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J Thorac Cardiovasc Surg 2005;129:782-790
© 2005 The American Association for Thoracic Surgery

Cardiopulmonary Support and Physiology

Combined administration of nitric oxide gas and iloprost during cardiopulmonary bypass reduces platelet dysfunction: A pilot clinical study

Ada Chung, PhDa,*, Stephen M. Wildhirt, MD, PhDb,*, Shoa Wang, MDa, Arvind Koshal, MDa, Marek W. Radomski, MD, PhD, DScc,*

a Departments of Pharmacology and Cardiothoracic Surgery, University of Alberta, Edmonton, Alberta, Canada
b Department of Cardiothoracic Surgery, German Heart Center Munich, Technical University of Munich, Munich, Germany
c Department of Integrative Biology and Pharmacology and Institute of Molecular Medicine for the Prevention of Human Diseases, University of Texas, Houston, Tex

Received for publication December 8, 2003; revisions received June 2, 2004; accepted for publication June 22, 2004.

* Address for reprints: Marek W. Radomski, MD, PhD, DSc, Center for Vascular Biology, Institute of Molecular Medicine, University of Texas-Houston, 6770 Bertner Ave, Suite C950J, Houston, TX 77030 (E-mail: Marek.Radomski{at}uth.tmc.edu).

BACKGROUND: Thrombocytopenia and platelet dysfunction are major mechanisms of cardiopulmonary bypass-induced postoperative hemorrhage. This study evaluated the effects of low amounts of nitric oxide, iloprost (prostacyclin analog), and their combination administered directly into the oxygenator on platelet function, platelet-leukocyte interactions, and postoperative blood loss in patients undergoing coronary artery bypass grafting.

METHODS: Blood samples from 41 patients randomized to the control, nitric oxide (20 ppm), iloprost (2 ng · kg–1 · min–1), or nitric oxide plus iloprost groups were collected during cardiopulmonary bypass. Platelets and leukocytes were enumerated. Platelet membrane glycoprotein Ib and glycoprotein IIb/IIIa, P-selectin, platelet-derived microparticles, leukocyte CD11b/CD18 (Mac-1), and platelet-leukocyte aggregate were quantified by means of flow cytometry. Collagen and thrombin receptor-activating peptide-induced platelet aggregation in whole blood was analyzed by means of aggregometry.

RESULTS: Both nitric oxide or iloprost attenuated cardiopulmonary bypass-induced thrombocytopenia, reduction of glycoprotein Ib and glycoprotein IIb levels, translocation of P-selectin, microparticle formation, Mac-1 upregulation, and suppression of collagen-induced aggregation. Nitric oxide plus iloprost was significantly more effective in preventing thrombocytopenia, microparticle formation, and P-selectin translocation. Moreover, this treatment preserved thrombin receptor-activating peptide-induced aggregation, which was not rescued by single treatments. Both nitric oxide and nitric oxide plus iloprost attenuated postoperative blood loss.

CONCLUSIONS: Nitric oxide plus iloprost reduced the deleterious effects of cardiopulmonary bypass, such as thrombocytopenia, platelet activation, platelet-leukocyte aggregate formation, and suppression of platelet aggregative responses. The reduced postoperative bleeding observed with this treatment suggests that this is a new and clinically feasible therapeutic option for patients subjected to cardiopulmonary bypass.




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