Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “ALKALOSIS”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 235 records · Page 13Linked to original sources
PubMed1992

A case of Cushing's syndrome associated with chronic respiratory failure due to metabolic alkalosis.

A case of Cushing's syndrome associated with chronic respiratory failure is presented. Although arterial blood gas analysis showed severe metabolic alkalosis, hypoxemia and mild hypercapnia, the patient had no evidence of pulmonary disease or neuromuscular disorder. Voluntary hyperventilation and inhalation of 100% oxygen (O2) revealed normalized arterial oxygen tension (PaO2). Following the recovery from metabolic alkalosis by the treatment with potassium chloride, PaO2 was elevated and arterial carbon dioxide tension (PaCO2) was lowered. Therefore, it was strongly suggested that the main cause of chronic respiratory failure was compensatory alveolar hypoventilation as a response to metabolic alkalosis.

Alkalosis↗
PubMed2004

Myoclonus and metabolic alkalosis from licorice in antacid.

A 90-year-old woman with hypertension developed metabolic alkalosis and myoclonus. Her medications included diltiazem hydrochloride, benidipine hydrochloride, kallidinogenase, procaterol hydrochloride, sennoside, dihydrocodeine phosphate, and KM powder antacid that contained 354 mg of licorice and 900 mg of sodium bicarbonate per 3.9 g of powder. Endocrinological studies showed slightly reduced plasma renin activity and normal plasma aldosterone concentration. A provisional diagnosis of licorice-induced metabolic alkalosis was established and the patient was successfully treated after correction of serum pH and cessation of the medications. Licorice-induced metabolic alkalosis must be considered in the differential diagnosis of myoclonus.

Aged↗
PubMed1993

Metabolic alkalosis induced by plasmapheresis in a patient with systemic lupus erythematosus.

We report a patient with systemic lupus erythematosus (SLE), who had developed metabolic alkalosis during plasmapheresis. The metabolic alkalosis could be promptly corrected by reducing the amount of citrate load. The development of metabolic alkalosis can be explained by the citrate load during plasmapheresis. Careful monitoring of acid base status is mandatory in patients with limited renal function and the reduction of citrate load may be advisable in plasmapheresis.

Adolescent↗
PubMed2000

Saline-resistant metabolic alkalosis, severe hypokalemia and hypertension in a 74-year-old woman.

The case of a 74-year-old woman with past history of hypertension and cerebrovascular accident admitted with pneumonia, dehydration, hypernatremia and severe hypokalemic alkalosis is presented. After correction of the hypertonic dehydration, the hypokalemia and alkalosis persisted in spite of aggressive potassium supplementation and the patient became hypertensive. Mineralocorticoid excess was suspected and excluded after extensive endocrinological testing. The use of aldactone failed to revert the abnormalities. Triamterene administration corrected the electrolytes and acid base aberrations, and dramatically improved the blood pressure control. This clinical picture is compatible with the diagnosis of Liddle's syndrome. Our patient exemplifies the unique occurrence of hypokalemic metabolic alkalosis in association with volume contraction at the start of the hospitalization and volume expansion later on her course.

Aged↗
PubMedDate not supplied

[An unexpected stage of alkalosis in the dynamics of the early posthemorrhagic period].

A study was made on acid-base metabolism in early posthemorrhagic period as exemplified by examination of patients presenting with gastrointestinal hemorrhage. It has been ascertained that hemorrhage is accompanied by a mixed variant of the acid-base state (ABS) deviation, namely metabolic lactate-acidosis and respiratory alkalosis. In the time-related course of posthemorrhagic period such deviations persist in patients with lethal outcome; with the disease running a favourable course the above deviations are found to return to normal quite soon. The development of complications leads to staging in ABC, its stages being as follows: stage I--the initial stage, stage II--persisting metabolic acidosis and respiratory alkalosis, stage III--alkalosis, stage IV--normalization, with stage III of ABS being encouraged by hypocapnia caused by function disorders of the lungs in early posthemorrhagic period, normalization of cell metabolism, increase in the rate of urination as a reflection of the third earlier identified stage of water metabolism, with the H+ excretion in the urine at the previous level. The identified ABS stage III threatens coming trouble, being accompanied by metabolic deviations together with a risk of function disorder of the myocardium.

