Objective: To investigate the effects of neutrophil (PMN) transmigration into inflammatory sites on cytosolic pH (pH1) regulation. Design: Exudative PMNs were obtained by bronchoalveolar lavage from rats sustaining endotoxin- induced lung injury. Circulating PMNs were purified with density-gradient centrifugation. Cytosolic pH was measured with single-cell fluorescence imaging using the pH-sensitive dye biscarboxyethyl-carboxyfluorescein. Results: Exudative PMNs showed impaired pH1 recovery from an induced acid load compared with circulating PMNs. Under conditions of extracellular acidosis, exudative PMNs showed impaired pH1 homeostasis and produced decreased superoxide compared with circulating cells. Inhibition of the sodium proton exchanger attenuated the differences in pH1 recovery, suggesting a mechanism underlying the pH1 regulatory dysfunction. All cells had comparable adenosine triphosphate levels and superoxide production at physiologic extracellular pH. Conclusion: Impaired pH1 regulation of exudative cells may mediate cellular dysfunction and impaired resolution of infection at inflammatory sites.
|Original language||English (US)|
|Number of pages||6|
|Journal||Archives of surgery|
|State||Published - Dec 1996|
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