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At least 379 records · Page 21Linked to original sources
PubMed1975

Experimentally induced intestinal obstruction in sheep: paradoxical aciduria in metabolic alkalosis.

Ewes with surgically prepared obstruction of the duodenum were used as a model in the study of ruminant metabolic alkalosis and paradoxical aciduria. Metabolic alkalosis occurred as a result of irreversible chloride loss, presumably into the abomasum and forestomachs. Analysis of data on serum and urinary electrolye concentrations provided limited support for the explanation of paradoxical aciduria in terms of chloride and potassium deficiencies. The accumulation undetermined anions in the serum indicated that the decreased urinary pH was due to the excretion of titratable acid.

Alkalosis↗
PubMed1989

Maintenance of metabolic alkalosis despite saline administration in the presence of ascites.

The administration of more than 15 L of saline over 10 days did not correct the metabolic alkalosis (plasma total CO2 35 mEq/L) of a patient with ascites secondary to ovarian carcinoma. Weight gain was more than 6 kg and urine chloride concentration remained less than 15 mEq/L. The tubular avidity for chloride and sodium which maintains metabolic alkalosis persisted in the face of saline administration, perhaps because of "ineffective" volume expansion.

Adenocarcinoma↗
PubMed1985

Prevention with molsidomine of coronary artery spasm caused by alkalosis.

A provocative test of coronary artery spasm caused by alkalosis was used to evaluate a possible anti-coronary artery spasm effect of molsidomine. The rapid infusion of an alkaline buffer followed by maximal voluntary hyperventilation in 10 patients with angina at rest led to the appearance of anginal pain and significant, transient ischemic changes of the ST segment resulting from alkalosis-induced coronary spasm. A second provocative test was performed under the same conditions, 24 hours later, after the administration of 4 mg of molsidomine. Molsidomine prevented the development of coronary artery spasm in 8 of the 10 patients in the study group. These preliminary results justify further clinical evaluation of molsidomine in the treatment of vasospastic angina.

Alkalosis↗
PubMed1986

Blood, urine, and ruminal fluid changes associated with metabolic alkalosis induced by duodenal obstruction.

Two Holstein heifers and a steer fitted with ruminal and duodenal cannulas were used to determine acid-base and electrolyte changes associated with metabolic alkalosis induced by duodenal obstruction. Obstruction was induced distally to the pylorus, but proximally to the common bile duct entrance. Ruminal fluid, blood, and urine samples were obtained before and after obstruction was induced. Duodenal obstruction resulted in increased blood pH, bicarbonate concentration, and base-excess values. Severe hypochloremia and hypokalemia were evident in 48 hours. Serum sodium concentration decreased only slightly. Packed cell volume and serum concentrations of urea nitrogen, creatinine, glucose, and inorganic phosphate increased, whereas calcium concentration showed no change. Renal chloride excretion reached near zero in 24 hours, whereas sodium and potassium excretions decreased in the steer, but were unchanged in the heifers. Urine creatinine concentration increased markedly in the heifers and steers. Acid urine was not evident up to 96 hours. Ruminal fluid pH decreased and chloride concentration increased in the steer, but remained unaffected in the heifers. Duodenal obstruction had no effect on rumen sodium, calcium, and magnesium concentrations, but the potassium concentration increased in the heifers. The degrees of alkalosis and electrolyte changes were greater in the steer than in the heifers.

Alkalosis↗
PubMed1985

Proximal tubule hydrogen ion transport processes in diuretic-induced metabolic alkalosis.

Transport systems involved in proximal tubule HCO-3 reabsorption were examined in disaggregated renal cortical tubules from rabbits with metabolic alkalosis. The acid-base disorder was induced by first treating the animals with furosemide, and then maintaining them on low Cl--high HCO-3 diets. On this regimen, the rabbits had increases in blood pH and total CO2 values and decreases in serum K+ concentrations. Urine Cl- concentrations were less than 15 mEq/L in all cases. Na+-H+ exchange was evaluated by incubating tubules in rotenone in an Na+-free medium to deplete them of Na+ and adenosine triphosphate. Then the tubules were resuspended in media containing 65 or 12.5 mEq/L Na+ at either pH 7.1 or pH 7.6. The rise in cell pH estimated by dimethadione distribution was taken as a measure of Na+-H+ exchanger activity. At the high incubation pH, Na+-H+ exchanger activity appeared to be the same in tubules taken from alkalotic rabbits compared with those prepared from normal rabbits. At the low incubation pH, the activity of this transport system appeared to be depressed by 40% to 50% in alkalosis, with kinetics that suggested a decreased Vmax for the exchanger. Na+-independent H+ transport, presumably reflecting activity of an H+-adenosine triphosphatase, was evaluated by preincubating tubules in a Na+-free medium in the presence of ouabain, and then sequentially exposing them to and removing them from a solution containing 20 mmol/L NH4Cl.(ABSTRACT TRUNCATED AT 250 WORDS)

Absorption↗
PubMed1985

Metabolic alkalosis with hypertonic dehydration in a patient with diarrhoea and magnesium oxide ingestion.

