SCKNTIFIC ADVANCC-S The Pattern of Early Lung Parenchymal and Air Space Injury Following Acute Blood Loss

Acute lung injury is a frequent clinical oc- currence 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. Ex- travasation of IV-administered (L2511-albumin was used to determine total lung and alveolar permeabil- ity. Permeability results were analyzed using their base-10 logarithmic transformations. Results: 86 an- imals were studied. Whole-lung myeloperoxidase activity was increased (control = 0.34 2 0.16 units, injured = 0.84 5 0.43 units, p < 0.01). while there was no difference in intra-alveolar leukocyte counts (injured = 1.85 ? 1.30 x lOVmL, control = 2.44 2 1.75 X 105/mL, p = 0.40), suggesting that the cellular com- ponent of the injury was more severe in the intravas- cular and interstitial spaces. There was a strong trend toward increased permeability in the intersti- tial compartment, and a significant increase in per- meability in the intra-alveolar compartment (whole- lung permeability: control = -0.27 2 0.19 units, injured = 0.10 -t 0.55 units, p = 0.06; alveolar per- meability: control = -2.00 ? 0.47 units, injured = - 1.32 2 0.49 units, p < 0.011, suggesting that the loss of integrity to macromolecules was not limited to the interstitium. Conclusion: Hemorrhage and resusci- tation resulted in an acute lung injury characterized by extravasation of intravascular protein into both the interstitium and the intra-alveolar space. Neutro- phi1 invasion of the lung was demonstrable only in the interstitial compartment. Key words: shock; lung; trauma-induced ARDS; posttraumatic respira- tory failure. ACADEMIC EMERGENCY MEDICINE 1998; 5:659-665

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