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PubMed1982

Glutamine metabolism in metabolic acidosis.

In chronic metabolic acidosis in the rat, there is increased ammoniagenesis, gluconeogenesis and renal extraction of glutamine with induction of renal phosphate-dependent glutaminase (PDG). Because the stimulus for these changes is not yet clear and also because acute acidosis is the more common clinical problem, the present study deals mainly with the metabolism of glutamine in acute metabolic acidosis. When acute metabolic acidosis is produced in rats by administration of mineral acid or by causing them to swim, thus inducing a severe lactic acidosis, a factor is found in the plasma which stimulates renal glutamine uptake and ammoniagenesis in vivo as well as in vitro. Acute acidosis does not induce synthesis of PDG in the kidney but causes a change in enzyme kinetics. The plasma factor not only enhances glutamine entry into cells, but apparently causes a conformational change in PDG, as shown by an increase in V1.0mM/Vmax. Intestinal metabolism of glutamine is also stimulated in vivo and in vitro by the plasma factor of acute acidosis.

Acidosis↗
PubMed1995

Renal tubular acidosis in the Silver-Russell syndrome.

Several patients with the Silver-Russell syndrome (SRS) attending our Genetics Clinic were diagnosed as having persistent metabolic acidosis. Since this abnormality has not been reported previously in the SRS, we reexamined 33 SRS patients to evaluate the frequency and type of metabolic acidosis, the clinical and laboratory findings, and the growth pattern in SRS patients with and without metabolic acidosis. Among them, 14 had a consistent decrease in HCO3- levels. Renal studies in acidotic patients showed urine pH of 5.8 and 24 h urine calcium of < 2.4 mg/kg/24 h; serum creatinine, excretion of glucose, and amino acids were normal, as were renal ultrasound and excretory urography findings. These data supported the diagnosis of renal tubular acidosis, probably type II; the patients were treated with oral bicarbonate and acidosis was corrected successfully. Clinical manifestations were similar in acidotic and non-acidotic patients. The nutritional indices at diagnosis and at last evaluation (at least 8 months after diagnosis) were abnormally low in all patients; however, acidotic patients, treated with bicarbonate, showed an improvement of nutritional status particularly in the weight/height index, although the difference between groups after follow-up did not reach statistical significance. We suggest that metabolic acidosis due to renal tubular acidosis, probably type II, may occur in children with the SRS and should be looked for and treated in all patients.

Abnormalities, Multiple↗
PubMed1978

[Lactic acidosis--a possible complication in buformin-treated diabetics (author's transl)].

Lactic acidosis is defined as a state of metabolic acidosis (arterial pH below 7.36) due to an increase in the blood concentration of lactate above 2 mEq/l. Lactic acidosis may occur under a variety of conditions; the biguanide-induced lactic acidosis is due to the toxic effects of biguanides (buformin, metformin, phenformin). The clinical picture is characterized by the occurrence of disturbances of consciousness, severe acidosis with Kussmaul's respiration, shock, hypothermia and in about 30% of all cases hypoglycemia. Apart from the general principles of intensive medical care, therapy should comprise correction of the acid-base-disturbances and elimination of the offending biguanide. The efficacy of hemodialysis in the treatment of biguanide-induced lactic acidosis is difficult to evaluate. By a more sensible use of biguanides, lactic acidosis secondary to drug administration should become a rare event.

Acidosis↗
PubMed1995

Colonic lactate metabolism and D-lactic acidosis.

