 (1.06.1998): F1015—F1019. http://dx.doi.org/10.1152/ajprenal.1998.274.6.f1015.
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In metabolic acidosis, the capacity of the proximal tubule for bicarbonate absorption is enhanced, whereas NaCl reabsorption is inhibited. Recent evidence indicates that transcellular NaCl absorption in the proximal tubule is mediated by apical membrane Cl−/formate exchange and Cl−/oxalate exchange, in parallel with recycling of these organic anions. We evaluated whether the effect of metabolic acidosis to inhibit NaCl reabsorption in the proximal tubule is due at least in part to inhibition of organic anion-dependent NaCl transport in this nephron segment. Absorption rates of bicarbonate ([Formula: see text]), chloride ( J Cl), and fluid ( J v) were measured in rat proximal tubule segments microperfused in situ. We confirmed that metabolic acidosis stimulates[Formula: see text]in tubules microperfused with 25 mM[Formula: see text], pH 7.4. For measurements of J Cl, tubules were microperfused with a low-bicarbonate (5 mM), high-chloride solution, simulating conditions in the late proximal tubule. Under these conditions, baseline J Cl and J v measured in the absence of formate and oxalate were not significantly different between control and acidotic rats. However, whereas addition of 50 μM formate or 1 μM oxalate to luminal and capillary perfusates markedly stimulated J Cland J v in control rats, formate and oxalate failed to stimulate J Cl and J v in acidotic rats. We conclude that metabolic acidosis markedly downregulates organic anion-stimulated NaCl absorption, thereby allowing differential regulation of proximal tubule NaHCO3 and NaCl transport.
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Gil, F. Zaladek, V. L. Costa Silva i M. F. Cavanal. "Effect of aluminium on urinary acidification in the rat: influence of parathyroid hormone". Clinical Science 81, s25 (1.10.1991): 465–70. http://dx.doi.org/10.1042/cs0810465.
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1. The influence of thyroparathyroidectomy and/or acidosis on renal function and specifically on acid excretion was studied in rats treated with a cumulative dose of 2 mg of aluminium. 2. Aluminium-treated and non-treated thyroparathyroidectomized rats showed a significant decrease in glomerular filtration rate and in the urinary/plasma inulin ratio without alteration in net acid excretion. 3. Non-treated thyroparathyroidectomized acidotic rats showed a significant fall in the amount of ammonium excreted and in overall acid excretion, suggesting that parathyroid hormone participates in an important way in the defence against metabolic acidosis. 4. The effects of acidosis, thyroparathyroidectomy and aluminium treatment on renal function parameters were not additive, suggesting a common final mechanism. In normal or acidotic aluminium-treated rats, thyroparathyroidectomy had no effect on renal acid excretion, suggesting that aluminium even in low doses inhibited the action of PTH on the renal tubule. 5. After exposure to aluminium, the relative inhibition of PTH on the renal tubule may become an additional factor that could contribute to the worsening of clinical conditions in which an inappropriate retention of acid loads can occur.
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AOTA, S., K. D. HOLMGREN, P. GALLAUGHER i D. J. RANDALL. "A Possible Role for Catecholamines in the Ventilatory Responses Associated with Internal Aciosis or External Hypoxia in Rainbow Trout Oncorhynchus Mykiss". Journal of Experimental Biology 151, nr 1 (1.07.1990): 57–70. http://dx.doi.org/10.1242/jeb.151.1.57.
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Plasma catecholamine levels and gill ventilation were measured in rainbow trout (Oncorhynchus mykiss) during acidosis and hypoxia. There was an increase in both plasma catecholamines and ventilation correlated with the acidosis. Fish exposed to hyperoxia prior to acid infusion did not show significant changes in catecholamines or ventilation. Those treated with the β-adrenergic antagonist propranolol before acidosis showed increases in catecholamines but not ventilation. Hypoxia was also associated with increases in endogenous catecholamines and ventilation, and the increase in ventilation could be partially blocked with propranolol. This increase in ventilation during hypoxia was not inhibited by asaline injection alone. It is proposed that catecholamines act to modulate ventilatory responses in fish under both acidotic and hypoxic conditions. If a central H+ chemoreceptor exists in fish to control breathing, it can be inhibited by hyperoxia or by β-receptor blockade.
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Purkerson, Jeffrey M., Eric V. Heintz, Aya Nakamori i George J. Schwartz. "Insights into acidosis-induced regulation of SLC26A4 (pendrin) and SLC4A9 (AE4) transporters using three-dimensional morphometric analysis of β-intercalated cells". American Journal of Physiology-Renal Physiology 307, nr 5 (1.09.2014): F601—F611. http://dx.doi.org/10.1152/ajprenal.00404.2013.
