An ex vivo model using human blood to perfuse pig lungs is used to study the hyperacute rejection response. Two separate components to this response have been identified, vasoconstriction and capillary leak. Using blockers of thromboxane synthesis we are able to attenuate the vasoconstriction; strategies which inhibit complement-mediated injury appear to block much of the capillary leak syndrome. Transgenic strategies are being developed to address these components separately and in conjunction.