D-Lactic acidosis is seen in patients with intestinal bypass or short bowels in whom colonic produced D-lactate accumulates. An intestinal bypassed patient with D-lactic acidosis had higher fecal D-lactate (122.4 mmol/liter) and L-lactate (90.1 mmol/liter) than described before in humans. D-Lactate fluctuated between 0.5 and 3.1 mmol/liter in plasma (normal < 0.1 mmol/liter) and between 1.1 and 52.8 mmol/liter in urine (normal < 0.7 mmol/liter) within a few hours, indicating that the human organism do metabolize and excrete D-lactate. The patient with D-lactic acidosis had a 10-fold increased DL-lactate production from glucose in fecal homogenates compared to 14 healthy controls and a patient with intestinal bypass, who did not have D-lactic acidosis. A 67% carbohydrate (starch)-enriched diet resulted in a minor elevation of fecal and plasma lactate, whereas 50 + 100 + 150 g of ingested lactose increased D-lactate in feces (84.0 mmol/liter) and plasma (2.3 mmol/liter) considerably in the patient with D-lactic acidosis. Intestinal prolongation (22 cm ileum) had a temporary effect on fecal and plasma D-lactate, but intestinal continuity was reestablished 26 months later because D-lactic acidosis recurred (plasma 8.6 mmol/liter, urine 101.3 mmol/liter). Large amounts of lactulose (160 g/day) to 12 normal individuals increased D-lactate to 13.6 +/- 3.5 mmol/liter in feces, but never increased D-lactate in plasma or urine. The in vitro fermentation of glucose in fecal homogenates increased DL-lactate, which disappeared after complete metabolization of the glucose. L-Lactate was converted to D-lactate and vice versa, and both were degraded to the short-chain fatty acids acetate, propionate, and butyrate. An infrequent, but elevated ability of the colonic flora to produce lactate may be a prerequisite for D-lactic acidosis to occur and may explain why the syndrome is so seldom seen even in patients with intestinal bypass or short bowels. The suggestion that D-lactate is not metabolized and hence accumulates is probably not valid.

Acidosis, Lactic↗
PubMed2001

Left ventricular contractility is reduced by hypercapnic acidosis and thoracolumbar epidural anesthesia in rabbits.

PURPOSE: We have previously observed that sympathetic blockade by epidural anesthesia (EA) modifies the cardiovascular response to marked hypercapnic acidosis in dogs. Our objective was to determine whether the combination of marked hypercapnic acidosis and EA reduce left ventricular contractility. METHODS: We randomly assigned 22 Japanese white rabbits anesthetized with isoflurane (1.0%) to two groups according to the absence (control group, n= 11) or presence (EA group, n= 11) of thoracolumbar EA. After epidural injection (0.5 mL.kg(-1) of 0.9% saline in the control group or 1% mepivacaine in the EA group) and during subsequent hypercapnia (mean arterial CO2 tension 85 mmHg), we measured left ventricular pressure, left ventricular volume by using conductance catheter and plasma catecholamine concentrations. Left ventricular contractility was assessed by the slope of the linear approximation of the left ventricular end-systolic pressure-volume relationship, [i.e., end-systolic elastance (Ees)]. RESULTS: The combination of hypercapnic acidosis and thoracolumbar EA caused a 65% decrease in Ees (P <0.05). Hypercapnic acidosis alone caused a 16% decrease (P <0.05) and thoracolumbar EA alone caused a 49% decrease in Ees (P <0.05). In the EA group, epidural injection caused an 85% decrease in the epinephrine concentration (P <0.05) and a 39% decrease in the norepinephrine concentration (P <0.05), even during hypercapnic acidosis. However, in the control group, hypercapnic acidosis caused no change in the circulating epinephrine concentration but a 74% increase in the circulating norepinephrine concentration (P <0.05). CONCLUSION: Combined hypercapnic acidosis and EA markedly reduce left ventricular contractility in an additive fashion in rabbits receiving general anesthesia.

Acidosis↗
PubMed1997

Acidosis alters the phosphorylation of Ser16 and Thr17 of phospholamban in rat cardiac muscle.

