Thromb Haemost 1990; 63(01): 006-012
DOI: 10.1055/s-0038-1645676
Original Article
Schattauer GmbH Stuttgart

Increased Whole Blood Viscosity during Coronary Artery Bypass Surgery

Studies to Evaluate the Effects of Soluble Fibrin and Poloxamer 188
Robert L Hunter
The Departments of Pathology and Anesthesiology, Emory University, Atlanta, Georgia, USA
,
Christine Papadea
The Departments of Pathology and Anesthesiology, Emory University, Atlanta, Georgia, USA
,
Christopher J Gallagher
The Departments of Pathology and Anesthesiology, Emory University, Atlanta, Georgia, USA
,
Donald C Finlayson
The Departments of Pathology and Anesthesiology, Emory University, Atlanta, Georgia, USA
,
Irene J Check
The Departments of Pathology and Anesthesiology, Emory University, Atlanta, Georgia, USA
› Author Affiliations
Further Information

Publication History

Received 31 March 1989

Accepted after revision 03 November 1989

Publication Date:
02 July 2018 (online)

Summary

This study was designed to test the hypothesis that soluble fibrin complexes resulting from the trauma of surgery could produce elevated blood viscosity, to characterize the soluble fibrin polymers, and to evaluate in vitro the effect of a new hemorheologic agent, poloxamer 188, on viscosity in these abnormal situations. Ten patients undergoing aortocoronary bypass surgery were studied before and at various times after surgery. By 6 h after surgery, the mean hematocrit decreased by 23%, fibrinogen decreased 48%, and erythrocyte sedimentation rate decreased 33%, whole blood viscosity at a low shear rate rose on average of 69% and soluble fibrin rose 118%. Over the 6-day observation period, the concentrations of soluble fibrin paralleled the changes in viscosity, whereas the concentrations of fibrinogen varied nearly inversely with viscosity. The effects of various forms of fibrinogen and fibrin were tested by additions to normal blood. Soluble fibrin polymers, but not fibrin monomers, increased blood viscosity two to three fold. Poloxamer 188 reduced the viscosity of all patient samples to the normal range. These data support the hypothesis that increased whole blood viscosity at low shear rates is caused by hydrophobic adhesion of fibrin polymers to red cells and that poloxamer 188 normalizes viscosity by effectively disrupting the weak hydrophobic bonds.

 
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