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Ann Thorac Surg 1999;67:972-977
© 1999 The Society of Thoracic Surgeons

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Original Articles

Inflammatory response to cardiopulmonary bypass using roller or centrifugal pumps

^a Department of Thoracic and Cardiovascular Surgery, Hôpital Henri Mondor, Créteil, France
^b Service d’Immunologie Biologique, Hôpital Henri Mondor, Créteil, France
^c Department of Cardiac Surgery, Free University Hospital, Amsterdam, the Netherlands

Accepted for publication September 4, 1998.

Address reprint requests to Dr Loisance, Department of Thoracic and Cardiovascular Surgery, Hôpital Henri Mondor, 51 Avenue du M^al de Lattre de Tassigny, 94010 Créteil Cedex, France
e-mail: loisance{at}univ-paris12.fr

	Abstract

Top Abstract Introduction Material and methods Results Comment Acknowledgments References

 
Background. The inflammatory response in 29 patients undergoing coronary artery bypass grafting using either roller or centrifugal (CFP) pumps was evaluated in a prospective study.

Methods. Patients were randomized in roller pump (n = 15) and CFP (n = 14) groups. Terminal complement complex activation (SC5b-9) and neutrophil activation (elastase) were assessed during the operation. Cytokine production (tumor necrosis factor-, interleukin-6, interleukin-8) and circulating adhesion molecules (soluble endothelial-leukocyte adhesion molecule-1 and intercellular adhesion molecule-1) were assessed after the operation.

Results. Release of SC5b-9 after stopping cardiopulmonary bypass and after protamine administration was higher in the CFP group (p = 0.01 and p = 0.004). Elastase level was higher after stopping cardiopulmonary bypass using CFP (p = 0.006). Multivariate analysis confirmed differences between roller pump and CFP groups in complement and neutrophil activation. After the operation, a significant production of cytokines was detected similarly in both groups, with peak values observed within the range of 4 to 6 hours after starting cardiopulmonary bypass. However, interleukin-8 levels were higher using CFP 2 hours after starting cardiopulmonary bypass (p = 0.02). Plasma levels of adhesion molecules were similar in both groups within the investigation period.

Conclusions. During the operation, CFP caused greater complement and neutrophil activation. After the operation, the inflammatory response was similar using either roller pump or CFP.

	Introduction

Top Abstract Introduction Material and methods Results Comment Acknowledgments References

 
The whole body inflammatory response induced by cardiopulmonary bypass (CPB) is considered to be mainly responsible for postoperative organ dysfunction in cardiac operations [1, 2]. This response is associated with the host defense mechanism related to massive blood activation that occurs by the CPB procedure. Two main sources of blood activation are distinguished: material-independent and material-dependent factors.

Of the material-independent factors, two have been adequately documented. The "controlled shock" situation during CPB, particularly of the hypooncotic pressure because of large crystalloid priming volumes, induces endotoxin translocation [3]. The associated cytokine release causes the clinical septiclike syndrome [2]. Retransfusion of pericardial shed blood, highly activated by its tissue contact and containing high concentrations of tissue plasminogen activator (tPA), results in high fibrinolytic activity [4]. Measures of low priming volumes and the routine use of aprotinin in the priming solution have reduced these two factors of material-independent blood activation [5, 6].

Of the material-dependent factors, the surface characteristics of the materials of the CPB circuit activate the complement system, inducing a cascade of inflammatory pathways [1]. Complement activation stimulates polymorphonuclear and mononuclear leukocytes to release inflammatory products, such as elastase and cytokines [3]. These inflammatory products affect endothelial function, causing capillary leak and microcirculatory disturbances leading to organ dysfunction [3]. The recent introduction of new material surface coating with heparin has reduced but not eliminated complement activation and its associated inflammatory response [7].

In the search of other factors potentially responsible for remaining blood activation during CPB, we will focus our attention on the effects of blood pumps used in the circuit. The routinely used roller pumps (RP) are known to generate shear forces causing hemolysis, lipid membrane ghosts, and spoliation from the tubing that might significantly contribute to impaired microcirculation [1]. Centrifugal pumps (CFP), originally developed for prolonged CPB, but now available for CPB, are considered to cause less blood trauma [8].

We conducted a prospective study in patients undergoing CPB for coronary artery bypass grafting in which all measures, such as low priming volume, aprotinin prime, and heparin-coated circuits, were taken to reduce blood activation. We evaluated the effects of using RPs or CFPs by measuring circulating concentrations of inflammatory mediators.

