Download PDF
Thorac Cardiovasc Surg 2003; 51(3): 138-141
DOI: 10.1055/s-2003-40314
Original Cardiovascular
© Georg Thieme Verlag Stuttgart · New York

Intracellular Adhesion Molecule-1 in Patients Developing Pulmonary Insufficiency after Cardiopulmonary Bypass

G.  Görlach1 , J.  Sroka1 , M.  Heidt1 , I.  Knez1 , A.  Sablotzki2 , M.  Schönburg1 , H.  Akintürk1 , P.  Roth1 , G.  Wozniak1 , P.  R.  Vogt1
  • 1Department of Cardiovascular Surgery, University Hospital, Giessen, Germany
  • 2Department of Anaesthesiology and Intensive Care Medicine, University Hospital, Giessen, Germany
Further Information

Publication History

Received: August 18, 2002

Publication Date:
30 June 2003 (online)

    Permissions and Reprints All articles of this category

Abstract

Objectives: Cardiopulmonary bypass activates adhesion molecules, which are associated with systemic inflammation and organ dysfunction. The intracellular adhesion molecule-1 (ICAM-1) has been evaluated in patients presenting pulmonary dysfunction after cardiac surgery. Materials and Methods: Postoperative serum levels of the ICAM-1 were measured in 40 patients who underwent isolated coronary artery bypass grafting, in 28 with uneventful postoperative recovery (70 %) (Group 1), and in 12 (30 %) with postoperative respiratory insufficiency (Group 2), defined by the need for prolonged (> 24 hours) mechanical ventilation using a fractional oxygen concentration of > 40 %. Results: Patients in group 1 were ventilated for 12.21 ± 4.86 hours and those in group 2 for 92.91 ± 48.14 hours (p < 0.001). ICAM-1 decreased from 145.98 ± 73.40 ng/ml to 81.15 ± 114.82 ng/ml in group 1, while in group 2 ICAM-1 showed a significant higher level and increased to 435.01 ± 130.02 ng/ml (p < 0.001). The leukocyte count increased in both groups as well as the C-reactive protein (CRP) during the postoperative course. The CRP behaves similar in both groups (p = 0.636) in contrast to the leukocyte count which was significantly higher in group 2 (p < 0.01). While none of the patients in group 1 died the mortality in group 2 was 50 % (p < 0.001). Conclusion: Respiratory insufficiency after cardiopulmonary bypass is associated with a distinct increase in the ICAM-1. The reason for the increase of the ICAM-1 in this small subset of patients has not been clarified.

