Pulmonary vascular effects of a fibrin(ogen)-derived vasoactive peptide.

We examined the effects of the 5 amino acid fibrin(ogen)-degradation product Ala-Arg-Pro-Ala-Lys (Peptide 6A) on pulmonary hemodynamics and vascular permeability in the isolated-perfused guinea pig lung. Infusion of this peptide (100 mumoles) resulted in a small increase in pulmonary vascular resistance. The pulmonary vasoconstrictor responses was not mediated by histamine or cyclooxygenase metabolites since neither H1 blockers nor meclofenamate inhibited the response. The capillary filtration coefficient (a measure of water transvascular permeability) did not change after Peptide 6A infusion. Small molecular weight fibrin(ogen)-degradation products may contribute to increased pulmonary vascular resistance associated with pulmonary intravascular coagulation, but not to the increase in lung hydraulic conductivity.