The effect of acidosis on the phosphorylation of Ser16 and Thr17 of phospholamban in rat cardiac muscle has been investigated using phosphorylation-site-specific antibodies to this protein. Ventricular myocytes were stimulated at 0.5 Hz for 5 min, in either control (pH 7.4) or acid (pH 6.5) physiological salt solution, in the absence or presence of isoprenaline. Site-specific phosphorylation of phospholamban was determined by Western blotting. Acidosis reduced phosphorylation of Ser16 in the absence of isoprenaline, but did not alter the isoprenaline-induced phosphorylation of Ser16. In contrast, acidosis increased Thr17 phosphorylation in the absence and presence of isoprenaline. Buffering intracellular Ca2+ ([Ca2+]i) with BAPTA inhibited the increase in Thr17 phosphorylation during acidosis but had no effect on Ser16 phosphorylation. We conclude that acidosis can alter the phosphorylation of Ser16 and Thr17 by inhibition of protein kinase A, and by an acidosis-induced increase in [Ca2+]i and the subsequent activation of a Ca2+/calmodulin-dependent protein kinase, respectively. The possible effect of these changes in phosphorylation on the activity of the Ca2+-ATPase of the cardiac sarcoplasmic reticulum during acidosis is discussed.

Acidosis↗
PubMed1998

Effect of acidosis on Ca2+-activated K+ channels in cultured porcine coronary artery smooth muscle cells.

Although acidosis induces vasodilation, the vascular responses mediated by large-conductance Ca2+-activated K+ (KCa) channels have not been investigated in coronary artery smooth muscle cells. We therefore investigated the response of porcine coronary arteries and smooth muscle cells to acidosis, as well as the role of KCa channels in the regulation of muscular tone. Acidosis (pH 7.3–6.8), produced by adding HCl to the extravascular solution, elicited concentration-dependent relaxation of precontracted, endothelium-denuded arterial rings. Glibenclamide (20 µM) significantly inhibited the vasodilatory response to acidosis (pH 7.3-6.8). Charybdotoxin (100 nM) was effective only at pH 6.9–6.8. When we exposed porcine coronary artery smooth muscle cells to a low-pH solution, KCa channel activity in cell-attached patches increased. However, pretreatment of these cells with 10 or 30 µM O, O′-bis(2-aminophenyl)ethyleneglycol-N,N,N′,N′-tetraacetic acid tetrakis(acetoxymethyl)ester (BAPTA-AM), a Ca2+ chelator for which the cell membrane is permeable, abolished the H+-mediated activation of KCa channels in cell-attached patches. Under these circumstances H+ actually inhibited KCa channel activity. When inside-out patches were exposed to a [Ca2+] of 10–6 M [adjusted with ethyleneglycolbis(β-aminoethylester)-N,N,N′,N′-tetraacetic acid (EGTA) at pH 7.3], KCa channels were activated by H+ concentration dependently. However, when these patches were exposed to a [Ca2+] of 10–6 M adjusted with BAPTA at pH 7.3, H+ inhibited KCa channel activity. Extracellular acidosis had no significant direct effect on KCa channels, suggesting that extracellular H+ exerts its effects after transport into the cell, and that KCa channels are regulated by intracellular H+ and by cytosolic free Ca2+ modulated by acute acidosis. These results indicate that the modulation of KCa channel kinetics by acidosis plays an important role in the determination of membrane potential and, hence, coronary arterial tone.

Acidosis↗
PubMed1983

Metabolic acidosis in the alcoholic: a pathophysiologic approach.

The purpose of this paper is to review the acid-base abnormalities in patients presenting with metabolic acidosis due to acute ethanol ingestion and to review the theoretical constraints on ethanol metabolism in the liver. Alcohol-induced acidosis is a mixed acid-base disturbance. Metabolic acidosis is due to lactic acidosis, ketoacidosis and acetic acidosis but the degree of each varies from patient to patient. Metabolic alkalosis is frequently present due to ethanol-induced vomiting. However, it could be overlooked because of an indirect loss of sodium bicarbonate (as sodium B-hydroxybutyrate in the urine). Nevertheless, the accompanying reduction in ECF volume may play an important role in the pathogenesis of alcoholic acidosis because it could lead to a relative insulin deficiency. Treatment of alcohol acidosis should include sodium, chloride, potassium, phosphorus, magnesium and thiamine replacements along with attention to concomitant clinical problems. Unless hypoglycemia is present, glucose need not be given immediately. We feel that insulin should be withheld unless life-threatening acidemia is present or expected. Lastly, alcohol need not be detected on admission to make the diagnosis of this metabolic disturbance. However, when present, it could contribute directly to the lactic, acetic and B-hydroxybutyric acidoses. With respect to the theoretical constraints on ethanol metabolism, it appears that "overproduction" of NADH in the liver is best averted by converting ethanol to B-hydroxybutyric acid.

