Abstract
Summary
Human C-reactive protein (CRP), whose concentration in serum is increased during acute inflammation, previously was shown to inhibit aggregation, activation of platelet factor 3, and release of both serotonin and β-glucuronidase in reactions involving human platelets. In the present study, rabbit as well as human CRP was found to dramatically inhibit both the rate and extent of thrombin-induced aggregation of washed rabbit platelets. Similarly, rabbit and human CRP both were found to inhibit the retraction of dilute rabbit clots, using an assay involving stimulation with excess thrombin and measurement of fluid volume expressed. These effects were observed using CRP concentrations (25-200 μg/mi) well within the range characteristically seen during reactions of inflammation and tissue destruction. Inhibition of clot retraction and cross-species inhibition of platelet aggregation are previously unreported properties of CRP. Thus, these observations further implicate CRP as a significant regulator of platelet function and emphasize the potential value of the rabbit as an experimental model in further studies of CRP.
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