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Ann Thorac Surg 1986;41:193-199
© 1986 The Society of Thoracic Surgeons
Departments of Surgery and Anesthesia, University of Alabama at Birmingham Medical Center, and the Veterans Administration Medical Center, Birmingham, AL, the Veterans Administration Medical Center, San Diego, CA, Brigham and Women's Hospital, Boston, MA, and Scripps Clinic and Research Foundation, La Jolla, CA
Accepted for publication April 11, 1985.
* Address reprint requests to Dr. John W. Kirklin, Division of Cardiothoracic Surgery, University of Alabama at Birmingham, University Station, Birmingham, AL 35294
Nineteen patients were prospectively selected and studied before and after the administration of protamine sulfate following cardiopulmonary bypass (CPB). After protamine administration, C3a, C4a, and C4d were elevated; the peak levels of C3a and C4a were in samples taken 10 minutes after protamine administration while those of C4d were in those obtained at 5 hours. Only C3a was elevated after CPB and before protamine administration. In vitro, only the combination of protamine sulfate and heparin, and neither alone, resulted in increased C3a and C4a. Administration of protamine was associated with small and transient decreases in total white blood cells, granulocytes, and platelets, and with small and transient reductions in systemic and pulmonary arterial and left and right atrial pressures. Systemic vascular resistance fell (p = 0.07), and pulmonary vascular resistance rose but the change could be due to chance (p = 0.29). These data and those reported by others support the inference that complement activation occurs during CPB by the alternative pathway and again during protamine administration by the classic pathway; and that this accompanies a whole-body inflammatory reaction with blood cell and hemodynamic changes which, when extreme, could result in a severe hemodynamic derangement.
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A. M. Gillinov, P. A. DeValeria, J. A. Winkelstein, I. Wilson, W. E. Curtis, D. Shaw, C. G. Yeh, A. R. Rudolph, W. A. Baumgartner, A. Herskowitz, et al. Complement inhibition with soluble complement receptor type 1 in cardiopulmonary bypass Ann. Thorac. Surg., March 1, 1993; 55(3): 619 - 624. [Abstract] [PDF]
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J. K. Kirklin Prospects for understanding and eliminating the deleterious effects of cardiopulmonary bypass Ann. Thorac. Surg., April 1, 1991; 51(4): 529 - 531. [PDF]
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G. J. R. Whitman, D. Martel, M. Weiss, A. Pochanapring, W. M. See, A. Hopeman, A. H. Harken, and I. M. Dauber Reversal of protamine-induced catastrophic pulmonary vasoconstriction by prostaglandin E1 Ann. Thorac. Surg., August 1, 1990; 50(2): 303 - 305. [Abstract] [PDF]
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R. S. Bonser, J. R. Dave, E. T. Davies, L. John, P. Taylor, H. Gaya, S. C. Lennox, and D. Vergani Reduction of complement activation during bypass by prime manipulation Ann. Thorac. Surg., February 1, 1990; 49(2): 279 - 283. [Abstract] [PDF]
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C. Aren Review article : Heparin and protamine during cardiac surgery Perfusion, July 1, 1989; 4(3): 171 - 181. [PDF]
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 R. J. Howard, C. Crain, D. A. Franzini, C. I. Hood, and T. E. Hugli Effects of Cardiopulmonary Bypass on Pulmonary Leukostasis and Complement Activation Arch Surg, December 1, 1988; 123(12): 1496 - 1501. [Abstract] [PDF]
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T. Tamiya, M. Yamasaki, Y. Maeo, T. Yamashiro, S. Ogoshi, and S. Fujimoto Complement Activation in Cardiopulmonary Bypass, with Special Reference to Anaphylatoxin Production in Membrane and Bubble Oxygenators Ann. Thorac. Surg., July 1, 1988; 46(1): 47 - 57. [Abstract] [PDF]
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A T. Pezzella, A. Ascioti, and P. Ricardi Noncardiogenic pulmonary oedema following cardiopulmonary bypass: report of two cases and review of the literature Perfusion, January 1, 1988; 3(1): 21 - 28. [Abstract] [PDF]
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W. van Oeveren and C. Wildevuur Review article : Blood compatibility of cardiopulmonary bypass circuits Perfusion, October 1, 1987; 2(4): 237 - 244. [PDF]
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P. J. Hendry, G. C. Taichman, and W. J. Keon The Myocardial Contractile Responses to Protamine Sulfate and Heparin Ann. Thorac. Surg., September 1, 1987; 44(3): 263 - 268. [Abstract] [PDF]
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