Acetates↗
PubMed2005

Response of protein synthesis to hypercapnia in rats: independent effects of acidosis and hypothermia.

Acute metabolic acidosis has been shown to inhibit muscle protein synthesis, although little is known on the effect of acidosis of respiratory origin. The aim of this study was to investigate the effect of acute respiratory acidosis on tissue protein synthesis. Rats (n = 8) were made acidotic by increasing the CO2 content of inspired air to 12% for 1 hour. Similar rats breathing normal air served as controls (n = 8). Muscle and liver protein synthesis rates were then measured with L-[ 2H5 ]phenylalanine (150 micromol per 100 g body weight, 40 mol%). The results show that protein synthesis is severely depressed in skeletal muscle (-44% in gastrocnemius, -39% in plantaris, and -24% in soleus muscles, P < .01) and liver (-20%, P < .001) in acidotic animals. However, because breathing CO2 -enriched air was found to lower body temperature by approximately 2 degrees C, in a second experiment (n = 10), the difference in body temperature between treated and control animals was minimized by gently wrapping rats breathing CO2 -enriched air in porous cloths. This second experiment confirmed that respiratory acidosis depresses protein synthesis in muscle (-22% in gastrocnemius, P < .001; -19% in plantaris, P < .01; and -4% in soleus, P = NS). However, no effect on liver protein synthesis could be detected, suggesting that liver protein synthesis may be sensitive to changes in body temperature but is not affected by acute respiratory acidosis for 1 hour. The results show that respiratory acidosis inhibits protein synthesis in skeletal muscle and indicates that acidosis, whether of metabolic or respiratory origin, may contribute to loss of muscle protein in patients with compromised renal or respiratory function.

Acidosis↗
PubMed1998

Extracellular presence of IL-8 in the astrocyte-rich cultured cerebellar granule cells under acidosis.

In order to evaluate the functional role of chemotactic cytokines in the regulation of brain function, we examined the effects of acidosis on the production of IL-8 in cultured neurons and/or astrocyte-rich cerebellar granule cells as assessed by the ELISA method. A time-dependent and significant production of IL-8 was detected in the extracellular fluid of astrocyte-rich cultured cells at 2, 3 and 6 hrs after treatment with acidified Krebs-HEPES buffer (pH 6.9), although such production did not appear in the fluid of neuron-rich cells. Additionally, microglia were detected by microscopic examination in both cultured cells under acidotic conditions. Only astrocyte-containing cultured cells produced a marked increase in intracellular IL-8 under acidotic conditions, although this production was much less than that seen in the extracellular fluid at 6 hrs under acidosis. The increase of IL-8 in astrocyte-rich cultures induced by acidosis was potentiated by treatment with glutamate, which enhanced the increase of cytosolic Ca2+ levels under acidosis, and was affected by extracellular Ca2+ conditions, by cyclosporine A, an inhibitor of calcineurin, and by trifluoperazine, an inhibitor of phospholipase A2. Significant inhibition of IL-8 production was detected after 6 hrs of pretreatment with trifluoperazine. Furthermore, the production of IL-8 under acidosis was associated with the appearance of astrocyte damage. These results suggest that Ca2+-dependent IL-8 is produced by astrocytes, but not neuronal cells, under acidosis, and that this production may be related to the process of cell dysfunction resulting from membrane destruction induced by acidosis.

Acidosis↗
PubMed1982

Distal renal tubular acidosis: pathogenesis and classification.

