Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0002063 (alkalosis)
 2,286 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In two patients with severe hypertension and moderately severe renal insufficiency, metolazone and furosemide were used in combination with propranolol, methyldopa, and hydralazine to augment control of blood pressure. This combination of diuretics also was used in five patients with refractory congestive heart failure. The patients developed severe electrolyte disturbances with a general pattern of hyponatremia. disproportionate hypochloremia, alkalosis, and phyokalemia. These abnormalities were transient in the patients with severe hypertension and moderately severe renal insufficiency. Effective long-term control of blood pressure was obtained. In the patients with heart failure, edema persisted. Due to the severity of the electrolyte derangements, metolazone and furosemide were discontinued. Because of potential untoward effects, this combination of diuretics should be used with caution.
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PMID:Severe electrolyte disturbances associated with metolazone and furosemide. 63 11

The additive natriuretic effect of a single dose of bendroflumethiazide, 5 mg., has been studied in patients with advanced congestive heart failure in long-term treatment with bumetanide, 4 mg., daily. Three permutation trial tests were performed including six patients each. In the first trial, the response to supplementary bendroflumethiazide, 5 mg., was definitely superior to that of additional bumetanide, 4 mg., in terms of renal output of sodium, chloride, potassium, water, and osmolar clearance. In the second trial, a similar pattern was found in patients receiving a combination of bumetanide, 4 mg., and spironolactone, 100 mg., daily. The third trial compared the effects of bendroflumethiazide, 5 mg., plus bumetanide, 4 mg.; of bendroflumethiazide, 5 mg.; and of bumetanide, 4 mg. In terms of natriuresis and chloruresis, the response to the combination of two drugs was significantly larger than the sum of the effects of other treatments. It is concluded that the combined effects of the drugs represent a supra-additive effect addition for sodium and chloride. A tentative explanation of the mechanism of interaction in terms of inhibition of renal tubular supplementary spironolactone, involve a tendency to development of hypokalemia, hypochloremia, and alkalosis, it is recommended that supplementary use of bendroflumethiazide in this setting is combined with the administration of potassium chloride or potassium-saving diuretics.
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PMID:The supra-additive natriuretic effect addition of bendroflumethiazide and bumetanide in congestive heart failure. Permutation trial tests in patients in long-term treatment with bumetanide. 109 Jan 32

Twenty-seven patients of hypertrophic pyloric stenosis operated on at our hospital between 1977 and 1991 were reviewed. The patients consisted of 22 boys and 5 girls, with males accounting for 81%. Seventeen of the 27 patients were the first children of their mothers. Vomiting was first noted between 10 and 58 days after birth with a mean of 26.5 days, and neonatal onset was observed in 67% of all patients. The body weight decreased after the onset in 17 patients, including 1 in which it decreased below the birth weight. Hypochloremia was the most frequent preoperative electrolyte imbalance, being observed in 41% of all patients. Alkalosis was noted in 17 of the 22 patients in which arterial blood gas analysis could be performed. The olive was palpated preoperatively in 24 (89%) of the 27 patients. The body weight increased in all patients after operation, and the mean daily increase was 26.7 g. The mean period of hospitalization after operation was relatively short at 8.3 days. Postoperative vomiting was observed in 16 patients (59%), with its mean duration being 26 days. All patients showed normal growth after operation, and no postoperative complications were noted.
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PMID:[Study on 27 surgical cases of hypertrophic pyloric stenosis at Kyoto City Hospital]. 147 21

An experimental model of hypertrophic pyloric stenosis was made by suture of the pyloric wall and gastrostomy in 10 rabbits under general anesthesia. Blood sampling indicated severe alkalosis and hypochloremia 3h 30 min after surgery. To correct the derangement, we tested an ion exchange resin (Dowex SAR), coated with a methacrylic hydrogel. A cartridge containing 18 g of this resin was inserted in an extracorporeal circuit. This chloride charged resin achieved uptake of HCO3- ions, and elution of Cl- ions. The electrolytic balance was fully restored after 10 min of treatment.
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PMID:Hemoperfusion with a new anion exchange resin corrects the metabolic alkalosis in pyloric stenosis: an experimental demonstration. 149 Jul 61