	Material and methods

Top Abstract Introduction Material and methods Results Comment Acknowledgments References

 
Study design
Twenty-nine patients undergoing elective coronary artery bypass grafting were randomly included in the study to be operated on using either RP or CFP. High-risk patients were included, particularly those receiving aspirin within 10 days before the operation and those with impaired left ventricular function as defined by ejection fraction less than 30%. Exclusion criteria included patients undergoing valvular surgery or ventricular aneurysm surgery, patients with impaired organ function (apart from myocardial ischemia), preoperative coagulopathy, diabetes mellitus, active inflammatory disease, or taking antiinflammatory drugs (except acetylsalicylic acid). Surgeons, physicians, and trial nurses involved in the postoperative care were blinded to the randomization.

RP group (n = 15)
The circuit consisted of an RP (Sarns 9000, 3M Health Care Group, Ann Arbor, MI), polyvinylchloride tubing coated with end point-attached covalently bonded heparin (CBAS Carmeda, Medtronic, Kerkrade, the Netherlands), closed venous reservoir, hollow-fiber oxygenator (Maxima Carmeda, Medtronic, Anaheim, CA), cardiotomy reservoir (Intersept, Medtronic), and an arterial line filter (Medtronic M 440).

CFP group (n = 14)
The circuit consisted of a CFP (Biopump, Medtronic Biomedicus, Inc, Eden Prairie, MN), polyvinylchloride tubing coated with end point-attached covalently bonded heparin (CBAS Carmeda, Medtronic), closed venous reservoir, hollow-fiber oxygenator (Maxima Carmeda, Medtronic), cardiotomy reservoir (Intersept, Medtronic) and an arterial line filter (Medtronic M 440).

Surgical procedure, extracorporeal circulation, and postoperative care
The extracorporeal circuit was primed with Ringer’s lactate solution with 5,000 IU heparin, 60 mL 8.4% sodium bicarbonate, and 1 g potassium chloride. Aprotinin (2 x 10⁶ KIU, in prime) was systematically added because most of the patients refered to our institution did not stop aspirin whithin 10 days before the operation; also, it reduced excessive thrombin generation and fibrinolysis. Heparin (300 IU/kg) was injected directly into the right atrium before cannulation. Immediately before starting CPB and depending on the hemodynamic state, 500 to 1000 mL blood was collected for immediate post-CPB autotransfusion. Cardiopulmonary bypass was performed with core cooling to 28°C and flow of 2.4 L · min^-1 · m^-2. After aortic cross-clamping, myocardial protection was achieved with cold anterograde crystalloid cardioplegia (Assistance publique-Hôpitaux de Paris solution, 1000 mL at 4°C). Anticoagulation during bypass was controlled by activated clotting time (ACT, Hemotec, Inc, Englewood, CO); additional heparin was administered if the activated clotting time was less than 600 seconds. If additional volume was required, macromolecular solution (Plasmagel, Fresemius France Pharma, Sovres, France) or human albumin solution (4%) was added to the circuit. During bypass, all intrapericardial blood was collected in the reservoir and retransfused through the aortic cannula. After cessation of CPB, protamine (1 mg/100 IU heparin) was administered intravenously, followed by the infusion of unmodified pump blood. All the patients were operated on according to a standardized surgical protocol: distal anastomosis first, proximal anastomosis after release of aortic cross-clamp.

Patients were discharged from the intensive care unit when they were extubated with no need for continuous monitoring or intravenous inotropic drugs, and after removal of the chest tubes. Volume of blood loss was measured from end of operation until 18 hours after arrival in the intensive care unit.

Blood sampling and measurements
Serial arterial blood samples were collected after induction of anesthesia (h0) for each marker, and at intervals of 2, 4, 6, and 24 hours after starting CPB (respectively, h2, h4, h6, and h24) for cytokines and adhesion molecules. For elastase, which served as a marker of neutrophil activation, blood samples were collected after stopping CPB. For SC5b-9, the marker of terminal complement complex activation, blood samples were collected after stopping CPB, after protamine administration, and at h24 postoperatively.

Blood samples were collected into sterile vacuum tubes with EDTA for cytokines and terminal complement complex measurements (tumor necrosis factor- [TNF-], interleukin-6 [IL-6], IL-8, and SC5b-9) or with trisodium citrate for elastase and soluble adhesion molecules (endothelial-leukocyte adhesion molecule-1 [ELAM-1] and intercellular adhesion molecule-1 [ICAM-1]) and immediately centrifuged. Aliquots of plasma were stored at -70°C and subsequently assayed in duplicate for each marker according to the manufacturer’s procedure. Tumor necrosis factor-, IL-6, and IL-8 enzyme-linked immunosorbent assays were from Medgenic Diagnostics (Biotechnie, Rungis, France), elastase from Merck (Merck-Clevenot, Saint Genevieve des Bois, France), ELAM-1 and ICAM-1 from R&D Systems (Abingdon, UK), and SC5b-9 from Quidel (InGen, Rungis, France). The limit of sensitivity of each assay undertaken was as follows: TNF-, 3 pg/mL; IL-6, 2 pg/mL; IL-8, 0.7 pg/mL; elastase, 4 µg/L; ELAM-1, 0.1 ng/mL; ICAM-1, 0.35 ng/mL; and SC5b-9, 16 ng/mL.

