Pulmonary edema: ischemia reperfusion endothelial injury and its reversal by c-AMP.

A review of the factors that oppose pulmonary edema formation (alveolar flooding) when capillary pressure is elevated are presented for a normal capillary endothelial barrier and for damaged endothelium associated with ischemia/reperfusion in rabbit, rat, and dog lungs. Normally, tissue pressure, the plasma protein osmotic pressure gradient acting across the capillary wall and lymph flow (Edema Safety Factors) increase to prevent the build-up of fluid in the lung's interstitium when capillary pressure increases. No measureable alveolar edema fluid accumulates until capillary pressure exceeds 30 mmHg. When the capillary wall has been damaged, interstitial edema develops at lower capillary pressures because the plasma protein osmotic pressure will not change greatly to oppose capillary filtration, but lymph flow increases to very high levels to remove the increased filtrate and the result is that capillary pressures can increase to 20-25 mmHg before alveolar flooding results. In addition, the mechanisms responsible for producing pulmonary endothelial damage with ischemia/reperfusion are reviewed and the effects of O2 radical scavengers, neutrophil depletion or altering their adherence to the endothelium, and increasing cAMP on reversing the damage to the pulmonary endothelium is presented.