Sodium Transport Across the Surface Membrane of Red Blood Cells in Hereditary Spherocytosis 1

Bertles, John F.

doi:10.1172/jci103487

Cited by 67 publications

(31 citation statements)

References 26 publications

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“…No correlation was observed between the magnitude of the Na' influx and the median corpuscular fragility for hereditary spherocytes from nine patients, which confirms the conclusions of Bertles (18). it seems likely that reticuloendothelial blockade of the patient's spleen makes at least some contribution.…”

Section: Resultssupporting

confidence: 74%

Red cell survival studies in hereditary spherocytosis

Wiley¹

1970

J. Clin. Invest.

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Section: Resultssupporting

confidence: 74%

Red cell survival studies in hereditary spherocytosis

Wiley¹

1970

J. Clin. Invest.

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“…In serum from a patient with obstructive jaundice, however, they gained cholesterol. As has been observed in normal red cells (12), this gain in cholesterol in vitro was not associated with (4,35). This leads to an increased rate of sodium extrusion and an accelerated rate of gucose consumption (4,36).…”

Section: Resultsmentioning

confidence: 65%

The role of membrane lipids in the survival of red cells in hereditary spherocytosis

Cooper¹,

Jandl²

1969

J. Clin. Invest.

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A B S T R A C T Red cells inObstructive jaundice causes an increase in membrane lipid, primarily cholesterol, and a decrease in the osmotic fragility of normal red cells. When HS red cells are transfused into patients with obstructive jaundice they also become less osmotically fragile. Moreover, when incubated in obstructive jaundice serum, they gain cholesterol. This acquisition of membrane lipid in vitro does not result in a change in their rate of glucose utilization or sodium efflux. However, the transformation to a less spheroidal shape in vivo permits them to traverse better the splenic circulation and survive longer.

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“…Whereas many hemolytic disorders (1)(2)(3)26) display increased passive permeability of the red blood cell membrane to cations with subsequent increased movement of the cation down its electrochemical gradient, these disorders are accompanied by a compensatory increase of the sodium outflux in an attempt to extrude sodium from the cell and maintain a normal intracellular environment. The intracellular sodium and potassium generally remain normal in these illnesses until just before the onset of hemolysis.…”

Section: Resultsmentioning

confidence: 99%

“…The transport of these cations has been studied in a variety of human illnesses, such as hereditary spherocytosis (1,2) and sickle-cell anemia (3), as well as nonhematologic diseases, such as severe uremia (4), disseminated neoplastic disorders (5), and extensive burns (5). Overman (6) studied the effects of Plasmodium knowlesi malaria upon the erythrocytic cation concentration in Rhesus monkeys.…”

Section: Introductionmentioning

confidence: 99%

Alterations of red blood cell sodium transport during malarial infection

Dünn¹

1969

J. Clin. Invest.

115

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A B S T R A C T Previous studies have suggested that malaria induces changes in erythrocytic membrane permeability and susceptibility to osmotic lysis. The present study investigated erythrocytic transport of sodium with cells from Rhesus monkeys infected with Plasmodium knowlesi. Red blood cell sodium concentration was significantly elevated in 37 parasitized animals (21.8 ±1.2 mM; mean +SEM), as compared to 23 control animals (10.0 +0.38 mM). The cellular sodium increased with the density of parasitemia and the cellular potassium decreased in proportion to the elevation of sodium. Nonparasitized as well as parasitized erythrocytes possessed this abnormality of cation metabolism. Effective chloroquine therapy reversed the changes over a period of 4 days.Active sodium outflux rate constants were depressed in animals with malaria (0.202 +0.012), as compared to controls (0.325 ±0.027). Passive sodium influx rate constants were higher in infected monkeys (0.028 +0.002) than in control animals (0.019 +0.002). The cross incubation of malarial plasma with normal red blood cells induced a 22% diminution in active sodium outflux but no changes were observed in sodium influx.It is concluded that malaria alters erythrocytic sodium transport in all erythrocytes. The elevated intracellular sodium concentration is the net result of decreased sodium outflux and increased sodium influx. The plasmodium organism or the affected host may produce a circulating substance that is deleterious to erythrocytic membrane cation transport.

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Sodium Transport Across the Surface Membrane of Red Blood Cells in Hereditary Spherocytosis 1

Cited by 67 publications

References 26 publications

Red cell survival studies in hereditary spherocytosis

Red cell survival studies in hereditary spherocytosis

The role of membrane lipids in the survival of red cells in hereditary spherocytosis

Alterations of red blood cell sodium transport during malarial infection

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