Statistical analysis
Data were stored and analyzed using the SPSS software package (SPSS for Windows, SPSS Inc, Chicago, IL). Quantitative variables were expressed as mean ± standard deviation, and univariate analysis was performed using t test or Mann-Whitney test when appropriate. Paired variables were analyzed using Wilcoxon test. Qualitative variables, expressed as percentages, were analyzed with ² test or Fisher’s exact test when appropriate. To investigate whether factors other than type of pump could influence maximal levels of SC5b-9 and elastase, stepwise multiple regression was performed. In this multivariate analysis, the type of pump was associated with the following variables: baseline values, sex, hemoglobin charge before CPB, ejection fraction less than 50%, volume of priming, heparin dose, aortic cross-clamp time, and duration of CPB. A two-tailed p < 0.05 level was retained for statistical significance.

	Results

Top Abstract Introduction Material and methods Results Comment Acknowledgments References

 
Demographic and perioperative data are detailed in Table 1 and blood element counts in Table 2. No difference occurred between groups except for hematocrit value and hemoglobin charge before CPB despite randomization of the patients. None of the patients died after the operation, and no adverse event was observed during the postoperative period.

View larger version (16K): [in this window] [in a new window]   Fig 1. Changes of plasma levels of SC5b-9. Data are represented as mean ± standard error of the mean and reported before the operation (preop), after stopping CPB, after protamine administration, and 24 hours after starting CPB (h24). (RP = roller pump; CFP = centrifugal pump; CPB = cardiopulmonary bypass.) *p < 0.05 vs CFP value; #p < 0.05 vs preop value.

View larger version (14K): [in this window] [in a new window]   Fig 2. Changes of plasma levels of elastase. Data are represented as mean ± standard error of the mean and reported before the operation (preop) and after stopping CPB. (RP = roller pump; CFP = centrifugal pump; CPB = cardiopulmonary bypass.) *p = 0.006 vs CFP value; #p = 0.001 vs preop value.

View larger version (13K): [in this window] [in a new window]   Fig 3. Changes of plasma levels of cytokines TNF- (A), IL-6 (B), and IL-8 (C). Data are represented as mean ± standard error of the mean and reported before starting CPB (h0), and 2 hours (h2), 4 hours (h4), 6 hours (h6), and 24 hours (h24) after starting CPB. (RP = roller pump; CFP = centrifugal pump; CPB = cardiopulmonary bypass.) A: #p < 0.01 vs h0 value; B: #p < 0.01 vs h0 value; C: *p = 0.02 vs CFP value; #p < 0.05 vs h0 value.

View larger version (14K): [in this window] [in a new window]   Fig 4. Changes of plasma levels of endothelial-leukocyte adhesion molecule ELAM-1 (A) and intercellular adhesion molecule ICAM-1 (B). Data are represented as mean ± standard error of the mean and reported before starting CPB (h0), and 2 hours (h2), 4 hours (h4), 6 hours (h6), and 24 hours (h24) after starting CPB. (RP = roller pump; CFP = centrifugal pump; CPB = cardiopulmonary bypass.) A: #p < 0.05 vs h0 value; B: #p < 0.01 vs h0 value.

	Comment

Top Abstract Introduction Material and methods Results Comment Acknowledgments References

 
This study was designed to assess whether CFP reduced the inflammatory response to CPB-mediated shear stress and subsequent lower blood activation. Although CFP is known to reduce hemolysis [8, 9], the inflammatory response detected during the operation was greater using CFP than RP, whereas late postoperative inflammatory response was similar with both devices.