An eight-week-old infant with diarrhoea and dehydration became markedly alkalotic after administration of magnesium oxide powder. The literature does not substantiate the premise that significant magnesium deficiency may occur during acute gastroenteritis in an otherwise healthy infant. Physicians should be warned about this form of therapy as a possible cause of metabolic alkalosis. The possibility of congenital alkalosis with diarrhoea should be considered in differential diagnosis.

Alkalosis↗
PubMed1979

[Physiopathological and clinical data on post-hypercapnic metabolic alkalosis. A case of severe hypercapnia treated with drugs and in an "iron lung"].

The Authors produce a further contribution on metabolic post-hypercapnic alkalosis on the basis of clinical observation of a patient with severe hypercapnia and respiratory failure undergoing intensive care as well as treatment with iron lung (Pulmolife). The improvement of respiratory acid-base umbalance was associated with alteration of electrolytic assessment, especially of the plasmatic chloride ratio. The Authors consider this remark as a starting point for a physiopathological pattern and a more complete analysis of the pathways which generate the metabolic post-hypercapnic alkalosis condition in such patients.

Alkalosis↗
PubMed1983

[Arterial hypertension with hypopotassemia and hypochloremic metabolic alkalosis caused by abuse of a nasal spray].

The case of a young woman, using a nasal spray containing corticosteroids, presenting hypertension systodiastolic, hypokalemia and hypochloremic metabolic alkalosis is presented. Clinical findings, similar to hyperfunction of the adrenal cortex, recovered quickly after discontinuation of the drug. The principal causes of hypertension associated with hypokalemia and hypochloremic metabolic alkalosis, are discussed and the importance of nasal spray, containing glucocorticoids and sympathetic agonists, as a cause of high blood pressure syndromes with different clinical expression and of difficult diagnosis is stressed. The importance of systemic absorption of drugs administered by nasal route is also emphasized.

Adolescent↗
PubMed1983

Characteristics of the inhibitory effect of alkalosis on insulin secretion.

Glucose-induced insulin secretion by the perfused sodium pentobarbital-anesthetized-rat pancreases was studied under different extracellular pH ranging from 7.4 to 7.8. Under our experimental conditions the amount of insulin released was inversely correlated to the pH increase. Besides, metabolic (CO2H- excess) or gaseous (low pCO2) type of alkalosis, were equally effective inhibiting insulin secretion. During a 16.6 mM glucose stimulus, sequential modifications of extracellular pH (7.4-7.8-7.4) caused a dramatic decrease in insulin secretion during alkalosis and an enhancement of its release during the second 7.4 period. The installment and remotion of the inhibition followed almost immediately the changes in the pH of the perfusates. These findings indicate that extracellular diminution of H+ concentration produces a gradual and quickly reversible decrease upon glucose-induced insulin secretion. These characteristics suggest that the inhibitory effect may be mediated through changes in intracellular and/or transmembrane ion fluxes coupled to the variations in H+ concentration.

Acid-Base Equilibrium↗
PubMed1983

Respiratory alkalosis early after stroke: its relation to loco-motor function.

In 27 acute stroke patients with hemi-motor deficit blood gases (paO2, paCO2 and blood pH) were determined within 72 hours and related to level of consciousness, site of brain lesion, findings of haemorrhage into the cerebral spinal fluid, extent of motor impairment and concomitant medical disorders. Sixteen subjects were followed for three weeks with repeated blood-gas sampling and assessment of motor control. Respiratory alkalosis occurred in 37%, hypoxia in 7% but acidosis in none. Blood gas abnormalities were significantly and positively associated only with the extent of motor impairment. Only small changes in blood gases were found during the three weeks follow-up. Initial findings of respiratory alkalosis predicted poor motor recovery during the follow-up period.

Aged↗
PubMed1984

Metabolic alkalosis in diabetic ketosis: a case report.

A mixed metabolic alkalosis and metabolic acidosis, resulting in an alkalemic state, occurred in a hyperlipemic patient with previously diagnosed non insulin dependent diabetes. The metabolic alkalosis, due to large loss of gastric HCl, was more severe than the diabetic acidosis and resulted in an alkaline blood pH. Initially the metabolic acidosis was due to ketoacidosis and coexistent lactic acidosis. During the improvement of the alkalemic and hyperglycemic state, lactic acidosis disappeared but a paradoxical rise of plasma NEFA and ketone body concentrations supervened so that the high anion gap metabolic acidosis was virtually unchanged. The rise of plasma NEFA was probably related to the marked removal of plasma triglycerides, by insulin activation of lipoprotein lipase, and consequent saturation of the pathways of fatty acid incorporation into adipose tissue.

Adult↗
PubMed1983

[Molsidomine prevention of coronary artery spasm caused by alkalosis].

