Affiliations: [a] Department of Chemical, Biological and Materials Engineering, University of Oklahoma, Norman, OK 73019, USA
| [b] Department of Medicine, University of Oklahoma Health Science Center, Oklahoma City, OK 73014, USA
Correspondence:
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Address for correspondence: Edgar A. O’Rear, Prof., School of Chemical, Biological and Materials Engineering, University of Oklahoma, 100 E. Boyd SEC T301, Norman, OK 73019, USA. Tel.: +1 405-325-4379; Fax: +1 405-32505813; E-mail: eorear@ou.edu.
Abstract: Background:Reperfusion injury often occurs with therapeutic intervention addressing the arterial occlusions causing acute myocardial infarction and stroke. The no-reflow phenomenon has been ascribed to leukocyte plugging and blood vessel constriction in the microcirculation. Objective:To assess possible red cell contributions to post-thrombolytic no-reflow phenomenon. Methods:Blood clots were formed by recalcifying 1 ml of citrated fresh human venous blood and then lysed by adding 1,000 units of streptokinase (SK) at several intervals within 1 hour. Red cell deformability was tested by both a microscopic photometric and a filtration technique, viscosity by a cone and plate viscometer, and erythrocyte aggregation by an optical aggregometer. Results:
Two sampling methods were devised for the microscopic photometric test, both of which indicated increases of erythrocyte stiffness after being lysed from the clot by SK. In accompanying experiments, the viscosity, aggregation and filterability of the post-lytic erythrocytes were assessed. Results indicated increased viscosity in Ringer’s, decreased aggregation index and filterability through a 5 μm pore size Nuclepore membrane.
Conclusion:Findings demonstrated that post-lytic changes in red cell deformability do occur which could contribute to the no-reflow phenomenon.