Key words

Pulmonary insufficiency - ICAM-1 - cardiopulmonary bypass

References

  • 1 Kirklin J K, Westaby S, Blackstone E H, Kirklin J W, Pacifico A D, Chenoweth D E. Complement and the damaging effects of cardiopulmonary bypass.  J Thorac Cardiovasc Surg. 1983;  89 854-857
    PubMedGoogle Scholar
  • 2 Smith C W, Marlin S D, Rothlein R, Toman C, Anderson D C. Co-operative interactions of LFA-1 and Mac-1 with intercellular adhesion molecule-1 in facilitating adherence and transendothelial migration of human neutrophil in vitro.  J Clin Invest. 1989;  83 2008- 2017
    PubMedGoogle Scholar
  • 3 Springer T A. Adhesion receptors of the immune system.  Nature. 1990;  346 425-435
    CrossrefPubMedGoogle Scholar
  • 4 Grunenfelder J, Zund G, Schoeberlein A, Schmid E R, Schurr U, Frisullo R, Maly F, Turina M. Expression of adhesion molecules and cytokines after coronary artery bypass grafting during normothermic and hypothermic cardiac arrest.  Eur J Cardiothorac Surg. 2000;  17 723-728
    CrossrefPubMedGoogle Scholar
  • 5 Grunenfelder J, Zund G, Schoeberlein A, Maly F E, Schurr U, Guntli S, Fischer K, Turina M. Modified ultrafiltration lowers adhesion molecule and cytokine levels after cardiopulmonary bypass without clinical relevance in adults.  Eur J Cardiothorac Surg. 2000;  17 77- 83
    CrossrefPubMedGoogle Scholar
  • 6 Galea J. Rebuck N, Finn A, Moat N. Expression of soluble endothelial adhesion molecules in clinical cardiopulmonary bypass.  Perfusion. 1998;  13 314-321
    PubMedGoogle Scholar
  • 7 Boldt J, Osmer C, Goerlach G, Hempelmann G. Hypothermic versus normothermic bypass: influence on circulating adhesion molecules.  J Cardiothorac Vasc Anaesth. 1996;  10 342-347
    PubMedGoogle Scholar
  • 8 Moat N E, Shore D F, Evans T W. Organ dysfunction and cardiopulmonary bypass: the role of complement and complement regulatory proteins.  Eur J Cardio-thorac Surg. 1993;  7 563-573
    CrossrefPubMedGoogle Scholar
  • 9 Braude S, Nolop K B, Fleming J S, Krausz T, Taylor K M, Royston D. Increased pulmonary transvascular protein flux after canine cardiopulmonary bypass. Association with lung neutrophil sequestration and tissue peroxidation.  Am Rev Respir Dis. 1986;  134 867-872
    PubMedGoogle Scholar
  • 10 Dreyer W J, Michael L H, Millman E E, Berens K L, Geske R S. Neutrophil sequestration and pulmonary dysfunction in a canine model of open heart surgery with cardiopulmonary bypass: evidence for a CD 18-dependent mechanism.  Circulation. 1995;  92 2276- 2283
    PubMedGoogle Scholar
  • 11 Smith C W, Marlin S D, Rothlein R, Toman C, Anderson D C. Cooperative interactions of LFA-1 and Mac-1 with intercellular adhesion molecule-1 in facillating adherence and transendothelial migration of human neutrophils in vitro.  J Clin Invest. 1989;  83 2008-2017
    PubMedGoogle Scholar
  • 12 Newman W, Dawson L, Carson C W. Soluble E-selectin is found in supernatants of activated endothelial cells and is elevated in the serum of patients with septic shock.  J Immunol. 1993;  150 644-654
    PubMedGoogle Scholar
  • 13 Weerwind P W, Maessen J G, van Tits L HJ. Influence of Duraflo II heparin-treated extracorporeal circuits on the systemic inflammatory response in patients having coronary bypass.  J Thorac Cardiovasc Surg. 1995;  60 525-529
    PubMedGoogle Scholar
  • 14 Boldt J, Osmer C, Schindler E, Linke L-C h, Stertmann W A, Hempelmann G. Circulating adhesion molecules in cardiac operations: influence of high-dose Aprotinin.  Ann Thorac Surg. 1995;  59 100-105
    CrossrefPubMedGoogle Scholar
  • 15 Menasche P, Peynet J, Lariviere J. Does hypothermia during cardiopulmonary bypass increase neutrophil-endothelium interactions?.  Circulation. 1994;  90 (part 2) 275-279
    PubMedGoogle Scholar
  • 16 Cremer J, Martin M, Redl H. Systemic inflammatory response syndrome after cardiac operations.  Ann Thorac Surg. 1996;  61 1714-1720
    CrossrefPubMedGoogle Scholar
  • 17 Rothenburger M, Markewitz A, Lenz T, Kaulbach H G, Marohl K, Kuhlmann W D, Weinhold C. Detection of acute phase response and infection. The role of procalcitonin and C-reactive protein.  Clin Chem Lab Med. 1999;  37 275-279
    CrossrefPubMedGoogle Scholar
  • 18 Dreyer W J, Michael L H, Millman E E, Berens K L. Neutrophil activation and adhesion molecule expression in a canine model of open heart surgery with cardiopulmonary bypass.  Cardiovasc Res. 5;  29 775-781
    PubMedGoogle Scholar
  • 19 Dreyer W J, Burns A R, Phillips S C, Lindses M L, Jackson P, Kukielka G L. Intercellular adhesion regulation in the canine lung after cardiopulmonary bypass.  J Thorac Cardiovasc Surg. 1998;  115 689- 693
    PubMedGoogle Scholar
  • 20 Byrne J G, Smith W J, Murphy M P. Complete prevention of myocardial stunning, contracture, low- reflow, and edema after heart transplantation by blocking neutrophil adhesion molecules during reperfusion.  J Thorac Cardiovasc Surg. 1992;  104 1589-1596
    PubMedGoogle Scholar
  • 21 Simpson P J, Todd R F, Fantone J C. Reduction of experimental canine myocardial reperfusion injury by a monoclonal antibody (anti -Mo1, anti-CD11b) that inhibits leukocyte adhesion.  J Clin Invest. 1998;  81 624-629
    PubMedGoogle Scholar
  • 22 Ma X L, Lefer D J, Lefer A M, Rothlein R. Coronary endothelial and cardiac protective effects of a monoclonal antibody to intercellular adhesion molecule-1 in myocardial ischemia and reperfusion.  Circulation. 1992;  86 937-946
    PubMedGoogle Scholar

MD Gerold Görlach

Department of Cardiovascular Surgery, University Hospital

Rudolf-Buchheim-Strasse 7

35385 Giessen

Germany

Phone: +49/641/99 44 333

Fax: +49/641/99 44 309

Email: Gerold.Goerlach@chiru.med.uni-giessen.de