A test provocation of coronary artery spasm by alkalosis was used to evaluate a possible anti-coronary artery spasm effect of molsidomine. The rapid infusion of an alkaline buffer followed by maximal voluntary hyperventilation in 10 patients with angina at rest led to the appearance of angina pain and significant, transient ischaemic changes of the ST segment, due to alkalosis induced coronary spasm. A second provocation test was performed under the same conditions, 24 hours later, after the prior administration of 4 mg of molsidomine. Molsidomine prevented the development of coronary artery spasm in 8 of the 10 patients in the study group. These preliminary results justify further clinical evaluation of molsidomine in the treatment of vasospastic angina.

Alkalosis↗
PubMed1984

[Results of therapy of severe metabolic alkalosis using hydrochloric acid infusions].

Severe metabolic alkalosis is often treated by infusion of arginine-HCl. Since we know that this substance leads to a supplemental increase of intracellular pH and fails to reduce intracellular bicarbonate concentration we use HCl for correction of this disturbance of acid-base equilibrium. 18 intensive-care patients with severe metabolic alkalosis were treated with an infusion of 0.2 m HCl. While base excess and sodium decreased significantly, chloride increased slightly. Arterial plasma pH, potassium, Hb, Hk, pCO2, pO2, and SO2 remained unchanged. Instructions for preparing different HCl solutions and advice on dosage are given.

Alkalosis↗
PubMed1983

Hypokalemic metabolic alkalosis caused by surreptitious vomiting: report of four cases.

Four women, aged 22 to 40 years, presented with severe hypokalemia and metabolic alkalosis. Three had related neuromuscular symptoms. All four patients denied vomiting or diuretic ingestion, and a diagnosis of Bartter's syndrome was entertained. A diagnosis of surreptitious vomiting was suspected from the characteristic urine electrolyte pattern: high values for sodium and potassium, and a chloride concentration of less than 5 mmol/l. Three patients excreted sodium and potassium primarily with bicarbonate and had an alkaline urine; the fourth patient excreted these cations primarily with an organic anion and had an acid urine (pH 5.5). Since self-induced vomiting may be a common method of weight reduction in young women, recognition of this characteristic urine electrolyte pattern will assist in the rapid diagnosis of hypokalemia and metabolic alkalosis of obscure cause.

Adult↗
PubMed1980

Insulin secretion during acid-base alterations. III: Role of extracellular calcium on the blocking effect of alkalosis.

Insulin secretion by the perfused rat pancreas and incubated islets of Langerhans challenged with glucose is hampered under metabolic alkalosis. In order to assess if the alteration was due to changes in extracellular ionic calcium availability at pH 7.8, perfusion and incubation media of different composition were used. Since sodium bicarbonate and bovine serum albumin diminish the ionic calcium concentration with a pH increase, they were substituted in the buffers by Hepes or dextran, respectively. Moreover, with the aid of ionic calcium measurement, its concentration was corrected in the pH 7.8 buffers to attain the corresponding value at pH 7.4. In spite of these changes the depressing effect of alkalosis was still present. These results suggest that the high pH renders beta cells low responders altering some intracellular step of the stimulus-secretion coupling rather than through a decrease of extracellular calcium.

Alkalosis↗
PubMed1980

Hypochloremic metabolic alkalosis following tolazoline-induced gastric hypersecretion.

Gastric hypersecretion following administration of tolazoline resulted in severe hypochloremic alkalosis in an infant with persistent fetal circulation. An initial bolus injection of 2 mg/kg was followed by an infusion of 5 mg/kg/hr for 24 hours. The infusion was then maintained at 2 mg/kg/hr for the next four days. Volume of gastric secretions exceeded 25 ml/kg/24 hr. Weaning from tolazoline and replacement of chloride and potassium corrected the metabolic alkalosis.

Alkalosis↗
PubMed1980

The use of intravenous hydrochloric acid in the treatment of thirty-four patients with metabolic alkalosis.

Since 1972, 34 patients with refractory metabolic alkalosis have been treated with intravenous hydrochloric acid at the teaching hospitals of the Medical College of Georgia. Intravenous hydrochloric acid lacks some of the problems associated with alternative methods of therapy. The acid must always be given through a central vein, and its effects should be monitored closely. The use of intravenous hydrochloric acid is a safe, effective way of preventing the deleterious effcts of severe metabolic alkalosis.

Adult↗
PubMed1980

Treatment of refractory congestive heart failure and normokalemic hypochloremic alkalosis with acetazolamide and spironolactone.

Combination therapy with a loop diuretic and an aldosterone antagonist can produce normokalemic hypochloremic alkalosis, a complication not previously documented in the literature. This report describes 74 patients who had severe congestive heart failure treated with a combination of furosemide and spironolactone in whom this complication developed. Acetazolamide corrected the metabolic abnormality. The combination of furosemide and spironolactone with intermittent courses of acetazolamide was very effective in the treatment of severe congestive heart failure complicated by normokalemic hypochloremic alkalosis.

Acetazolamide↗