Distal renal tubular acidosis results from ineffective addition of hydrogen ions to the lumen of the distal nephron. The syndrome is manifested by hyperchloremic metabolic acidosis often associated with hypokalemia. More recently, it has been recognized that hyperkalemia rather than hypokalemia can be a dominant feature of some cases of distal renal tubular acidosis. It has been generally accepted that all cases of this syndrome ultimately resulted from a similar mechanism. The prevailing view was that the abnormality underlying distal renal tubular acidosis was that of inability to either generate or maintain a steep pH gradient across the distal nephron. Recent advances in our understanding of the process of distal acidification have provided evidence that different mechanisms can alter distal hydrogen ion secretion. In this article, the significance of the various indices of urinary acidification and their use in the characterization of the mechanism underlying distal renal tubular acidosis are revised. A classification of distal renal tubular acidosis on the basis of mechanism is presented. The importance of plasma potassium and renal potassium excretion in the evaluation of patients with distal renal tubular acidosis is emphasized.

Acidosis, Renal Tubular↗
PubMed1983

Drug and chemical-induced metabolic acidosis.

Metabolic acidosis produced by drugs and/or chemicals can be conveniently divided into those with an increase in the anion gap (anion gap = Na- (Cl + HCO3)) and those with a normal anion gap. The increase in the anion gap is due to the accumulation of unmeasured organic anions, such as lactate or acetoacetate and beta-hydroxybutyrate, as occurs in ketoacidosis and lactic acidosis, or the accumulation of toxic anions such as formate or glycolate, as occurs with the ingestion of methanol or ethylene glycol. Increased concentrations of lactic acid may also be present in the toxic forms of metabolic acidosis. The most common drugs and chemicals that induce the anion gap type of acidosis are biguanides, alcohols, polyhydric sugars, salicylates, cyanide and carbon monoxide. In normal anion gap acidosis the reduction in bicarbonate is balanced by a reciprocal increase in the chloride concentration so that the sum of the two remains unchanged. Normal anion gap acidosis is caused by carbonic anhydrase inhibitors, hydrochloride salts of amino acids, toluene, amphotericin, spironolactone and non-steroidal anti-inflammatory drugs. The mechanism by which these substances produce metabolic acidosis and the therapy are discussed.

Acidosis↗
PubMed2003

[Metformin-associated lactic acidosis precipitated by acute renal failure].

In type II diabetes treated with metformin, lactic acidosis is a rare but severe complication. Commonly patients with lactic acidosis show signs of shock, tissue hypoxia, acute hepatic or renal failure and the link between metformin therapy and lactic acidosis may be coincidental, associated or causal. Excessive plasma metformin concentrations show that lactic acidosis is due to a toxicological mechanism. The case of a 65-year-old woman with type II diabetes, in whom severe type B2 lactic acidosis secondary to metformin was precipitated by acute renal failure, is presented. The association of diuretics with non-steroidal anti-inflammatory drugs and colchicine was responsible for a volume depletion and an acute renal failure. Initial serum creatinine was 643 micromol x l(-1) and arterial blood gas analysis revealed a pH of 7.01. Aggressive volume expansion and correction of the acidosis with intravenous bicarbonate therapy failed. At the intensive care unit, calculated anion gap was 35 mmol x l(-1) (normal range 10-18) and lactate concentration was 12.4 mmol x l(-1), liver profile was normal. Prolonged haemodialysis using bicarbonate dialysate resulted in a favourable outcome. Toxicology confirmed retrospectively the presence of a plasma concentration of metformine of 20 mg x l(-1) (normal <2). One month after this episode she has made a recovery of tubular necrosis, although no longer prescribed metformin. Metformin should be temporally stopped when acute renal failure occurs or is anticipated; patient with acute renal failure and high calculated anion gap should benefit from lactate measurements. Early bicarbonate haemodialysis is an adequate treatment of lactic acidosis caused by accumulation of metformin associated with acute renal failure

Acidosis, Lactic↗
PubMed1990

Effect of chronic respiratory acidosis on urinary calcium excretion in the dog.

