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PubMed2005

Metabolic acidosis aggravation and hyperkaliemia in hemodialysis patients treated by sevelamer hydrochloride.

Reports on acid-base side effects of sevelamer hydrochloride (SH), a new aluminum (Al)- and calcium (Ca)-free phosphate binder are rare and conflicting. In a retrospective analysis, we evaluated SH impact on metabolic acidosis and serum potassium (K) in hemodialysis (HD) patients. Two groups of stable HD patients were studied. Group A included 17 patients, M/F=15/2, 64 (42-80) years old, dialyzed since 130 (34-253) months, under SH for 24 months. Group B serving as controls was made of 7 patients, M/F=4/3, 67 (48-91) years old, dialyzed since 67 (27-174) months, under CaCO3 and/or Al(OH)3 as phosphate binders also for 24 months. Bicarbonate (BIC), K, Ca, phosphorus (P), Ca x P, alkaline phosphatase (ALP), and intact parathyroid hormone (iPTH) were recorded before (MO) and at the end (M24) of 24-month SH or CaCO3-Al(OH)3 treatment in group A and B patients. In group A, BIC fell from 20.02 +/- 1.43 to 17.89 +/- 2.30 mEq/ L, P=.002; and K rose from 5.45 +/- 0.51 to 5.75 +/- 0.49 mEq/L, P=0.02. In group B, BIC (19.8 +/- 3.03 to 19.0 +/- 3.3 mEq/L) and K (5.01 +/- 0.8 to 4.9 +/- 1.1 mEq/L) had nonsignificant changes. In group A, iPTH rose from 132.82 +/- 124.08 to 326.89 +/- 283.91 pg/mL, P=.0008; P fell from 5.92 +/- 1.48 to 4.9 +/- 1.01, P=.02; and Ca x P decreased from 52.04 +/- 9.7 to 45.58 +/- 10.42 mg2/dL2, P=.04. In group B, changes in iPTH from 240.71 +/- 174.7 to 318.57 +/- 260.2 pg/mL, P from 4.9 +/- 0.5 to 4.8 +/- 1.3 mg/dL, and CaxP product from 44.3 +/- 6.6 to 44 +/- 11.2 mg2/dL2 were nonsignificant. The changes observed in Ca and ALP in both groups were nonsignificant. Correlations in group A between metabolic acidosis (BIC) and SH doses, or iPTH and BIC, Ca, or P changes, were also found to be nonsignificant. Long-term use of SH, effectively controlling serum P levels and Ca x P values, is associated with acidosis aggravation and hyperkaliemia. Worsening of secondary hyperparathyroidism, also noted, needs to be confirmed and could be related to Ca/Al salt discontinuation and to metabolic acidosis aggravation itself.

Acidosis↗
PubMed2005

Recurrent D-lactic acidosis in a child with short bowel syndrome.

D-lactic acidosis is a rare complication in children with short bowel syndrome. It results from fermentation of dietary carbohydrate by luminal bacteria in the small bowel caused by bacterial overgrowth. We present the case of a 14-year-old boy who had been diagnosed with short bowel syndrome from surgical treatment of midgut volvulus five years previously. His nutritional status was maintained by total parenteral nutrition and enteral feeding as tolerated. During hospitalization, episodic confusion and hyperpnea developed. The investigation showed severe metabolic acidosis with serum bicarbonate of 9 mmol/L and a wide anion gap. The serum D-lactic acid was 11.21 mmol/L. There was no evidence of renal or hepatic failure. Therefore, D-lactic acidosis from enteral carbohydrate overload was diagnosed. The treatment was correction of metabolic acidosis by sodium bicarbonate infusion and carbohydrate restriction. The results of the therapy were satisfactory. Early detection and appropriate treatment is necessary to avoid morbidity and mortality following this complication of short bowel syndrome.

Acidosis, Lactic↗
PubMed1992

Beneficial effect of MCI-154, a cardiotonic agent, on ischemic contractile failure and myocardial acidosis of dog hearts: comparison with dobutamine, milrinone and pimobendan.

