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At least 1,225 records · Page 68Linked to original sources
PubMed1990

A patient with hyperkalemia and metabolic acidosis.

Uptake of potassium by extrarenal tissues, primarily muscle and liver, represents a major defense mechanism in the maintenance of normokalemia following an acute elevation in the serum potassium concentration. Insulin, epinephrine, and aldosterone all play major roles in maintaining the normal distribution of potassium between the intracellular and extracellular environment. In addition to hormonal regulation, changes in blood pH and tonicity also exert a strong influence on extrarenal potassium metabolism. Last, the serum potassium concentration per se directly influences its own cellular uptake and this transport mechanism appears to be inhibited by uremia.

Acidosis↗
PubMed1983

Lactic acidosis: current concepts.

Lactic acidosis is now a widely recognized disorder in clinical medicine. Experimental studies during the past decade demonstrate an important role of lactate disposal mechanisms in the pathogenesis of lactic acidosis. Such factors as decreased cardiovascular reserve, inadequate liver perfusion and alterations in liver intracellular pH appear to limit the normally large capacity of the liver to dispose of lactic acid. The continued high mortality of this disorder has led to a re-examination of the conventional, empirical treatment of lactic acidosis with sodium bicarbonate. Available data suggest that alkali may cause or exacerbate the conditions of excessive lactate production, decreased cardiac reserve and inadequate hepatic lactate disposal which exist in this disorder. In contrast, dichloroacetate therapy shows strikingly beneficial results, at least in early experimental studies.

Acidosis↗
PubMed2002

Metabolic acidosis in the intensive care unit.

Metabolic acidosis is a common occurrence in critically ill patients. Understanding the pathological mechanisms underlying the generation of protons will enable the clinician to quickly recognize these disorders and establish an acceptable treatment strategy. This article presents a logical approach to metabolic acidosis.

Acid-Base Imbalance↗
PubMed1987

Blood rheology in the newborn infant.

The blood in neonates shows several peculiar properties which affect its rheological properties. 1. The haematocrit in neonates may be as high as 0.65 l/l without any clinical signs. 2. Both plasma viscosity and red cell aggregation are markedly lower in neonates than in adults because of low protein levels in neonates. This results in decreased blood viscosity at given haematocrit, particularly at low shear forces. 3. Deformability of neonatal red cells is similar to that of adult cells when studied under controlled conditions (e.g. rheoscope, ektacytometer). However, neonatal red cells are less filterable and require higher pressures for entering narrow micropipettes than adult red cells due to the larger size of neonatal red cells. 4. Neonatal leukocytes require higher pressure for the passage of 5 microns filter pores or 5 microns micropipettes than adult cells. The following haemorheological disorders have been observed in neonates: 1. Polycythaemia in infants with late cord-clamping, severe asphyxia, growth retardation and diabetic mothers. 2. Markedly decreased red cell deformability in septicaemia, necrotizing enterocolitis and in vitamin E deficiency (after exposure to oxidizing agents). 3. Moderately decreased red cell deformability in infants with diabetic mothers, growth retardation and severe acidosis. 4. Increased red cell aggregation in septicaemia. 5. Lack of red cell aggregation in immature neonates. 6. Decreased ability of leukocytes from septic neonates to pass filter pores and micropipettes. Treatment may be either haemodilution (in polycythaemia) or exchange transfusion (in septicaemia and necrotizing enterocolitis). Haemorheological drugs have not been used in neonates.

Blood Flow Velocity↗
PubMed1998

The management of metformin overdose.

Only two cases of deliberate self-poisoning with metformin have been described in the literature. We report the management of three cases, all of which presented with severe lactic acidosis. Two cases had a fatal outcome. The options for treatment and previous cases reported in the literature are reviewed. Recommendations for the management of metformin overdose include early recognition, intensive support of the cardiovascular system, the correction of metabolic acidosis and the maintenance of body temperature. The use of venovenous haemofiltration against a non-lactate containing fluid may improve outcome when sodium bicarbonate alone fails to reverse severe systemic acidosis.

Acidosis, Lactic↗
PubMed2000

Ammonium chloride potentiation of streptozotocin-induced diabetes in juvenile pigs.

In preparation for direct vital microscopic evaluation of microcirculatory dynamics in the diabetic pig myocardium, we were initially unsuccessful in inducing sustained hyperglycemia in juvenile pigs using streptozotocin according to previously reported methods. Therefore, we modified the technique in a way previously unreported in an effort to improve the success rate of diabetes induction. In the first set of 9 pigs, we followed described methods of intravenous injection with 150 mg/kg streptozotocin. In the second group of 9, the technique was modified. The change was based on human studies with ammonium chloride and animal experiments with alloxan, and consisted of the addition of a period of pretreatment with ammonium chloride. Of the nine pigs not treated with ammonium chloride, only two developed sustained hyperglycemia in excess of 17 mmol/L (300 mg/dl), and only after reinjection with a full dose of streptozotocin within 7 days of the first injection. Conversely, of the ammonium chloride pretreated pigs, eight of nine developed diabetes. We conclude that the addition of ammonium chloride to produce systemic acidosis prior to streptozotocin injection improves the efficacy of the drug.

Acidosis↗
PubMed1968

Study of fatal cases of Friedreich's ataxia.

A study of 82 fatal cases of Friedreich's ataxia showed that over half the patients died of heart failure while nearly three-quarters had evidence of cardiac dysfunction during life. A high incidence of diabetes mellitus (23%) was another finding, and four patients developed diabetic ketosis terminally.

Acidosis↗