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Defective energy metabolism in stored granulocytes
Author(s) -
Lane T.A.,
Lamkin G.E.
Publication year - 1982
Publication title -
transfusion
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.045
H-Index - 132
eISSN - 1537-2995
pISSN - 0041-1132
DOI - 10.1046/j.1537-2995.1982.22583017460.x
Subject(s) - incubation , zymosan , adenosine triphosphate , extracellular , chemotaxis , chemistry , opsonin , metabolism , neutrophile , biochemistry , endocrinology , medicine , biology , in vitro , receptor
Previous studies suggested that a general metabolic defect might be responsible for impaired chemotaxis of stored granulocytes (PMN). We studied PMN energy metabolism in fresh and stored PMN. Adenosine triphosphate (ATP) decreased slightly in unstimulated PMN after 48 hours of storage at room temperature. Exposure of fresh PMN to opsonized zymosan resulted in a 12 percent decrease in ATP. In contrast, PMN stored for 24 or 48 hours at room temperature and then exposed to opsonized zymosan, showed significant decreases in ATP. Incubation of fresh or stored, stimulated (opsonized zymosan) or resting PMN with potassium cyanide resulted in no change in the pattern of ATP decrements during storage. Likewise, incubation of fresh or stored, stimulated or resting PMN in the presence or absence of extracellular glucose, resulted in no change in the pattern of ATP decrements during storage. Preincubation of PMN with 2‐deoxy‐glucose obscured the differences in ATP maintenance between fresh and stored PMN. ATP decrements were also observed in unstimulated PMN which had been stored at high cell concentrations. Decrements in ATP correlated stronglywith decreased glucose (r = .82) and pH (r = .89) in the storage medium. These decrements were partially reversed by incubation of PMN in fresh buffer. The ATP decrements in stored, concentrated granulocyte preparations thus were prevented by maintenance of pH. ATP decrements were not prevented by additional glucose. Thus, in PMN stored for 24 or 48 hours at room temperature, there was a defect in ATP maintenance which was occult in unstimulated cells, but was evoked by the energy‐dependent process, phagocytosis. These findings are compatible with a major role for glycolysis and glycogenolysis in maintaining ATP in fresh and stored PMN. Storage of PMN at high cell concentrations was accompanied by impaired ATP maintenanceand decreased pH in the storage medium, both of which were preventable by addition of alkali to the PMN concentrate prior to storage.