The ability of various peptides cleaved by plasmin from human fibrinogen and fibronectin or fibrinogen- and fibronectin- related synthetic peptides to induce histamine release from mast cells and collagenase and elastase from PMN- leukocytes was examined. Low molecular weight fibrinogen degradation products showed dose dependent secretion of collagenase. These peptides (mol. wt. 1.4 kD) at the concentration of 10⁻⁵ M released about 47% of collagenase and 13% of elastase. Synthetic fib- rinopeptides A and В had a similar strong collagenase releasing potency and also released histamine from mast cells. Peptides from plasmin digestion of fibronectin containing cell attachment site with sequence Arg-Gly-Asp-Ser and also synthetic peptide reproducing this aminoacid sequence at the concentration of 1000 µg/ml released about 50% of collagenase and 55% of elastase from PMN-leukocytes. Moreover peptides containing cell attachment and gelatin binding site induced histamine release from mast cells. The association of fibrinogen and fibronectin degradation with activation of mast cells may motivate the treatment with antihistaminic drugs of all pathological conditions where the intensive protein degradation takes place.
Isolated, cultured rat neonatal cardiac myocytes were placed in medium suppled menfed with mitochondrial respiratory inhibitor potassium cyanide which caused a rapid adenosine triphosphate (ATP) depletion. These myocytes with the impaired energy metabolism (“hypoxia-like state”) were exposed to unstimulated human neutrophils. Effect of human neu rophils on the myocy es m the “hypoxia-like state” was quantified as a total change in the amount of ATP in cardiac cells. After 5 hours of incubation of neu rophils with the myocytes in the “hypoxia-like state” an additional decrease (of 50 per cent) in ATP content was observed. Since catalase (which destroys hydrogen peroxide) prevented the further decline in ATP level in the myocy es with impaired energy metabolism, it seem that hydrogen peroxide and possibly their products are responsible for this effect. These results suggest that unstimulated human neu rophils af er activation by the contact with injured cardiac cells caused further decrease of ATP level in target cells.