The effects of MCI-154, a cardiotonic agent with Ca++ sensitizing actions, on the ischemic contractile failure and myocardial acidosis were studied in the dog heart, in which the left anterior descending coronary artery (LAD) was partially occluded for 90 min, and compared with those of dobutamine, milrinone, pimobendan and isosorbide dinitrate (ISDN). Partial occlusion of LAD decreased segment shortening (measured by sonomicrometry) and myocardial pH (assessed by a micro glass pH electrode) in the ischemic myocardium. MCI-154, when administered i.v. 30 min after ischemia, improved the segment shortening in the ischemic zone, whereas dobutamine, milrinone and pimobendan failed to improve it when the drugs increased peak positive left ventricular dP/dt. Among the cardiotonic agents tested only MCI-154 attenuated myocardial acidosis during ischemia. The degree of the attenuation of acidosis by MCI-154 was equivalent with that by ISDN. However, the improvement of the ischemic zone segment shortening by MCI-154 was more pronounced than that by ISDN. These results suggest that in addition to the attenuation of myocardial acidosis the positive inotropic action of MCI-154, presumably increasing the responses of myofilaments to Ca++, may be possibly responsible for the improvement of regional contractile function in the ischemic myocardium. Thus, MCI-154 may be useful in the management of ischemic heart failure.

Acidosis↗
PubMed2005

Metformin lactic acidosis and anaesthesia: myth or reality?

AIMS: To determine whether a causal or coincidental relationship is indicated in the literature between metaformin and lactic acidosis and to recommend clinical guidelines for the withdrawal of metformin prior to surgery. METHOD: A broad review of the literature related to metformin associated acidosis was carried out. (There are few publications specifically related to metformin treatment and anaesthesiology). RESULTS: When metformin-associated lactic acidosis occurs, a concurrent pathology or contraindication to the use of metformin is often found. Anaesthesia and surgery can generate or aggravate concurrent pathologies. CONCLUSION: Although no association has been shown between metformin and lactic acidosis under usual conditions of use, vigilance is required when metformin is used prior to surgery. The following clinical guideline is proposed: to withdraw (when possible) metformin 48 hours prior to surgery and to wait until the patient's biological and clinical parameters return to normal before reintroducing it.

Acidosis, Lactic↗
PubMed1990

Decreased colostral immunoglobulin absorption in calves with postnatal respiratory acidosis.

The effect of postnatal acid-base status on the absorption of colostral immunoglobulins by calves was examined in 2 field studies. In study 1, blood pH at 2 and 4 hours after birth was related to serum IgG1 concentration 12 hours after colostrum feeding (P less than 0.05). Decreased IgG1 absorption from colostrum was associated with respiratory, rather than metabolic, acidosis, because blood PCO2 at 2 and 4 hours after birth was negatively related to IgG1 absorption (P less than 0.05), whereas serum bicarbonate concentration was not significantly related to IgG1 absorption. Acidosis was frequently observed in the 30 calves of study 1. At birth, all calves had venous PCO2 value greater than or equal to 60 mm of Hg, 20 of the calves had blood pH less than 7.20, and 8 of the calves had blood bicarbonate concentration less than 24 mEq/L. Blood pH values were considerably improved by 4 hours after birth; only 7 calves had blood pH values less than 7.20. Calves lacking risk factors for acidosis were examined in study 2, and blood pH values at 4 hours after birth ranged from 7.25 to 7.39. Blood pH was unrelated to IgG1 absorption in the calves of study 2. However, blood PCO2 was again found to be negatively related to colostral IgG1 absorption (P less than 0.005). Results indicate that postnatal respiratory acidosis in calves can adversely affect colostral immunoglobulin absorption, despite adequate colostrum intake early in the absorptive period.

Absorption↗
PubMed1990

Molecular mechanisms of glial cell swelling in acidosis.

The mechanism of glial swelling in acidosis were investigated in an in vitro model. C6 glial cells were exposed to pH levels between 7.4 and 6.2. The cell volume response was determined by flow cytometry. Cell swelling of 110% to 115% was observed if pH was reduced to 6.8 or below. This effect was independent of the length of exposure to acidosis. Swelling induced by pH could be attenuated by (a) inhibition of the Na+/H+ antiporter by amiloride, (b) replacement of bicarbonate by HEPES, and (c) inhibition of carbonic anhydrase by acetazolamide. Absence of Na+ ions from the incubation medium completely prevented acidosis-induced glial swelling. Inhibition of the Cl-/HCO3- antiporter reduced swelling only in its first phase. The results suggest that glial swelling in acidosis may be from an activation of anion and cation antiporters as an attempt to maintain a normal intracellular pH. It is concluded that swelling of glial cells in the ischemic penumbra zone evolves along similar mechanisms.

Acetazolamide↗
PubMed1990

[Lactic acidosis].