It is currently believed that the two chronic acidemic disorders exert disparate effects on urinary calcium excretion: chronic metabolic acidosis induces consistent hypercalciuria, but no appreciable change or even a decrease in calcium excretion is reported to attend chronic respiratory acidosis. Whereas the effect of metabolic acidosis is well documented, little work has been carried out in chronic hypercapnia. In fact, most of the studies on chronic respiratory acidosis were short in duration, had employed only mild hypercapnia, or had failed to control carefully the prevailing metabolic conditions. We have carried out balance observations in nine dogs exposed to a 10% CO2 atmosphere in an environmental chamber for a period of two weeks. Chronic respiratory acidosis led to a significant increase in urinary calcium excretion from a mean control value of 0.4 +/- 0.1 mmol/day to 0.6 +/- 0.1 mmol/day during both week 1 and 2 of hypercapnia (P less than 0.05). Hypercalciuria occurred even though filtered load of calcium fell. Mean fractional excretion of calcium increased significantly during each week of hypercapnia averaging 0.60 +/- 0.12% during control, 1.05 +/- 0.13% during week 1, and 1.26 +/- 0.17% during week 2 of hypercapnic exposure (P less than 0.05). There were no changes in plasma levels of immunoreactive parathyroid hormone or 1,25-dihydroxyvitamin D3. These findings suggest that chronic respiratory acidosis, just like chronic metabolic acidosis, augments urinary calcium excretion by a direct depressive effect on the tubular reabsorption of calcium.

Acid-Base Equilibrium↗
PubMed2005

Acidosis causes endoplasmic reticulum stress and caspase-12-mediated astrocyte death.

Endoplasmic reticulum (ER) stress leads to activation of caspase-12, which in turn can lead to activation of caspase-3 and cell death. Here we report that transient acidosis induces ER stress and caspase-12-mediated cell death in mouse astrocytes. After a 3-hour incubation at pH 6.0, astrocytes exhibited delayed cell death associated with nuclear condensation and fragmentation. Cell death was reduced by the protein synthesis inhibitor cycloheximide, further suggesting an active cell death program. Acidosis increased the expression of the ER chaperone protein GRP-78, indicative of ER stress. Acidosis also increased caspase-12 mRNA expression, caspase-12 protein expression, cleavage of caspase-12 to its active form, and activation of caspase-3. Each of these effects was suppressed in astrocytes pretreated with caspase-12 antisense phosphorodiamidate morpholino oligodeoxynucleotides (PMOs). Caspase-12 antisense PMOs also reduced the cell death induced by acidosis. Immunoprecipitation studies showed dissociation of both caspase-12 and Ire1-alpha from GRP-78, thereby suggesting a mechanism by which acidosis can initiate the ER stress response. To evaluate caspase-12 activation in vivo, rats were subjected to middle cerebral artery ischemia-reperfusion. Immunostaining of brain sections harvested 24 hours later showed increased caspase-12 expression and nuclear condensation in astrocytes of the periinfarct region exposed to acidosis during ischemia. These findings suggest that acidosis induces ER stress and caspase-12 activation, and that these changes may contribute to delayed cell death after ischemia.

Acidosis↗
PubMed1999

Acidosis potentiates oxidative neuronal death by multiple mechanisms.

Both acidosis and oxidative stress contribute to ischemic brain injury. The present study examines interactions between acidosis and oxidative stress in murine cortical cultures. Acidosis (pH 6.2) was found to potentiate markedly neuronal death induced by H2O2 exposure. To determine if this effect was mediated by decreased antioxidant capacity at low pH, the activities of several antioxidant enzymes were measured. Acidosis was found to reduce the activities of glutathione peroxidase and glutathione S-transferase by 50-60% (p < 0.001) and the activity of glutathione reductase by 20% (p < 0.01) in lysates of the cortical cultures. Like acidosis, direct inhibition of glutathione peroxidase with mercaptosuccinate also potentiated H2O2 toxicity. Because acidosis may accelerate hydroxyl radical production by the Fenton reaction, the effect of iron chelators was also examined. Both desferrioxamine and N,N,N',N'-tetrakis(2-pyridylmethyl)ethylenediamine, two structurally different iron chelators, significantly reduced H2O2-induced neuronal death under both pH 7.2 and pH 6.2 conditions. These results suggest that the increased cell death produced by severe acidosis during cerebral ischemia may result in part from exacerbation of oxidative injury. This exacerbation may result from both impaired antioxidant enzyme functions and increased intracellular free iron levels.