Acid-Base Equilibrium↗
PubMed2004

Effect of extracellular hypertonicity and alkalosis on endothelial-derived EA.hy 926 cells in vitro.

Endothelial and local metabolic mechanisms contribute in concert to the regulation of blood flow. In vivo extracellular alkalosis induces a vasoconstriction, hyperosmolarity a vasodilatation. The interaction between local metabolic and endothelial mechanisms is poorly understood. Therefore we investigated in endothelial-derived EA.hy926 cells the secretion of endothelial modulators of vascular tone under hypertonic stress with and without alkalosis: hyperosmolality was generated by either the addition of NaHCO subset 3 (25, 50, 100 mM, pH up to > 8) or mannitol (50, 100, 200 mM) to the cell culture media. The cells were studied using automated cell counting, measurement of the activity of the lactate dehydrogenase (LDH) and a bromo-deoxyuridine (BrdU) cell proliferation assay. Endothelin and cGMP, a surrogate marker for nitric oxide (NO), were measured with specific ELISAs. EA.hy 926 cells formed stable monolayers in vitro. The secretion of endothelin, but not of cGMP was inversely correlated with the osmolality of the incubation media: the endothelin concentration in the supernatants decreased in both mannitol- and NaHCO subset 3 -treated cells in a concentration-dependent manner (152.4 +/- 6.2 pg/ml (control) to 24.4 +/- 2.4 pg/ml (200 mM mannitol), res. to 18.2 +/- 2.7 pg/ml (100 mM NaHCO subset 3). Neither hypertonic bicarbonate nor mannitol solutions decreased the monolayer cell density or cell viability during the 6 hour incubation period. In conclusion, EA.hy926 cells are quite resistant against a 6-hour hypertonic/alkaline stress. Hypertonicity decreases the secretion of endothelin and has no effect on cGMP. At each level of hypertonicity the endothelin concentration was similar in the NaHCO subset 3 and mannitol media arguing against a direct role of endothelin in alkalosis-induced vasoconstriction in vivo. The decreased secretion of endothelin during hypertonicity could contribute to the hyperosmolal vasodilation seen in vivo.

Alkalosis↗
PubMed1992

[The mechanism maintaining severe metabolic alkalosis].

The pathogenesis of severe metabolic alkalosis was studied from the following three points of view; 1) effect of administration of alkalosing agents in rats, 2) amino acids in blood and muscle and 3) renal ammoniagenesis in control and K-depleted rats. The weight gain was significantly depressed in all kinds of alkalosis. Lysine increased remarkably, especially over 10 times in muscle, but Fischer's ratio decreased significantly in blood and muscle of K-depleted rats. Glutamine is the main source in ammoniagenesis, and ammonia (NH4+) is the main substance of H+ secretion from kidney. Though the concentration of glutamine was unchanged in blood and muscle, ammoniagenesis increased 2.5 times, compared with control in renal tubules suspension of K-depleted rat. In conclusion, increase in renal ammonia production would be one of the most important ways to maintain severe metabolic alkalosis.

Alkalosis↗
PubMed1991

Replacement of chloride deficit by use of 1.8% NaCl to correct experimentally induced hypochloremic metabolic alkalosis in sheep.