The rare congenital lactic acidosis is a consequence of enzyme defects. The acquired form is relatively common in critically ill patients. The altered metabolism of pyruvate and the imbalance between lactate production and utilization have a central role in the pathogenesis of this disease. The physiologic compensating mechanisms are generally not sufficient for complete correction of acidosis. In most of the cases the basic disease is the one that should be treated. The correction of the acidosis must be careful, because overtreatment may worsen acidosis, or may cause severe post-treatment alkalosis.

Acidosis, Lactic↗
PubMedDate not supplied

[Lactic acidosis and intensive care. 16 cases (author's transl)].

Sixteen cases of lactic acidosis are reported: 7 phenformin treated diabetes, 5 cardiovascular diseases (2 myocardial infractions, 2 pulmonary embolisms, 1 heart failure). In 2 patients no etiology was found. Concomittant renal failure or liver diseases were found in respectively 9 and 4 cases. Patients presented the usual criteria of lactic acidosis: clinical, polypnea, severe hypotension (9/16), peripheral symptoms of shock (12/16), hypothermia (9/16), abdominal pain (9/16): biologically, acidosis (pH = 6,99 +/- 0,01, HCO3- = 5,9 +/- 1,5 mmol), hyperlactatemia (14,1 +/- 3,6 mmol/l) with hig lactate/pyruvate ratio (105 +/- 73), and anion gap (24,3 +/- 4,2 mmol/l). Sodium bicarbonate infusion was performed in all cases (2,5 to 42 mmol/kg). Few cases required volhemic expansion or furosemid induced diuresis. One patient was treated with extrarenal dialysis. 13 patients were alkalinised with less than 185% of estimated deficit measured from alkalin reserve: 12 died. 3 patients received 185% more than this deficit, associated with furosemid (1,8 to 12,5 mg/kg): only one patient died ten days after by casual disease, with lactatemia of 3,2 mmol/l. In spite of the small number of patients, these findings suggest that an early and massive alkalinisation, with large doses of furosemid, can improve the severe lactic acidosis prognosis.

Acidosis↗
PubMed1989

[Lactic acidosis in recovered asphyctic newborn infants].

Thirty newborn babies delivered by elective caesarean section were studied. They were randomly placed in two groups. The first group consisted of newborns who scored 3 or less on the Apgar scale at one minute and 8 or more after five minutes. The other group included newborns which scored 8 or higher at one minute and 9 at five minutes. Blood samples were obtained from the umbilical cord which allowed for the measuring of the infants' pH, serum gases and pyruvic lactic acid levels. An increased level lactate was found in asphyctic infants. Five cases presented lactic acidosis which continued to be persistent in four of them an hour after they were born. Although increased levels of lactate were found also in the control group, they never presented lactic acidosis. No correlation was found between the pH and lactate levels nor between lactate and bicarbonate. A clear correlation between lactic acidosis and fetal distress was documented. It was concluded that lactate quantification is a useful indicator of neonatal asphyxia. Lactic acidosis; Apgar scores; asphyxia.

Acidosis, Lactic↗
PubMed1989

Cerebral acidosis in focal ischemia.

The discovery in the 1970s that hyperglycemia accompanying cerebral ischemia adversely affected survival led to a significant research effort on the biochemical, histological, and clinical consequences of cerebral acidosis. In this article, we review the methods used currently to measure cerebral pH and discuss the means the cell has to control its pH environment. We then discuss the influence of both normoglycemic and hyperglycemic cerebral ischemia on pH and conversely the effect of acidosis on cerebral blood flow (CBF), glycolysis, mitochondrial function, the blood-brain barrier, cellular volume control, the formation of cerebral edema, and the histological damage resulting from ischemia. We conclude with a discussion of how acidosis could worsen the derangement in calcium homeostasis known to occur as a consequence of ischemia, and review methods now available to counteract cerebral acidosis.

Acidosis↗
PubMed1989

Stimulation of rat-kidney hexose monophosphate shunt dehydrogenase activity by chronic metabolic acidosis.

The effect of chronic metabolic acidosis on the kinetic behaviour of renal glucose 6-phosphate dehydrogenase and 6-phosphogluconate dehydrogenase have been investigated. Acidosis induced a significant increase in both enzyme activities at all substrate concentrations used. Saturation curves of both dehydrogenases were hyperbolic with no evidence of sigmoidicity. Maximum activities were found after 7 days of acidosis with no significant change in the Km values. The results suggest that stimulated renal hexose monophosphate dehydrogenases activities are probably due to an increased intracellular concentration of these enzymes. The relationship between these changes and those generated in the metabolic acidosis are also discussed.

