Conclusions

Our knowledge of how fluid and solutes cross the endothelial barrier has now been expanded to incorporate cellular events, but the major findings from animal models of endothelial barrier dysfunction have not been adequately tested in the clinical setting. However, the recent finding that nitric oxide can protect the lung against ischemia-reperfusion damage in animal models ( Mooreefa/ 1.996b) may have important clinical implications, since this compound is already in use for treating pulmonary hypertension. It is quite possible that exciting new therapies for the successful treatment of endothelial barrier damage caused by the inflammatory process will be developed in the near future.

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