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J Thorac Cardiovasc Surg 1994;108:184-185
© 1994 Mosby, Inc.

LETTERS TO THE EDITOR

Plasma elastase concentrations and pulmonary function after cardiopulmonary bypass

Peter Mair, MD, Johannes Mair, MD, Ingo Seibt, Wilhelm Furtwaengler, MD, Doris Balogh, MD, Bernd Puschendorf, MD

Department of Anesthesia and Intensive Care Medicine
Department of Medical Chemistry and Biochemistry
University Innsbruck School of Medicine
Innsbruck, Austria

To the Editor:

Postbypass pulmonary dysfunction remains a relevant problem in patients undergoing heart operations with extracorporeal circulationGo 1 Experimental data suggest that activated leukocytes contribute to lung injury after cardiopulmonary bypass. Go 2 Leukocyte depletion by mechanical filtration istherefore recommended during cardiopulmonary bypass. Go 2 To determine the role of activated leukocytes in a clinical setting, we measured pulmonary function and plasma elastase concentrations as a marker of leukocyte activation Go 3 in patients undergoing aorta-coronary artery bypass operations.

Twenty-six patients undergoing elective, uncomplicated aorta-coronary bypass operations were investigated (age, 61.2 ± 7.0 years; mean ± standard deviation). In all patients, standard cardiopulmonary bypass techniques with moderate systemic hypothermia, aortic crossclamping, and cardioplegic arrest were used (bypass time, 117 ± 32.9 minutes; aortic crossclamp time, 59.4 ± 18.7 minutes; mean ± standard deviation). During aortic crossclamping, lungs were not ventilated and continuous positive airway pressure (8 mm Hg) was applied. Venous blood samples were drawn before anesthesia, before operation, before cardiopulmonary bypass (0 to 2, Fig. 1), with aortic unclamping, at 1, 2, 3, 4, 8, 12, 16, 20, and 24 hours later (3 to 12, Fig. 1), and daily thereafter for 7 days (13 to 19, Fig. 1). Elastase{alpha}1 proteinase inhibitor complex concentrations were measured with an immunoassay (PMN-Elastase IMAC; Merck, Darmstadt, Germany). Postbypass pulmonary function was assessed by the quotient of arterial partial pressure of oxygen to fraction of inspired oxygen (PaO2/FiO2) 1 and 3 hours after aortic unclamping. Go 4



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  		Fig. 1. Elastase plasma concentrations in relation to postbypass pulmonary function data, given as mean ± standard error of the mean. ACC, aortic crossclamping; group 1, Pao2/Fio2< 200; group 2, Pao2/Fio2 between 200 and 300/ group 3, Pao2/Fio2> 300.

 
Plasma elastase concentrations showed a marked increase after initiation of cardiopulmonary bypass (p < 0.0001, repeated-measures analysis of variance). Peak values occurred 1 to 4 hours after aortic unclamping, followed by a rapid subsequent decrease within 12 hours (Fig. 1). There were no close, significant correlations between elastase concentration and bypass time, aortic crossclamp time, or plasma free hemoglobin concentrations. Pulmonary function after cardiopulmonary bypass varied over a wide range (PaO2/FiO2 quotients ranging from 93 to 560). There was no significant close correlation between elastase concentration and PaO2/FiO2 quotients 1 and 3 hours after aortic unclamping. Eleven patients (group 1) had PaO2/ FiO2 ratios of less than 200, indicating severely impaired pulmonary function; eight patients (group 2) had PaO2/FiO2 ratios between 200 and 300, indicating moderately impaired pulmonary function. Seven patients showed normal pulmonary function after extracorporeal circulation (PaO2/FiO2 > 300). Neither plasma elastase peak concentration (one-factor analysis of variance) nor plasma elastase time courses (two-factor repeated-measures analysis of variance) differed significantly in these three groups of patients (Fig. 1).

Aorta-coronary bypass operations with cardiopulmonary bypass cause leukocyte activation, as shown by the marked increase in plasma elastase concentrations. Among various potential sources of pulmonary dysfunction after extracorporeal circulation, however, leukocyte activation seems to be a minor determinant of postbypass pulmonary function in this clinical setting.

References

  1. Latson TW, Kickler TS, Baumgartner WA. Pulmonary hypertension and noncardiogenic pulmonary edema following cardiopulmonary bypass associated with an antigranulocyte antibody. Anesthesiology 1986;64:106-11.[Medline]
  2. Bando K, Pillai R, Cameron DE, et al. Leukocyte depletion ameliorates free radical–mediated lung injury after cardiopulmonary bypass. J THORAC CARDIOVASC SURG 1990;99:873-7.[Abstract]
  3. Neumann S, Gunzer G, Henrich N, Lang H. "PMN-elastase assay": enzyme immunoassay for human polymorphnuclear elastase complexed with alpha-1-proteinase inhibitor. J Clin Chem Clin Biochem 1984;22:693-7.[Medline]
  4. Murray JF, Matthay MA, Luce JM, Flick MR. An expanded definition of the adult respiratory distress syndrome. Am Rev Respir Dis 1988;138:720-3.[Medline]



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