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PubMed1987

Effect of systemic acid-base balance on ileal secretion.

We previously reported that systemic pH and HCO3 concentration affect ileal water and electrolyte absorption. To determine whether these effects could influence an ongoing secretory process, we measured transport in ileal loops exposed to either saline or 50-75 micrograms cholera toxin in mechanically ventilated Sprague-Dawley rats anesthetized with pentobarbital sodium. The effects of acute respiratory and metabolic acidosis and alkalosis were then examined. Decreases in systemic pH during respiratory acidosis caused equivalent increases in net water (54 +/- 8 microliters . cm-1 . h-1) and Na absorption (7 +/- 1 mu eq . cm- . h-1) and smaller increases in Cl absorption in cholera toxin compared with saline loops. These increases reversed the net secretion of these ions observed during alkalemia in the cholera toxin loops to net absorption. Metabolic acidosis and alkalosis and respiratory compensation of systemic pH of these metabolic disorders also altered cholera toxin-induced secretion in a direction consistent with the pH change. The increase in net HCO3 secretion caused by cholera toxin was unaffected by the respiratory disorders and did not vary with the HCO3 concentration in the metabolic disorders. These findings suggest that the systemic acid-base disorders that characterize intestinal secretory states may themselves alter intestinal absorptive function and fluid losses.

Acid-Base Equilibrium↗
PubMed2001

Acute ethylene chlorohydrin poisoning: experience of a poison control center.

BACKGROUND: Ethylene chlorohydrin (CAS 107-07-3), a chemical once used in hastening grape vine sprouting in Taiwan, has caused severe toxicity upon acute exposure. Although such use of ethylene chlorohydrin is now prohibited in Taiwan, poisoning still occurs following its illegal use. Since data concerning human ethylene chlorohydrin poisoning remain rare, we report our experience in treating acute ethylene chlorohydrin-poisoned patients. METHODS: A retrospective analysis was conducted to evaluate patients with ethylene chlorohydrin poisoning reported to Taiwan Poison Control Center during 1985-1998. RESULTS: Seventeen patients with ethylene chlorohydrin poisoning were identified. There were 11 male and 6 female patients, ranging in age from 2 to 70 years (median 53 years). The intent of exposure was suicide in 5, accident in 9, and occupational exposure in 3 patients. Oral ingestion was the most common route of exposure (14 patients). Seven out of the 17 patients died within 24 hours due to metabolic acidosis and respiratory failure. Ethanol therapy, used in 2 patients, had no apparent benefit. Moderate or mild poisoning was characterized by gastrointestinal effects only and an uneventful recovery. CONCLUSIONS: Ethylene chlorohydrin can result in severe metabolic acidosis, respiratory failure, coma, and death after acute exposure.

Accidents↗
PubMed2002

Effects of acid-base abnormalities on blood capacity of transporting CO(2): adverse effect of metabolic acidosis.

OBJECTIVE: To investigate the effects of some acid-base abnormalities on blood capacity of transporting CO(2). DESIGN: Prospective study. SETTING: General and Cardiosurgical ICUs of a University hospital. PATIENTS: Six groups of ten patients characterized by: metabolic alkalosis; respiratory alkalosis; absence of acid-base abnormalities; metabolic acidosis; uncompensated respiratory acidosis; and compensated respiratory acidosis. MEASUREMENTS AND RESULTS: The CO(2) dissociation curve, Haldane effect, and the ratio Ra-v between Ca-vCO(2) and Pa-vCO(2) were calculated from arterial and mixed-venous blood gas analyses. The CO(2) dissociation curve was shifted upwards by metabolic alkalosis and compensated respiratory acidosis and downwards by metabolic acidosis. The slope of the curve was unaffected, but CO(2) transport not due to Haldane effect was significantly lower in respiratory acidosis since the slope was less steep at higher PCO(2) values. In comparison with controls, patients affected by metabolic acidosis showed lower Haldane effect values (0.18+/-0.15 vs 0.59+/-0.26 ml of CO(2) per ml of arterial-mixed venous O(2) content difference; P <.05) and Ra-v values (0.43+/-0.10 vs 0.84+/-0.17 ml of CO(2) transported by 100 ml of blood per Torr of arterial-mixed venous PCO(2) gradient; P <.05). CONCLUSIONS: Our findings suggest that acid-base abnormalities, particularly metabolic acidosis, markedly affect blood capacity of transporting CO(2) and may worsen tissue hypercarbia associated with hypoperfusion. However, because of possible errors due to small measurements and the assumptions of the method, in the future definitive clarification will require the construction of original CO(2) dissociation curves for each acid-base abnormality.

Acidosis↗
PubMed1979

Respiratory response to HCl acidosis in dogs after carotid body denervation.

To test the participation of the carotid bodies in the respiratory response to metabolic acidosis, six dogs were infused with HCl for 2 h followed by HCl feeding to prolong the acidosis to 48 h. This protocol was repeated after carotid body denervation (CBD). Mean control PCO2 rose by 7.3 Torr after CBD. PCO2 fell comparably during acidosis before and after CBD at all time periods from 30 to 48 h and returned to control levels by 72 h. The pH ranged from 7.10 to 7.30 during acidosis pre- and post-CBD. The decreases in pH and bicarbonate concentration did not differ significantly at any time interval between the pre- and post-CBD studies. This study indicates that in dogs moderately severe HCl acidosis stimulates ventilation acutely and chronically through a central mechanism in the absence of the carotid bodies.

