A standardized, reproducible Ivy bleeding time technic has been described which permits one to obtain accurate bleeding time data in man. The technic was used to standardize an aspirin tolerance test in which 60 normal males had a control bleeding time; were given, on a double blind basis, either placebo or 1 Gm. of aspirin, and had a second bleeding time 2 hours later. The control values were: mean, 5 min.; mean ± 2 st. dev., 2 min., 30 sec. to 10 min. The values after placebo were: mean, 5 min., 30 sec.; mean ± 2 st. dev., 2 min., 30 sec. to 11 min. The values after aspirin were: mean, 9 min., 30 sec.; mean ± 2 st. dev., 4 min. to 21 min. The difference between the mean bleeding time after placebo and after aspirin was highly significant (p < 0.001). The distribution of the bleeding times after aspirin suggested that normal subjects do not respond to aspirin as a single population. The degree of prolongation of the bleeding time and the large size of the drops of blood observed in some subjects suggested to us that small amounts of aspirin may exert a significant effect upon hemostasis in normal individuals.

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Heparin was administered to 34 normal subjects by intravenous injection (100 mu/kg) and the template bleeding time was significantly increased both 10 min and 120 min following injection. Before heparin the bleeding time was 5-3 +/- 1.0 min (mean +/- 1 SD); 10 min after injection it was 9.8 +/- 5.6 min (P less than 0.001); and 120 min after injection it was 7.2 +/- 3.9 min (P less than 0.001). Increases in the bleeding time were unrelated to changes in platelet count, and independent of heparin's effect on plasma coagulation. In blood drawn 10 min and 120 min following heparin injection, there was significantly less [14C]5-HT released from platelet-rich plasma (PRP) in response to collagen, 0.41 mM epinephrine and 8 micron ADP, although in vitro addition of heparin (0.1 mu/ml, 0.5 mu/ml and 2.5 mu/ml) to baseline PRP of three subjects did not depress [14C]5-HT release. Our experiments suggest that intravenous administration of a therapeutic dose of heparin can cause a significant reversible inpairment of platelet haemostatic properties, possibly by an indirect mechanism.

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