Five adult 40- to 50-kg female sheep were surgically fitted with a reentrant cannulae placed in the proximal part of the duodenum just distal to the pylorus. By diversion of abomasal outflow, this model has been shown to produce hypochloremic metabolic alkalosis accompanied by dehydration, hypokalemia, and hyponatremia. Each sheep was subjected to 3 separate, 12-hour IV treatment trials, in each case preceded by a control period of 48 hours, and a diversion period of 36 to 96 hours, during which a hypochloremic (Cl- less than or equal to 60 +/- 2 mEq/L) metabolic alkalosis with hypokalemia and hyponatremia was produced. Treatment 1, consisting of 6 L of isotonic Na gluconate, was designed to replace volume without replenishing the Cl-1 deficit. Although hydration improved, plasma Cl- decreased further, and the sheep became increasingly weak and depressed. Treatment 2, consisting of 2 L of 1.8% NaCl, was designed to replace the Cl- deficit without replacing total volume. Plasma Na+ and Cl- concentrations returned to normal during the 12 hours of treatment; acid-base balance and plasma K+ concentrations returned to normal within 36 hours of treatment. During treatment 3 (control, no treatment), measured metabolic values changed minimally. We concluded that the IV replacement of Cl- without K+ is effective in the correction of experimentally induced hypochloremic metabolic alkalosis in sheep.

Alkalosis↗
PubMed1989

Furosemide and sodium bicarbonate-induced alkalosis in the horse and response to oral KCl or NaCl therapy.

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)

Alkalosis↗
PubMed1989

Haemodynamic effects of respiratory alkalosis independent of changes in airway pressure in anaesthetized newborn dogs.

We have recently reported a decrease in cardiac output in newborn dogs during respiratory alkalosis which is independent of changes in airway pressure. The present study was designed to characterize the mechanism responsible for this reduction in cardiac output. Twelve newborn coonhounds were anaesthetized with pentobarbital, paralyzed with pancuronium and hyperventilated to an arterial carbon dioxide tension (PaCO2) of 20 torr. Subsequent changes in PaCO2 were achieved by altering the FiCO2. Measurements were made after 30 min at either 40 or 20 torr PaCO2. The sequence of PaCO2 levels was randomized. Compared to normocarbia, respiratory alkalosis resulted in significantly decreased cardiac output (279 +/- 16 to 222 +/- 10 ml/min per kg, mean +/- SEM, P less than 0.001), stroke volume (1.60 +/- 0.10 to 1.24 +/- 0.06 ml/kg; P less than 0.001), maximum left ventricular dP/dt (1629 +/- 108 to 1406 +/- 79 mmHg/s, P less than 0.01) and left ventricular end diastolic pressure (3.9 +/- 0.4 to 2.9 +/- 0.3 mmHg; P less than 0.001). The decrease in cardiac output during respiratory alkalosis is manifest through a decrease in stroke volume, which is due, at least in part, to the decrease in left ventricular end diastolic pressure. The decrease in maximum left ventricular dP/dt is likely a reflection of the decrease in preload, however, a change in myocardial contractility cannot be excluded. We speculate the decrease in filling pressure may be due to an increase in venous capacitance.

Alkalosis, Respiratory↗
PubMedDate not supplied

Metabolic alkalosis induced by regional citrate hemodialysis.

Two patients are described in whom regional citrate dialysis (RCD) and induced metabolic alkalosis with marked increases in serum HCO3, which were sustained during the period of repeated treatments. As currently employed, RCD of necessity delivers large amounts of potential bicarbonate (several hundred mEq) to the patient and may cause severe metabolic alkalosis. Studies should be carried out to determine an effective method to avoid this complication whenever repeated RCD is necessary or is used in patients with pre-existing alkalosis.

Adult↗
PubMed1988

Involvement of lipoxygenase and cyclo-oxygenase pathways in hypoxia and metabolic alkalosis produced by canatoxin in rats.