Acidosis↗
PubMed1999

Renal responses of trout to chronic respiratory and metabolic acidoses and metabolic alkalosis.

Exposure to hyperoxia (500-600 torr) or low pH (4.5) for 72 h or NaHCO(3) infusion for 48 h were used to create chronic respiratory (RA) or metabolic acidosis (MA) or metabolic alkalosis in freshwater rainbow trout. During alkalosis, urine pH increased, and [titratable acidity (TA) - HCO(-)(3)] and net H(+) excretion became negative (net base excretion) with unchanged NH(+)(4) efflux. During RA, urine pH did not change, but net H(+) excretion increased as a result of a modest rise in NH(+)(4) and substantial elevation in [TA - HCO(-)(3)] efflux accompanied by a large increase in inorganic phosphate excretion. However, during MA, urine pH fell, and net H(+) excretion was 3.3-fold greater than during RA, reflecting a similar increase in [TA - HCO(-)(3)] and a smaller elevation in phosphate but a sevenfold greater increase in NH(+)(4) efflux. In urine samples of the same pH, [TA - HCO(-)(3)] was greater during RA (reflecting phosphate secretion), and [NH(+)(4)] was greater during MA (reflecting renal ammoniagenesis). Renal activities of potential ammoniagenic enzymes (phosphate-dependent glutaminase, glutamate dehydrogenase, alpha-ketoglutarate dehydrogenase, alanine aminotransferase, phosphoenolpyruvate carboxykinase) and plasma levels of cortisol, phosphate, ammonia, and most amino acids (including glutamine and alanine) increased during MA but not during RA, when only alanine aminotransferase increased. The differential responses to RA vs. MA parallel those in mammals; in fish they may be keyed to activation of phosphate secretion by RA and cortisol mobilization by MA.

Acidosis↗
PubMed1976

Acute respiratory failure precipitated by a carbonic anhydrase inhibitor.

A 60-year-old white man with chronic bronchitis was noted to develop acute respiratory failure and metabolic acidosis four days after being started on methazolamide (Neptazane) for an ophthalmologic problem. The patient was intubated with ventilator support and improved after his metabolic acidosis resolved. Caution is emphasized in the use of carbonic anhydrase inhibitors in patients with obstructive airway disease.

Acidosis, Respiratory↗
PubMed1993

Acid-base status in paediatric Plasmodium falciparum malaria.

We measured the acid-base status of children with falciparum malaria in order to determine the prognostic significance and rate of resolution of acidaemia in patients with severe disease. We prospectively studied 141 Malawian children who were admitted to Hospital, with falciparum malaria, 60 of whom had cerebral malaria (unrousable coma, unable to localize a painful stimulus). Of the 60 patients with cerebral malaria 25 (42%) were acidaemic (capillary blood pH < 7.3); of 81 children with uncomplicated malaria 4 (5%) were acidaemic (p < 0.0001). Eleven patients died; of these, eight presented with cerebral malaria, eight with acidaemia and seven with both. The strong association of altered acid-base status with disease severity and mortality was independent of other previously identified predictors of illness and death in malaria. Acidaemia was not associated with shock, bacteraemia or hypoxaemia. Acidaemic patients had a slower mean respiratory rate and a higher incidence of respiratory rhythm abnormalities than other patients, suggesting that acidaemia is in part the result of inadequate respiratory compensation for metabolic acidosis. Although acidaemia is quickly corrected by fluids and antimalarial drugs, specific therapy to correct acidaemia needs evaluation in children with severe malaria.

Acidosis↗
PubMed1975

Immediate effects of alkaline infusion in infants with respiratory distress syndrome.

Nineteen infants with acidosis associated with RDS were studied following the infusion of: (1) 0.58M (7%) THAM over 30 seconds; (2) molar bicarbonate over 30 seconds; (3) molar bicarbonate over 2 minutes; and (4) molar bicarbonate over 5 minutes. PaC02 fell after THAM; PaC02 rose sharply after bicarbonate and remained elevated 10 minutes after infusion. The pH rose abruptly in all infants and remained significantly elevated 10 minutes after infusion. Pa02 changes were variable; no infant had immediate improvement in Pa02. The changes in osmolality, hematocrit, and colloid osmotic pressure describe the immediate osmotic hemodilution following the infusion of hypertonic base.

Acid-Base Equilibrium↗
PubMed2003

A deletion in the human QP-C gene causes a complex III deficiency resulting in hypoglycaemia and lactic acidosis.

Mitochondrial respiratory chain complex III (ubiquinol-cytochrome c reductase) consists of 11 subunits, only one (cytochrome b) being encoded by the mitochondrial DNA. Disorders of complex III are comparatively rare but are nevertheless present as a clinically heterogeneous group of diseases. To date, no mutation in any of the nuclear-encoded subunits has been described. We report here a deletion in the nuclear gene UQCRB encoding the human ubiquinone-binding protein of complex III (QP-C subunit or subunit VII) in a consanguineous family with an isolated complex III defect. In the proband, a homozygous 4-bp deletion was identified at nucleotides 338-341 of the cDNA predicting both a change in the last seven amino acids and an addition of a stretch of 14 amino acids at the C-terminal end of the protein. Both parents were found to be heterozygous for the deletion, which was absent from 55 controls. Low temperature (-196 degrees C) spectral studies performed on isolated mitochondria from cultured skin fibroblast of the proband showed a decreased cytochrome b content suggestive of a role for the QP-C subunit in the assembly or maintenance of complex III structure.

Acidosis, Lactic↗