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(Circulation. 1998;97:117.)
© 1998 American Heart Association, Inc.

Correspondence

Extracorporeal Circulation

Harel Gilutz, MD

Cardiology Division, Faculty of Health Sciences, Ben Gurion University of the Negev, Soroka Medical Center, Beer-Sheva, Israel

To the Editor:

The original work of Sanjay Kaul et al, "Inhibition of Acute Stent Thrombosis Under High-Shear Flow Conditions by a Nitric Oxide Donor, DMHD/NO,"¹ is a well-designed and controlled study. When it comes to drawing clinical implications, the authors did not address a major limitation of this study: the thrombogenic effect of extracorporal circulation (EC).

EC initiates humoral and cellular responses leading to enhanced thrombogenicity through integrated multifactorial pathways. It was recently shown that during EC, there is an activation of the complement system and that the terminal components C5a and C5b-9 directly contribute to platelet and neutrophil activation.² In a different study (non-EC), it was shown that C3d fixation to erythrocytes resulted in decreased membrane deformability.³

EC induces proteolytic activity, causing pronounced platelet degranulation⁴ and erythrocyte membrane damage, leading to formation of echinocytes.⁵ A decrease of erythrocyte deformability due to a change in sodium contents as well as decreased 2,3-DPG content was observed.⁶ Thus, prolonged artificial circulation provokes structural reorganization in erythrocytes, thereby affecting both blood rheology and gas exchange.⁷ Direct shear-induced platelet aggregation, mediated by binding of von Willebrand factor to platelet glycoprotein Ib, which caused degranulation, was also demonstrated.⁸

A very important forgotten concept is the "inversion phenomenon" of blood viscosity in the microcirculation, which takes into consideration the rheology of cell aggregates and single cells.⁹ The appearance of sludgelike aggregates in the blood will cause an immediate amplification of the resistance to the point of no flow.

Thus, it is reasonable to assume that the actual viscosity in EC experiments is much higher than that calculated by the flow and radius and has a great impact on flow conditions and thrombus formation. We should bear these facts in mind when we attempt to integrate these EC ex vivo studies into the clinical world.

References

1. Kaul S, Makkar RR, Nakamura M, Litvack FI, Shah PK, Forrester JS, Hustsell TC, Eigler NL. Inhibition of acute stent thrombosis under high-shear flow conditions by a nitric oxide donor, DMHD/NO. Circulation. 1996;94:2228–2234.[Abstract/Free Full Text]

2. Rinder CS, Rinder HM, Smith BR, Fitch JC, Smith MJ, Tracey JB, Matis LA, Squinto SP, Rollins SA. Blockade of C5a and C5b-9 generation inhibits leukocyte and platelet activation during extracorporeal circulation. J Clin Invest. 1995;96:1564–1572.

3. Sung KL, Freedman J, Chabanel A, Chien S. Effect of complement on the viscoelastic properties of human erythrocyte membrane. Br J Haematol. 1985;61:455–466.[Medline] [Order article via Infotrieve]

4. Mellgren K, Friberg LG, Hedner T, Mellgren G, Wadenvik H. Blood platelet activation and membrane glycoprotein changes during extracorporeal life support (ECLS): in vitro studies. Int J Artif Organs. 1995;18:315–321.[Medline] [Order article via Infotrieve]

5. Reinhart WH, Ballmer PE, Rohner F, Ott P, Straub PW. The influence of extracorporeal circulation on erythrocytes and flow properties of blood. J Thorac Cardiovasc Surg. 1990;100:538–545.[Abstract]

6. Otsuki M. The function of red blood cells under open-heart surgery with extracorporeal circulation without donor blood. Masui. 1992;41:1627–1634.[Medline] [Order article via Infotrieve]

7. Boiarinov GA, Smirnov VP, Snopova LB, Tarasova AI, Filippova TA. Erythrocyte and microcirculatory functions during artificial circulation. Biull Eksp Biol Med. 1987;103:281–283.[Medline] [Order article via Infotrieve]

8. Borgdorff P, Kok WE, Vis MA, van den Bos GC. Vasodilation by shear-induced platelet aggregation in extracorporeal circuits. Am J Physiol. 1994;266:H891–H897.[Abstract/Free Full Text]

9. Dintenfass L. Red cell aggregation in cardiovascular diseases and crucial role of inversion phenomenon. Angiology.. 1985;36:315–326.

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