Effect of Gut Ischemia on Pulmonary Barrier Dysfunction and Pulmonary Edema. Figure 15a shows the dynamics of pulmonary occludin levels (as a proxy for pulmonary barrier dysfunction) in a representative run with a sub-lethal initial "%Isch" = 11 over a 72 hour run. Levels of both Cytoplasm Occludin and Cellwall Occludin nadir at ~24 hrs, then show gradual recovery as inflammation subsides. TJ protein levels continue to rise towards 72 hours. This pattern is consistent with that seen clinically in the recovery of pulmonary edema secondary to inflammatory causes. Figure 15b shows a screenshot for this representative run at the end of 72 hours, demonstrating a mostly recovered pulmonary epithelial surface. Figure 15c shows the dynamics of pulmonary occludin levels in a representative run with a lethal initial "%Isch" = 13. Level of both Cytoplasm Occludin and Cellwall Occludin are seen to drop consistent with progressive activation of pulmonary endothelium and production of NO, leading to pulmonary TJ failure. This run is terminated at 24 because endothelial damage is nearly complete, as seen in the corresponding screenshot in Figure 15d. Figure 15d Letter A points to black cubes representing "dead" endothelial cell agents. These agents "die" owing to a decrease in the available maximal "oxy" level to below the threshold for generalized endothelial agent activation. The impaired systemic oxygenation due to pulmonary leak arises from pulmonary epithelial barrier failure. Letter B points to the only remaining intact pulmonary epithelial cell agents. Letter C points to the only remaining intact gut epithelial cell agents. Letter D points to the only remaining patches of surviving endothelial agents (red areas seen through the failed gut barrier).