The Standardized Normal Ivy Bleeding Time and Its Prolongation by Aspirin

A standardized, reproducible Ivy bleeding time technic has been describedwhich permits one to obtain accurate bleeding time data in man. Thetechnic 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 hourslater. 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 differencebetween the mean bleeding time after placebo and after aspirin was highlysignificant (p < 0.001). The distribution of the bleeding times after aspirinsuggested that normal subjects do not respond to aspirin as a single population. The degree of prolongation of the bleeding time and the large size ofthe drops of blood observed in some subjects suggested to us that smallamounts of aspirin may exert a significant effect upon hemostasis in normalindividuals.

Submitted on January 10, 1969 Accepted on April 23, 1969     

The Mode of Inheritance of PTA Deficiency: Evidence for the Existence of Major PTA Deficiency and Minor PTA Deficiency

Plasma thromboplastin antecedent (PTA) activity was measured with aquantitative assay in the available members of the families of eight propositiwith severe PTA deficiency. PTA deficiency was found to exist in two forms:major PTA deficiency, characterized by PTA levels of up to 20 per cent of ourstandard reference plasma and by the potential for serious surgical bleeding,and minor PTA deficiency, characterized by PTA levels between 30 and 65per cent of our standard reference plasma and by the absence of significantsurgical bleeding. Minor PTA deficiency was found in parents and childrenof subjects with major PTA deficiency.

It would appear that the gene for PTA deficiency is an incompletely recessive or "intermediate" gene which produces major PTA deficiency in the homozygote and minor PTA deficiency in the heterozygote.

Submitted on March 27, 1961 Accepted on May 16, 1961     

Evidence that platelet accelerator (platelet factor 1) is adsorbed plasma proaccelerin

1. Human platelets possess an accelerator activity equal to about six per centof the proaccelerin activity of normal citrated plasma. This accelerator activityis only slightly reduced by 10 washings.

2. Thrombin increases platelet accelerator activity as much as ten fold. Thismeans that platelet accelerator activity behaves like proaccelerin (plasma Acglobulin) rather than accelerin (serum Ac-globulin).

3. Platelets from a patient with parahemophilia (congenital proaccelerindeficiency) possess only a trace of accelerator activity. They acquire a normalamount of accelerator activity after contact with normal platelet-poor plasma.

4. Trypsin destroys 90 per cent or more of the platelet accelerator activityof normal platelets without altering their appearance. Trypsinized plateletsregain normal accelerator activity upon incubation with normal platelet-poorplasma.

5. These findings strongly suggest that the platelet accelerator (plateletfactor 1) is adsorbed plasma proaccelerin.

Submitted on April 15, 1955 Accepted on July 5, 1955