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Bovine fibrinopeptide B and human fibrinopeptide A given in minute concentrations to rabbits, dogs, and lambs caused pulmonary hypertension, decreased effective pulmonary blood flow, decreased lung compliance, decreased ventilatory conductance, increased frequency and volume of ventilation, and increased differences in arterial and alveolar Pco2 and Po2. These effects appeared immediately after injection of the peptides into the lesser circulation, increased for 15 to 30 min, and were detectable for as long as 70 min. Mean aortic pressure, heart rate, stroke volume, left and right atrial pressures, and cardiac output showed no systematic changes after injection of these peptides. On the contrary, bovine fibrinopeptide A given in equimolar doses elicited none of the pulmonary responses but induced increases in heart rate, stroke volume, and cardiac output without consistent changes in mean pulmonary or aortic pressure. These responses appeared within 3 min, increased for 5 to 10 min, and disappeared within an hour. Some possible relationships of fibrinopeptides to clinical syndromes characterized by respiratory distress, hypoxemia, pulmonary vasoconstriction, and diminished lung compliance are briefly discussed. It is speculated that the lung may be an active site of fibrinopeptide catabolism and that accelerated fibrinogen-fibrin conversion may cause pulmonary failure through fibrinopeptide-induced vasoconstriction and reduction in compliance.