Acute lung injury is a frequent clinical occurrence following blood loss and trauma. The nature of this injury remains poorly understood. Objective : To examine the relative parenchymal and intra-al-veolar distribution of inflammation in a rat model of hemorrhage and resuscitation. Methods : Rats were anesthetized and subjected to hemorrhage followed by resuscitation with shed blood and saline. Myelo-peroxidase activity of lung homogenates and cytology of bronchoalveolar lavage fluid were used to measure total lung and intra-alveolar neutrophil invasion. Extravasation of IV-administered [ 125 I]-albumin was used to determine total lung and alveolar permeability. Permeability results were analyzed using their base-10 logarithmic transformations. Results : 86 animals were studied. Whole-lung myeloperoxidase activity was increased (control = 0.34 ± 0.16 units, injured = 0.84 ± 0.43 units, p < 0.01), while there was no difference in intra-alveolar leukocyte counts (injured = 1.85 ± 1.30 times 10 5 mL, control = 2.44 ± 1.75 times 10 5 mL, p = 0.40), suggesting that the cellular component of the injury was more severe in the intravas-cular and interstitial spaces. There was a strong trend toward increased permeability in the interstitial compartment, and a significant increase in permeability in the intra-alveolar compartment (whole-lung permeability: control =—0.27 ± 0.19 units, injured = 0.10 ± 0.55 units, p = 0.06; alveolar permeability: control = -2.00 ± 0.47 units, injured = -1.32 ± 0.49 units, p < 0.01), suggesting that the loss of integrity to macromolecules was not limited to the interstitium. Conclusion : Hemorrhage and resuscitation resulted in an acute lung injury characterized by extravasation of intravascular protein into both the interstitium and the intra-alveolar space. Neutrophil invasion of the lung was demonstrable only in the interstitial compartment
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