Spatial and temporal correlation between leukocyte behavior and cell injury in postischemic XXXX skeletal muscle microcirculation.

@entity71210 @entity2667 @entity3624 @entity71209 @entity22139 @entity35 @entity551 @entity121 @entity130
BACKGROUND: Although leukocyte adhesion and capillary plugging are postulated to play a role in postischemic tissue injury, there is only limited evidence demonstrating the relationship between tissue leukocyte accumulation and cell injury in terms of their temporal sequence and spatial distribution. EXPERIMENTAL DESIGN: This study was designed to study in vivo neutrophil behavior and its correlation with cell @entity121 . The microcirculation of the @entity35 spinotrapezius muscle was observed in vivo using dual-color digital microfluorography to simultaneously visualize leukocyte traffic and cell death (irreversible nuclear damage) on the basis of @entity22139 and @entity2667 , respectively. A 1-hour period of hemorrhagic @entity551 (40 mm Hg) followed by reperfusion was carried out to induce @entity121 . RESULTS: @entity551 was followed by an increase in leukocyte recruitment in two different ways: capillary obstruction and @entity71209 . Upon reperfusion, a majority of the leukocytes were initially dispersed from the muscle capillaries and venules, but then the number of leukocytes plugging capillaries and adherent to venules increased again in a time-dependent manner. The number of leukocytes obstructing capillaries was closely correlated with the @entity551 . The cell injury became detectable initially at the end of the @entity551 period and then increased explosively after reperfusion before a significant leukocyte accumulation. Reperfusion-induced @entity130 was seen predominantly in reperfused capillaries without plugging leukocytes. A majority of the initially damaged nuclei were those of myocytes in the pericapillary space, but no nuclei of capillary endothelium was involved. @entity71210 , a novel inhibitor of @entity3624 oxidase, significantly attenuated the early increase in @entity121 and subsequent venular leukocyte adhesion after reperfusion. CONCLUSIONS: These results suggest the involvement of an endothelium-dependent mechanism involving @entity3624 oxidase in postischemic irreversible @entity130 . It is conceivable that leukocytes adherent to venules as well as those plugging capillaries play only minor roles in the initial mechanism of reperfusion injury.