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The purpose of this study was to examine the three-dimensional (3-D) expression and distribution of anion transporters pendrin (SLC26A4) and anion exchanger (AE)4 (SLC4A9) in β-intercalated cells (β-ICs) of the rabbit cortical collecting duct (CCD) to better characterize the adaptation to acid-base disturbances. Confocal analysis and 3-D reconstruction of β-ICs, using identifiers of the nucleus and zona occludens, permitted the specific orientation of cells from normal, acidotic, and recovering rabbits, so that adaptive changes could be quantified and compared. The pendrin cap likely mediates apical Cl−/HCO3− exchange, but it was also found beneath the zona occludens and in early endosomes, some of which may recycle back to the apical membrane via Rab11a+ vesicles. Acidosis reduced the size of the pendrin cap, observed as a large decrease in cap volume above and below the zona occludens, and the volume of the Rab11a+ apical recycling compartment. Correction of the acidosis over 12–18 h reversed these changes. Consistent with its proposed function in the basolateral exit of Na+ via Na+-HCO3− cotransport, AE4 was expressed as a barrel-like structure in the lateral membrane of β-ICs. Acidosis reduced AE4 expression in β-ICs, but this was rapidly reversed during the recovery from acidosis. The coordinate regulation of pendrin and AE4 during acidosis and recovery is likely to affect the magnitude of acid-base and possibly Na+ transport across the CCD. In conclusion, acidosis induces a downregulation of AE expression in β-ICs and a diminished presence of pendrin in apical recycling endosomes.
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Gude, Vinayaka, i Steven Corns. "Integrated Deep Learning and Supervised Machine Learning Model for Predictive Fetal Monitoring". Diagnostics 12, nr 11 (17.11.2022): 2843. http://dx.doi.org/10.3390/diagnostics12112843.
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Asphyxiation associated with metabolic acidosis is one of the common causes of fetal deaths. The paper aims to develop a feature extraction and prediction algorithm capable of identifying most of the features in the SISPORTO software package and late and variable decelerations. The resulting features were used for classification based on umbilical cord pH data. The algorithms developed here were used to predict cord pH levels. The prediction system assists the obstetricians in assessing the state of the fetus better than the category methods, as only about 30% of the patients in the pathological category suffer from acidosis, while the majority of acidotic babies were in the suspect category, which is considered lower risk. By predicting the direct indicator of acidosis, umbilical cord pH, this work demonstrates a methodology, which uses fetal heart rate and uterine activity, to identify acidosis. This paper introduces a forecasting model based on deep learning to predict heart rate and uterine contractions, integrated with the classification algorithm, resulting in a robust tool for predictive fetal monitoring. The hybrid algorithm resulted in a model capable of providing future conditions of the fetus, which obstetricians can use for diagnosis and planning interventions. The ensemble classification algorithm had a test accuracy of 85% (n = 24) in predicting fetal acidosis on the features extracted from the cardiotocography data. When integrated with the classification model, the results from the prediction model (long short-term memory network) can effectively identify fetal acidosis 2 or 4 min in the future.
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Preti, Beatrice, Jasna Deluce i Siddhartha Srivastava. "Type B Lactic Acidosis in a Solid-Tumour Malignancy Without Liver Metastases". Canadian Journal of General Internal Medicine 16, nr 2 (21.06.2021): 38–42. http://dx.doi.org/10.22374/cjgim.v16i2.427.
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Malignancy-induced type B lactic acidosis is a rare, yet fascinating, cause of refractory acidosis in patients with cancer, often unresponsive to usual medical treatments. Case reports usually discuss the paraneoplastic phenomenon in hematologic malignancies; however, we present the case of a 72-year-old woman with metastatic breast cancer, who initially presented to hospital with an elevated lactate in the absence of acidosis. She appeared to improve with fluids; however, she then represented 2 weeks later with a severe metabolic acidosis and undetectable high lactate level. Ultimately, the patient did not respond well to supportive care, and the decision was made to pursue comfort-directed therapy. RésuméL’acidose lactique de type B induite par une tumeur est une cause rare, mais extrêmement intéressante, d’acidose réfractaire chez les patients cancéreux et qui, souvent, ne répond pas aux traitements médicaux habituels. Les études de cas traitent généralement du phénomène paranéoplasique des tumeurs malignes hématologiques; toutefois, nous présentons le cas d’une femme de 72 ans atteinte d’un cancer du sein métastatique, qui s’est d’abord présentée à l’hôpital pour un taux élevé de lactate dans le sang, mais sans acidose. Son état a semblé s’améliorer grâce à un apport de liquides; toutefois, elle s’est présentée de nouveau à l’hôpital deux semaines plus tard pour une acidose métabolique grave et un taux élevé de lactate indétectable. Au bout du compte, la patiente n’a pas bien répondu aux soins de soutien, et il a été décidé d’appliquer les soins de confort.