Acidosis↗
PubMed1989

Distal renal tubular acidosis in recurrent renal stone formers.

Renal acidification ability was examined in 90 recurrent renal stone formers, using fasting morning urinary pH levels followed by a short ammonium chloride loading test in subjects with pH levels above 6.0. Fifteen patients (16.6%) revealed a distal renal tubular acidification defect: one patient (1.1%) had complete distal renal tubular acidosis and 14 (15.5%) incomplete distal renal tubular acidosis. Our results confirm that distal renal tubular acidification defects are associated with a more severe form of stone disease and make distal renal tubular acidosis one of the most frequent metabolic disturbances in renal stone formers. Distal renal tubular acidosis (dRTA) was relatively more common in female stone formers and most often found in patients with bilateral stone disease (36%). Since prophylactic treatment in renal stone formers with renal acidification defects is available, this has important therapeutic implications. The pathological sequence in renal stone formers with dRTA is discussed.

Acidosis, Renal Tubular↗
PubMed1987

In vivo measurements of tissue pH of the heart, brain, liver, spleen, and skeletal muscle following therapy of severe metabolic uraemic acidosis with infusion of bases: an experimental study on the limitation of the Mellemgaard-Astrup equation.

The intracellular tissue pH of the heart, brain, liver, spleen, and skeletal muscle of nephrectomized rats was determined in vivo from the distribution of 14C-labelled DMO (5,5-dimethyl-2-4-oxazolidinedione) following acute variation of arterial plasma pH (pHe) by CO2 inhalation or sodium bicarbonate administration in the range of pHe 6.9-7.7, or following correction of severe metabolic uraemic acidosis with sodium bicarbonate or Tris (hydroxymethyl) aminomethane (THAM) infusion according to the Mellemgaard-Astrup equation. It was found that: (a) during severe uraemic acidosis administration of sodium bicarbonate according to the Mellemgaard-Astrup equation leads to a stable correction of the extracellular disturbance while a comparable amount of THAM has a less pronounced effect; (b) in the first 60-120 min following therapy of severe chronic uraemic acidosis there is an overcorrection of intracellular tissue pH when compared to acute acidosis of the same degree. PHi of the investigated tissues increased more following sodium bicarbonate administration than following THAM; (c) the amount of base required for the correction of the overall acid-base status of the organism cannot be determined from the extracellular measurements alone; (d) when the normal acid-base correlation between blood and tissues is disturbed, measurements of arterial acid-base parameters can give misleading information about the whole body acid-base status and may result in failure of therapy.

Acid-Base Equilibrium↗
PubMed1976

Contribution of tissue acidosis to ischemic injury in the perfused rat heart.

The isolated perfused working rat heart preparation has been used to study the effects of respiratory acidosis on myocardial metabolism and contractilly. Hearts were perfused with 5 mM glucose and 10(-2) U/ml of insulin in order to enhance metabolsim of glucose relative to that of fatty acids. After perfusion with Krebs bicarbonate medium at pH 6.6, hearts rapidly ceased performing external work and peak left ventricular pressure fell by 75% after 5 minutes. Oxygen consumption, rate of ATP generation and overall glycolytic flux also declined rapidly. After about 2 minutes of perfusion, the fall of glycolytic flux showed a partial reversal, which was largely accounted for by increased lactate production, so that glucose oxidation decreased further. The reversal of glycoltic flux could be accounted for by partial release of H+ inhibition of phospho-fructokinase by increased tissue levels of adenosine 5'-diphosphate (ADP), adenosine monophosphate (AMP) and P1 and decreased levels of adenosine triphosphate (ATP) and creatine phosphate. The increased proportion of glucose uptake converted to lactate together with an increase of the tissue lactate/pyruvate ratio could be accounted for by inhibition of the malate-aspartate cycle combined with tissue hypoxia. Lactate accumulated in the tissue as a result of a decreased permeability of the plasma membrane to lactate. Decreased oxygen delivery to the myocardium was caused by secondary constriction of the coronary vessels. In further experiments, the coronary flow was regulated by an external pump which delivered fluid at a controlled rate into the aortic cannula above the coronary arteries, and the degree of tissue hypoxia was monitored by measuring changes of pyridine nucleotide reduction state by surface fluorescence techniques. The effects of acidosis uncomplicated by possible hypoxia were compared directly with those produced by ischemic hypoxia. The effects of acidosis under these conditions were similar to those described above, and to those produced by ischemia. From these and other data it is concluded that the effects of ischemia are caused by a lowering of the intracellular pH, which decreases the rate of energy production relative to the rate of energy demand. However, it is suggested that the primary cause of the decreased peak systolic pressure with either acidosis or ischemia is not a result of a defect of energy metabolism, but is due to alteration of the calcium cycle of the heart. Possible causes of irreversible heart failure after prolonged ischemia are discussed.

