J Thorac Cardiovasc Surg 1999;117:1045-1046
© 1999 Mosby, Inc.
Effect of normoxic cardiopulmonary bypass on leukocyte elastase release
Y. John Gu, MD, PhD,
Piet W. Boonstra, MD, PhD,
Willem van Oeveren, PhD
Blood Interaction Research
Department of Cardiothoracic Surgery
Thorax Center
University Hospital
Hanzeplein 1
9700 RB Groningen, The Netherlands
Effect of normoxic cardiopulmonary bypass on leukocyte elastase release
To the Editor:
We read with great interest the recent paper by Ihnken and coworkers
1 about the reduction of oxygen-derived free radicals and nitric oxide by normoxic cardiopulmonary bypass (CPB). In their article, the authors showed that normoxic CPB reduced release of neutrophil elastase in patients undergoing cardiac operations. They wrote, "this is the first time that a PO2-dependent elastase release on CPB is described."
Recently, we have undertaken a prospective study on 60 patients undergoing cardiac operations to compare the efficiency and safety of different membrane oxygenators. A large variation in PO2 appeared during perfusion, which gave us an opportunity to assess whether elastase release during CPB was dependent on the level of PO2. During CPB, arterial PO2 was measured 5 times: at the start of cooling, during cooling down to 32°C, on stabilized hypothermia at 28°C, during rewarming to 32°C, and at the end of CPB. Elastase was measured before and at the end of CPB from blood samples taken from the radial artery using the same method that Ihnken and associates described (enzyme-linked immunosorbent assay; Merck, Darmstadt, Germany). Results showed that PO2 varied between 107 and 440 mm Hg at the start of cooling and between 80 and 308 mm Hg on stabilized hypothermia during CPB. On an average of the 5 time points during CPB, PO2 varied between 128 and 317 mm Hg. Elastase increased in the majority of patients at the end of CPB with a concentration ranging between 41 to 490 ng/mL, or a percentage increase (release) of 47% to 742% compared with baseline concentration before CPB. However, there was no correlation either between PO2 and elastase concentration at the end of CPB or between PO2 and the percentage increase compared with the baseline elastase (Fig. 1).
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Fig 1. Scattergrams showing no relationship between arterial PO2 and systemic elastase concentration determined at the end of CPB (A) or the percentage increase at the end of CPB compared with the baseline elastase (B). PO2 is the average of 5 blood gas samples determined during CPB (see text for details).
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Our results suggest that systemic elastase release during CPB is not dependent on PO2. For years, elastase release during CPB has been known to be largely attributed to blood interaction with the artificial surface of the extracorporeal circuit. 2,3 Modification of the material surface of the circuit has been associated with a reduction in elastase release either during clinical CPB 4 or in a simulated model of CPB. 5 It could well be that normoxic CPB had reduced the cardiac source of elastase but that the effect had been systematically counteracted by other factors, such as blood-material interaction. Thus whether PO2 plays a role in controlling local or systemic elastase release is of interest, but needs to be confirmed by later studies as normoxic CPB becomes more prevalent than hyperoxic CPB.
12/8/96853
References
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Butler J, Pillai R, Rocker GM, Westaby S, Parker D, Shale DJ. Effect of cardiopulmonary bypass on systemic release of neutrophil elastase and tumor necrosis factor. J Thorac Cardiovasc Surg 1993;105:25-30. [Abstract]
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Gu YJ, van Oeveren W, Akkerman C, Huyzen RJ, Boonstra PW, Wildevuur CRH. Heparin-coated circuits reduce the inflammatory response to cardiopulmonary bypass. Ann Thorac Surg 1993;55:917-22. [Abstract]
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