Neutrophil activation and severity of tissue hypoxia during tourniquet-induced forearm ischemia in man.

Neutrophil activation and adhesion to the endothelium are thought to be central in the inflammatory response to reperfusion after ischemia. This study explores whether the severity of tissue hypoxia can be related to a biochemical measure. Venous blood was sampled from 20 volunteers undergoing tourniquet-induced forearm ischemia for 10 min and subsequent reperfusion. Samples were analyzed for neutrophil count, neutrophil hydrogen peroxide generation measured by flow cytometry, plasma thromboxane (a marker of platelet activation), the endogenous antioxidant glutathione peroxidase, and thrombomodulin, a marker of endothelial cell damage. Forearm oxygen saturation by near-infrared spectroscopy was monitored throughout the experiment. Neutrophil hydrogen peroxide generation fell from an initial mean fluorescent intensity (MFI) of 0.91 +/- 0.07 to 0.77 +/- 0.09 (mean +/- SE) during ischemia (P < 0.05) and this reduction correlated with severity of hypoxia (r = 0.56, P < 0.01). Plasma levels of glutathione peroxidase were also reduced during ischemia (P < 0.05) whereas plasma thromboxane levels rose (P < 0.05). There were no significant changes in plasma levels of thrombomodulin or circulating neutrophil count. In conclusion, alterations in a measurement of neutrophil function reflect the changes in tissue oxygenation and may act as a biochemical predictor of the severity of an ischemic injury.