Critical Care · 7 authors, 6 centres
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In a rat model of warm pulmonary ischemia followed by reperfusion of 30 minutes to 4 hours, significant increases in neutrophils, macrophages, and T cells were observed alongside apoptosis and oedema in the absence of necrosis. These findings characterize the cellular infiltrates contributing to warm ischaemia–reperfusion injury relevant to acute respiratory distress syndrome.
Fifty rats were randomized into eight groups to evaluate warm pulmonary ischaemia–reperfusion injury. Five groups underwent 60 minutes of warm ischaia followed by reperfusion periods of 30 minutes to 4 hours, with an additional group flushed using isolated lung perfusion and two sham groups. Neutrophils, macrophages, T cells, apoptosis, and oedema were assessed using H&E staining, immunohistochemistry, and TUNEL assay. Neutrophils increased from 30 minutes to 4 hours of reperfusion with a bimodal pattern. Macrophages doubled and T cells increased fourfold during early reperfusion.