This paper reports on the metabolic alkalosis produced in rats by canatoxin, a neurotoxic principle extracted from Canavalia ensiformis seeds. Rats receiving canatoxin showed increased blood bicarbonate concentration with alkaline pH and no change in pCO2. A fall in pO2 was also seen. A dose-dependent relationship between pO2 decrease and bicarbonate increase was also observed with the toxin, suggesting that hypoxia may result from respiratory compensation. Canatoxin-induced hypoxia was both lipoxygenase and cyclo-oxygenase dependent but metabolic alkalosis was only blocked with cyclo-oxygenase inhibitors. Canatoxin activates the lipoxygenase pathway and probably increases leukotriene (LT) production. Since LT may release cyclo-oxygenase products, this may explain the metabolic alkalosis observed with canatoxin.

Acid-Base Equilibrium↗
PubMed1977

Hypokalemic, metabolic alkalosis induced by high-dose ampicillin sodium.

A case of hypokalemic metabolic alkalosis precipitated by high-dose intravenous ampicillin sodium is discussed. Cases of hypokalemic metabolic alkalosis attributable to ampicillin sodium have not been reported previously. There have been reports of this phenomenon associated with high doses of penicillin sodium and carbenicillin disodium. The possible mechanism of antibiotic-induced hypokalemic metabolic alkalosis is discussed. It is suggested that most cases of antibiotic-induced hypokalemia respond to oral or intravenous potassium chloride.

Alkalosis↗
PubMed1983

Renal tubular acidosis in a patient with recurrent metabolic alkalosis.

A 7-month-old infant with failure to thrive and recurrent episodes of vomiting and metabolic alkalosis was evaluated. Urine pH, serum bicarbonate, and urine PCO2-blood PCO2 studies were consistent with the diagnosis of distal renal tubular acidosis (RTA-type I). Analysis of serum potassium and chloride levels during periods of alkalosis and acidosis revealed that potassium depletion and hypochloremic volume contraction served to maintain the alkalotic state despite the presence of an underlying chronic acidosis. This case represents an unusual presentation for renal tubular acidosis and suggests that, under certain conditions, renal tubular acidosis may predispose to the maintenance of a metabolic alkalosis.

Acidosis, Renal Tubular↗
PubMed1984

[Treatment of experimental metabolic alkalosis by sorbamine].

A new infusion solution called alkamine has been developed for the treatment of metabolic alkalosis. It contains amino acids in the form of hydrochlorides (arginine, lysine and histidine hydrochlorides), potassium chloride and sorbit. The solution has been tested in anesthetized cats with experimental metabolic alkalosis induced by the injection of sodium hydrocarbonate solution. In control experiments without any therapy, a stable alkalytic shift of acid-base balance in the blood, a fall in the blood pressure, hypopotassemia and death of the animals within the first days were observed after experiments. The treatment of metabolic alkalosis by alkamine (25 experiments) entailed a complete correction of acid-base balance and hypopotassemia, stabilization of blood pressure and the survival of 23 out of the 25 animals. Alkamine solution has been approved for clinical trials by the Pharmacological Committee of the Ministry of Health of the USSR.

Acid-Base Equilibrium↗
PubMed1984

[A case of hypochloremic alkalosis in a newborn infant].

A full term neonate in which by accident a metabolic alkalosis was found, is described. The origin of the metabolic alkalosis was excessive vomiting by the mother during the days prior to delivery. The simplified form of the Henderson Hasselbalch equation is used to describe the factors responsible for the generation of metabolic alkalosis. Consequences for the neonate are mentioned, especially the vasoconstriction of the cerebral vessels is discussed. Treatment should be rehydration and administration of sodium-chloride.

Adult↗
PubMed1981

Buffered hydrochloric acid: a modern method of treating metabolic alkalosis.

Twenty-one patients with metabolic alkalosis were treated successfully with intravenous hydrochloric acid (HCl) buffered in an amino acid solution (TPN). No complications of HCl were seen. TPN was used to meet energy needs and provide a buffering effect through the interaction of HCl and amino acids. Buffered HCl therapy should be considered as the initial treatment in patients with metabolic alkalosis associated with congestive heart failure, renal failure, hepatic failure, cerebral edema, or refractory metabolic alkalosis.

Alkalosis↗