Physiology and morphology of pulmonary microvascular injury with shock and reinfusion.

Abstract

The effect of hemorrhagic shock and reinfusion of the shed blood on lung microvasculature was studied in 10 anesthetized dogs during a control, a shock (40-50 mmHg aortic pressure), and a reinfusion period. Pulmonary capillary hydrostatic and oncotic pressures decreased, whereas lung lymph flow and lymph-to-plasma albumin and globulin ratios increased with shock and with reinfusion, indicating an increased microvascular permeability. Calculated pore radius increased with reinfusion (p less than 0.05), whereas pore number increased both with shock and with reinfusion in eight dogs. Comparison of the autopsy results of these experiments with those of previous control and shock animals showed that with reinfusion there was a rise in lung wet-to-dry weight ratios and increased granulocytes by light microscopy. By electron microscopy, the granulocytes were intravascular, and there was alveolar wall edema without endothelial or epithelial damage. We conclude that the morphological changes in the lung with reinfusion are minimal and that our data are consistent with the hypothesis that granulocytes may cause the observed microvascular injury and interstitial edema.