ABSTRACT
The intravenous administration of heterologous polyclonal antibodies to pulmonary angiotensin-converting enzyme (ACE) causes acute fatal pulmonary edema. Examination of the lungs reveals platelet and leukocyte aggregation in the pulmonary capillaries, fibrin deposition, and alveolar edema. Endothelial injury is manifest by bleb formation and the disintegration of the cell membranes. The rapidity of the onset of pulmonary injury and the intravascular aggregation of the observed formed elements are similar to those described in other experimental immunologic lung injury. R. N. Pinckard have studied a rabbit model of IgE-induced systemic anaphylaxis in which the aggregates of platelets and leukocytes develop in the pulmonary vascular bed. The chapter shows that goat antibodies directed against purified rabbit pulmonary ACE are anticatalytic in vitro, and when given in vivo to unanesthetized rabbits, the antibodies caused a reduction in the pressor response to an administration of angiotensin and potentiated the depressor response to administered bradykinin.