Acidosis↗
PubMed2001

Acute metabolic acidosis decreases muscle protein synthesis but not albumin synthesis in humans.

Chronic metabolic acidosis induces negative nitrogen balance by either increased protein breakdown or decreased protein synthesis. Few data exist regarding effects of acute metabolic acidosis on protein synthesis. We investigated fractional synthesis rates (FSRs) of muscle protein and albumin, plasma concentrations of insulin-like growth factor-I (IGF-I), thyroid-stimulating hormone (TSH), and thyroid hormones (free thyroxin [fT(4)] and triiodothyronine [fT(3)]) in seven healthy human volunteers after a stable controlled metabolic period of 5 days and again 48 hours later after inducing metabolic acidosis by oral ammonium chloride intake (4.2 mmol/kg/d divided in six daily doses). Muscle and albumin FSRs were obtained by the [(2)H(5)ring]phenylalanine flooding technique. Ammonium chloride induced a significant decrease in pH (7.43 +/- 0.02 versus 7.32 +/- 0.04; P < 0.0001) and bicarbonate concentration (24.6 +/- 1.6 versus 16.0 +/- 2.7 mmol/L; P < 0.0001) within 48 hours. Nitrogen balance decreased significantly on the second day of acidosis. The FSR of muscle protein decreased (1.94 +/- 0.25 versus 1.30 +/- 0.39; P < 0.02), whereas the FSR of albumin remained constant. TSH levels increased significantly (1.1 +/- 0.5 versus 1.9 +/- 1.1 mU/L; P = 0.03), whereas IGF-I, fT(4), and fT(3) levels showed no significant change. We conclude that acute metabolic acidosis for 48 hours in humans induces a decrease in muscle protein synthesis, which contributes substantially to a negative nitrogen balance. In contrast to prolonged metabolic acidosis of 7 days, a short period of acidosis in the present study did not downregulate albumin synthesis.

Acidosis↗
PubMed2006

Relationship between intertwin delivery interval and metabolic acidosis in the second twin.

This study sought to assess the relationship between intertwin delivery interval (ITDI) and metabolic acidosis in the second twin at birth using a retrospective twin delivery cohort from a tertiary-level teaching hospital. Twin births were identified from an obstetrical database during a 10-year period from 1994 to 2004. Mean arterial cord pH and base deficit among different ITDIs were compared by analysis of variance. Logistic regression models were used to estimate effects of ITDI on metabolic acidosis. The incidence of metabolic acidosis in the second twin was defined as pH < 7.0, and base deficit was defined as >or= 12 mmol/L at birth. After excluding those pregnancies with both twins delivered by cesarean section, birthweight less than 750 g of either twin, antepartum death of either twin, or second twins with missing cord arterial pH, we had 310 twin pairs left for final analysis. Mean pH was significantly lower and base deficit significantly higher for second twin after ITDI exceeded 60 minutes. The incidence of metabolic acidosis increased with increasing ITDI (chi2 test for linear trend, P = 0.02) and the risk of metabolic acidosis (odds ratio, 22.6; 95% confidence interval, 2.5 to 494.1) was increased in the second twins with ITDI longer than 60 minutes compared with those with ITDI less than 15 minutes. The incidence of metabolic acidosis increases with increasing ITDI and there is a statistically significant increased risk of neonatal acidosis after longer than 60 minutes compared with less than 15 minutes of ITDI.

Acidosis↗