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Hemorrhage and resuscitation induce delayed inflammation and pulmonary dysfunction in mice
J A Claridge1, R I Enelow, J S Young
1Trauma Research Laboratory, University of Virginia Health System, Charlottesville, Virginia, 22908-0709, USA.
Background:
It is well known that hemorrhagic shock induces inflammatory changes. Our objective was to study the histologic and biochemical changes in the lung and evaluate alterations in respiratory function after hemorrhage and resuscitation (H/R) in mice.
Methods:
After 30 min of hemorrhagic shock, mice were resuscitated with shed blood to restore mean arterial blood pressure to baseline. A sham group was anesthetized and instrumented for 30 min, but did not undergo hemorrhage. Myeloperoxidase (MPO) levels were measured and histologic analysis was performed on lung tissue. Pulmonary function was evaluated using whole-body plethysmography (WBP) 1, 3, and 5 days postprocedure. Alveolar function was evaluated by measuring carbon monoxide uptake via gas chromatography 5 days after H/R.
Results:
Five days after H/R, mice exposed to shock had significantly higher lung MPO levels and showed greater histologic evidence of lung injury. Airway resistance (Penh) in the sham mice was 0.91 +/- 0.06 versus 1.21 +/- 0.09 in the hemorrhage group (P < 0.01). Alveolar function was significantly decreased in the H/R group (70.8 +/- 3.6%) compared with shams (81.6 +/- 1.8%) (P < 0.05).
Conclusions:
Hemorrhage and resuscitation cause delayed biochemical, histologic, and physiologic changes in the lung. These were marked by increased lung MPO, increased neutrophils, and decreased alveolar function. The alterations of pulmonary function and structure were most severe 5 days after H/R.
