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Blood, 15 November 2000, Vol. 96, No. 10, pp. 3630-3636
TRANSFUSION MEDICINE
o-Raffinose cross-linked hemoglobin improves the
hemostatic defect associated with anemia and thrombocytopenia
in rabbits
David H. Lee,
Leslie Bardossy,
Nichole Peterson, and
Morris A. Blajchman
From the Departments of Medicine and Pathology,
Queen's University, Kingston, Ontario, Canada; and the
Department of Pathology and Molecular Medicine, McMaster University,
Hamilton, Ontario, Canada.
Several different preparations of cross-linked hemoglobin
(CLHb) are being evaluated for their efficacy and safety as red cell
substitutes in a variety of preclinical and clinical settings. Because
CLHb is known to sequester nitric oxide (NO) and inhibit NO-mediated
processes, we hypothesized that CLHb would have a hemostatic effect by
enhancing platelet reactivity, inducing vasoconstriction, or both.
Infusion of o-raffinose CLHb shortened the prolonged microvascular bleeding time and decreased blood loss from ear incisions
in rabbits rendered anemic and thrombocytopenic. Moreover, this
hemostatic effect persisted for at least 24 hours after infusion. Phenylephrine induced a degree of vasoconstriction similar to that
induced by CLHb but did not shorten the bleeding time or decrease blood
loss, suggesting that vasoconstriction alone cannot account for the
hemostatic effect of CLHb. There was no evidence of CLHb-induced
activation of coagulation in vivo, since infusion of CLHb did not
increase circulating levels of thrombin-antithrombin complex. In vitro,
CLHb abolished the inhibitory effect of the NO donor
3-morpholinosydnonimine on platelet aggregation and enhanced the
aggregation of stimulated but not resting platelets. This potentiating
effect was not attenuated by the addition of superoxide dismutase or
catalase. To evaluate the potential arterial thrombogenicity of CLHb, a
model of carotid artery thrombosis was developed in rabbits without
thrombocytopenia or anemia. Compared with albumin infusion, CLHb
infusion shortened the time to complete carotid occlusion. These data
suggest that CLHb may shift the thromboregulatory balance toward clot
formation, resulting in decreased bleeding in anemic and
thrombocytopenic rabbits and possibly increasing arterial
thrombogenicity in normal rabbits.
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