Abstract

The first (control) group of rabbits breathed ambient air whereas the second was exposed to low level carbon monoxide (CO, 50 ppm by volume) for 24 hr continuously for 8 weeks. The third group was exposed to 300 ppm CO for 4 weeks. The fourth group was exposed to 300 ppm CO for the same period of time as the third group but in addition they were also given epsilon amino caproic acid (EACA) orally, and the results compared to Group III. Per cent oxyhemoglobin (HbO2), per cent hemoglobin (Hb) and per cent carboxyhemoglobin (HbCO) were monitored in all groups. Tests of fibrinolysis were monitored and showed acceleration of the whole blood clot lysis and euglobulin lysis times (ELT). A fibrin plate test confirmed the increased lysis and serum fibrin and/or fibrinogen degradation products (FDP) were elevated in the CO exposed animals. No changes were observed in the same tests in the rabbits exposed to ambient air. The fourth group of animals receiving EACA showed inhibition of lysis and decrease in serum FDP. Alpha-1-antitrypsin and alpha-2-macroglobulin assays in all groups showed no change. Microscopic examination of the large vessels in these test groups showed endothelial damage which indicates a possible source for a plasminogen activator release, or lead to action of Hageman factor and activated plasma plasminogen proactivator.

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