Acidosis, Respiratory↗
PubMed1988

MCl-176, a novel calcium channel blocker, attenuates the ischemic myocardial acidosis induced by coronary artery occlusion in dogs.

The effect of MCl-176 [2-(2,5-dimethoxyphenylmethyl)-3-(2-dimethylaminoethyl)-6- isopropoxy-4(3H)-quinazolinone hydrochloride], a novel calcium channel blocker, on ischemic myocardial acidosis was studied in the dog heart, in which the left anterior descending coronary artery was partially occluded for 90 min (partial occlusion). Myocardial pH (measured by a micro glass pH electrode) was about 7.60 in the nonischemic normal heart. The myocardial pH decreased rapidly in response to partial occlusion, and reached the steady state of about 6.85 within 30 min (i.e., the myocardial [H+] increased after partial occlusion). Saline or drug was injected i.v. 30 min after partial occlusion, and the drug effect was observed till the end of partial occlusion. Myocardial [H+], that had been increased by partial occlusion, restored slightly after the saline injection, and the restoration was about 30% 60 min after the injection. MCl-176 increased this spontaneous restoration of myocardial [H+] with a decrease in blood pressure and heart rate; the restoration induced by 0.1 mg/kg of MCl-176 was 74% 60 min after the injection. Even in the paced heart, MCl-176 (0.1 mg/kg) attenuated the ischemia-induced myocardial acidosis. Propranolol (1 mg/kg) also attenuated the myocardial acidosis, the restoration being 82%. These results indicate that MCl-176 attenuates the myocardial acidosis during ischemia as does propranolol, and that the mechanism of action of MCl-176 is not due primarily to a decrease in heart rate.

Acidosis↗
PubMed1986

[Increase of the depressive effect of verapamil in acidosis].

The effect of pH on the negative chronotropic response to slow channel blockers was studied in isolated rat atria incubated at pH 7.39 (control group) and at pH 7.03 (group in acidosis). Cumulative concentration-response curves for verapamil, nitrendipine and nifedipine were done recording the spontaneous electrical activity 20 min after each drug addition. Both verapamil and dihydropyridines produced a depression of sinoatrial automatism, but only verapamil showed an enhanced effect in acidosis. The change in atrial rate was significantly greater in acidosis than in the control group with verapamil concentrations from 3 X 10(-9) to 10(-7) M. This enhancement of the negative chronotropic effect of verapamil by acidosis resembles a similar modification to the one observed in the inotropic response. Our experiments suggest a synergistic mechanism in the inhibition of Ca2+ channels by H+ and verapamil, but not for H+ and dihydropyridines.

Acidosis↗
PubMed1986

Type II renal tubular acidosis in a mare.

Persistent, severe metabolic acidosis complicated the operative and postoperative period in a 4-year-old mare with colic. On the basis of clinical and laboratory findings, a renal tubular disorder was diagnosed. Renal tubular acidosis is rare in horses. In the only report found on the subject, type I renal tubular acidosis was described in 2 horses. Bicarbonate titration studies in our case helped document type II renal tubular acidosis in this mare.

Acidosis, Renal Tubular↗
PubMedDate not supplied

Hyperchloremic metabolic acidosis as a clue to recto-urethral fistula in an infant with anal atresia.

An infant with high anal atresia and transverse colostomy, in whom initial radiologic evaluation of the urinary tract had been normal, developed hyperchloremic metabolic acidosis at 24 days of age. Gastroenteritis and renal tubular acidosis as possible causes for this metabolic disturbance were excluded, which prompted a repeat investigation of the possibility of a communication between the urinary tract and the rectum. A recto-urethral fistula was demonstrated by urethrography. Analysis of the fluid obtained from the left colon as compared to urine in the bladder and voided urine demonstrated that electrolyte exchange was taking place in the colon, resulting in hyperchloremic hypokalemic acidosis. Treatment with oral sodium bicarbonate and daily lavage of the left colon resulted in normalization of the acid-base status and catch-up growth of the baby. Hyperchloremic acidosis associated with anal atresia and recto-urinary communication appears to be uncommon. However, early diagnosis and treatment of the metabolic derangement are of importance as it may determine the infant's overall prognosis.

Acidosis↗