Metabolic alkalosis was induced in 10 clinically normal horses by administration of furosemide (1 mg/kg of body weight, IM) followed 4.5 hours later by sodium bicarbonate (NaHCO3; 500 g in 8 L water) via nasogastric tube. Furosemide diuresis resulted in a mean weight loss of 21.1 kg, which was associated with small, but significant, increases in venous blood pH, bicarbonate, and plasma protein concentrations (P less than 0.001), while plasma potassium, chloride, and calcium concentrations declined significantly (P less than 0.001). Oral administration of the hypertonic NaHCO3 solution resulted in clinical evidence of hypovolemia, which was accompanied by a marked increase (P less than 0.001) in plasma protein concentration. Seven of the 10 horses developed signs of neuromuscular excitability, as evidenced by muscle fasciculations, and 5 of the horses developed diaphragmatic flutter. Hypernatremia was transiently induced, but it resolved as the horses were allowed access to water. The alkalosis induced by furosemide and NaHCO3 was profound and persisted for a 24-hour period and was associated with marked hypochloremia and hypokalemia. Partial replacement of the electrolyte deficits and correction of the metabolic alkalosis was attempted, using 1,000 mEq of NaCl or KCl given as an isotonic solution via nasogastric tube. In the KCl-treated group, there was a prompt and significant decline in venous blood pH and bicarbonate concentration (P less than 0.001) accompanied by a significant increase in plasma potassium concentration (P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Furosemide and sodium bicarbonate-induced alkalosis in the horse and response to oral KCl or NaCl therapy. 255 Dec 2

In 1962 Bartter et al. described a clinical syndrome characterized by growth and mental retardation, hypokalemic alkalosis, increased aldosterone secretion rate and increased plasma angiotensin II concentration in the presence of normal blood pressure. The inheritance pattern has been reported as autosomal recessive or as sporadic. Since that time 37 cases have been reported in pediatric age, describing a wide spectrum of clinical and biochemical features. For the diagnosis the following criteria must be present: hypokalemia, hypochloremia, alkalosis, hyperreninemia in the presence of a normal blood pressure and elevated urinary K and Cl excretion, in the absence of other conditions that might cause similar features. A case of Bartter's disease is herein reported with our experience in the diagnosis, treatment and follow-up.
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PMID:[Hypokalemia and hypoevolutism. Description of a case of Bartter's syndrome]. 263 84

In critically ill patients, nonrespiratory (metabolic) alkalosis is the most common acid-base disturbance; it is caused by hypochloremia and/or by hypoproteinemia. Information on the concentration of plasma proteins should be included when evaluating acid-base status.
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PMID:Acid-base disorders in critical care medicine. 265 46

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.
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PMID:Blood, urine, and ruminal fluid changes associated with metabolic alkalosis induced by duodenal obstruction. 396 93

Metabolic alkalosis was induced in dogs by administering ethacrynic acid and sustained by feeding a chloride-deficient diet. At the height of the alkalosis extracellular fluid was expanded "isometrically," i.e., with an infusion that duplicated plasma sodium, chloride, and bicarbonate concentrations. Correction of metabolic alkalosis promptly followed such expansion and was attributed to the selective retention by the kidneys of chloride from the administered solution. Since plasma chloride concentration was not increased as an immediate consequence of the infusion, it is concluded that the change in renal tubular function that led to the selective retention of chloride must have been mediated by factors independent of filtrate chloride concentration.A decrease in circulating mineralocorticoid level, as a consequence of volume expansion, does not seem to account for this change in tubular function since identical studies in dogs receiving excessive amounts of 11-deoxycorticosterone acetate during the day of infusion yielded similar findings. Moreover, no other consequence of volume expansion appears to be sufficient to cause this change in tubular function in the absence of metabolic alkalosis; when the alkalosis was corrected with hydrochloric acid before infusion, isometric expansion of extracellular volume did not induce selective chloride retention. We suggest that isometric expansion during metabolic alkalosis causes a decrease in proximal sodium reabsorption that relinquishes filtrate to a more distal site in the nephron and that this site may retain chloride preferentially when hypochloremia or chloride deficiency is present.
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PMID:Correction of metabolic alkalosis by the kidney after isomertric expansion of extracellular fluid. 564 61

Anion gap acidosis is generally regarded as featuring a rather precise balance between the decrement in plasma HCO-3 and the increment in anion gap plasma Cl- remaining normal. In theory, therefore, the finding of hypochloremia in conjunction with an anion gap acidosis should evidence a coexisting metabolic alkalosis. In the clinical setting, however, hypochloremia is occasionally found in patients with anion gap acidosis but without exposure to a recognized alkalosis-inducing process. To examine the possibility that an element of hypochloremia might, under certain circumstances, be an integral part of the underlying acidosis, we studied three forms of anion gap acidosis in unanesthetized, nephrectomized rats. In protocol I, 7 mEq/kg H+ as H2SO4 was infused over 1 hour. In protocol II, 24 mEq/kg H+ as D,L-lactic acid was infused over 3 hours. In protocol III, rats were maintained in the anephric state for approximately 28 hours to permit uremic acidosis to develop. In each protocol, plasma C1- fell significantly (-8.0, -12.0, and -7.0 mEq/L in protocols I, II, and III, respectively) and contributed substantially to the observed increment in anion gap. A possible explanation for this acidosis-induced hypochloremia is expansion of the extracellular compartment secondary to the extrusion of cellular cation that occurs in the process of buffering.
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PMID:Hypochloremia as a consequence of anion gap metabolic acidosis. 673 48


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