Thromb Haemost 1966; 15(03/04): 349-364
DOI: 10.1055/s-0038-1649437
Originalarbeiten — Original Articles — Travaux Originaux
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The Effect of Adrenaline Infusions on Blood Coagulation in Normal and Haemophilia B Dogs[*]

A.H Özge
1   Department of Physiological Sciences, Ontario Veterinary College, Guelph; Blood and Vascular Disease Research Unit, Departments of Medicine and Pathology, University of Toronto
,
H.C Rowsell
1   Department of Physiological Sciences, Ontario Veterinary College, Guelph; Blood and Vascular Disease Research Unit, Departments of Medicine and Pathology, University of Toronto
,
H.G Downie
1   Department of Physiological Sciences, Ontario Veterinary College, Guelph; Blood and Vascular Disease Research Unit, Departments of Medicine and Pathology, University of Toronto
,
J.F Mustard
1   Department of Physiological Sciences, Ontario Veterinary College, Guelph; Blood and Vascular Disease Research Unit, Departments of Medicine and Pathology, University of Toronto
› Author Affiliations
Further Information

Publication History

Publication Date:
27 June 2018 (online)

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Summary

The addition of trace amounts of adrenaline to whole blood in plasma in vitro increased factor VIII, factor IX and whole plasma activity in the thromboplastin generation test. This was dose dependent.

Adrenaline infusions less than 22 (μg/kg body weight in normal dogs accelerated clotting, increased factor IX, factor VIII and whole plasma activity in the thromboplastin generation test and caused a fall in blood pH. In a factor IX deficient dog, there was no increase in factor IX activity. After adrenaline infusions, however, the other changes occurred and were of the same order of magnitude as in the normal. Adrenaline in doses greater than 22 μg/kg body weight did not produce as great an effect on clotting in normal or factor IX deficient dogs. The platelet count in the peripheral blood was increased following the infusion of all doses of adrenaline. These observations suggest that the accelerating effect of adrenaline on clotting is not mediated through increase in activity of a specific clotting factor.

* This work was supported in part by grants from the Ontario Heart Foundation, Department of Veterans Affairs and the National Institutes of Health, U.S. Public Health Service H-6951 and H-6912.