The early inflammatory response initiated immediately after starting CPB, as reflected by markers released during the CPB procedure, is known to affect the complement system and neutrophils [1, 2]. We observed higher complement and neutrophil activation when using CFP. These results are opposed to those of Moen and associates [9], who reported that CFP ex vivo causes less complement activation than RP during prolonged CPB. However, this experimental setting did not simulate the biomaterial-independent blood activation generated by impaired organ perfusion. They further reported their clinical experience using CFP, but the extent of the inflammatory response induced by pumps was masked by the benefit provided by heparin coating [10]. The mechanism by which CFP was associated with a greater early inflammatory response than RP remains speculative. Because other elements of the extracorporeal circuits were identical, it may enhance qualitative differences of the organ perfusion provided by both devices. It would imply that a relative hypoperfusion occurred using CFP although less microparticles were expected to be embolized into the bloodstream. Without a special add-on device, such as in our protocol, a CFP delivers completely nonpulsatile perfusion, whereas even a conventional RP delivers slight pulsatility [11]. Previous comparisons of these flow regimens have demonstrated that pulsatile perfusion better preserves the microcirculation and organ perfusion [12] and that nonpulsatile perfusion is associated with higher endotoxemia [13] and elastase release [14]. The production of endotoxin detected after release of the aortic cross-clamp, as a marker of mucosal injury after inadequate intestinal perfusion, is involved in activation of the complement system [15] and release of elastase from neutrophils [16]. In our study the pump outflow imposed by the perfusionists was similar using RP and CFP. However, the amount of regional blood flow during hypothermic CPB despite constant pump outflow is still open to debate. The cold-induced vasoconstriction of the splanchnic area is of major importance when hypothermia is used, as we did, despite the maintenance of generally accepted levels of mean arterial blood pressure and perfusion blood flow [17]. Because CFPs are sensitive to afterload pressure [18], inadequate intestinal perfusion during hypothermic CPB would more likely occur than by using RPs, thus providing additional inflammatory response to that initiated by blood-material contact. It would additionally imply that normothermic CPB is required for safe use and expected benefit of CFP.

The pattern of release of cytokines into the bloodstream indicates that inflammatory response also occurred late after the CPB procedure. The production of these inflammatory mediators covered the first postoperative day with peak values observed within the range of 4 to 6 hours after starting CPB, which is in agreement with a previous report [19]. The only difference that we found between the two pumps affected the IL-8 production, which was higher 2 hours after starting CPB using CFP. It may be related to a correlation of IL-8 levels at this time with elastase levels as previously reported [20]. It may also be explained by the fact that the rapid increase of IL-8 in blood does not fit very well with the time frame required for a synthesis of other cytokines [20]. However, this single difference in cytokine response after CPB occurred when the amount of IL-8 did not exceed 25% of the peak value. This suggests some contribution other than the pumps to the cytokine response. In other words, shear forces generated by pumping and their consequences on organ perfusion represented a minor source of blood activation whereas multifactorial sources were of major importance. Moreover, routine hypothermia delays the inflammatory response that occurs when rewarming the patient during the end of CPB [21]. Therefore, all these additional factors may be responsible for a background noise of blood activation that led us to be unable to discriminate, 24 hours after the operation, the influence of CFP and RP in the production of these inflammatory mediators.

Neutrophil-endothelial interactions represent the end point of this post-CPB inflammatory process. Release of oxygen free radicals and proteases from activated neutrophils in contact with endothelial cells is known to be the main cause of the neutrophil-related damage of the endothelium [1, 2]. Thus, circulating adhesion molecules are believed to be markers of microvascular injury, tissue damage, and extent of inflammatory response. In this study, the pattern of release of adhesion molecule paralleled those previously reported by Boldt and colleagues [22]. The decrease of adhesion molecule concentration in the postoperative period has been attributed by these authors to hemodilution induced by CPB. It is likely that the expression of ELAM-1 and ICAM-1 on the endothelial surface was upregulated to the same extent by cytokines, thus explaining the similar levels of circulating adhesion molecules detected in blood during the first postoperative day. It cannot be argued that potential differences between groups would be masked by aprotinin. Indeed, aprotinin has been proved to not influence plasma levels of circulating adhesion molecules [22] or the cytokine response [23] in the clinical setting of CPB.

A contribution of pumps to blood activation has been found during the operation but not detrimentally in our patients undergoing CPB for coronary artery bypass grafting. Whereas CFP is known to reduce hemolysis and was expected to minimize embolization of microparticles from tubing and fragmented blood cells, RP allowed less complement and neutrophil activation. In the clinical setting of CPB, hypothermia might be avoided for CFP use to compensate for deleterious effects of its nonpulsatile flow, to limit the inflammatory response that may be owing to impaired intestinal perfusion. Nevertheless, the contribution of pumping likely represents a minor source of blood activation that occurs early whereas other multifactorial sources are of major importance in the late inflammatory response.

	Acknowledgments

Top Abstract Introduction Material and methods Results Comment Acknowledgments References

 
The authors thank Gérard Bajan, Thierry Moiré, Jean Luc Ermine, François Roman, Romuald Rycklink, Christiane Chenal, and Evelyne Sainte-Marie for their technical assistance and Karine Marson for blood sampling.

	References

Top Abstract Introduction Material and methods Results Comment Acknowledgments References

 

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This Article Abstract Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Personal Folders Download to citation manager Author home page(s): Christophe Baufreton Piet G.M. Jansen Daniel Y. Loisance Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Baufreton, C. Articles by Loisance, D. Y. Search for Related Content PubMed PubMed Citation Articles by Baufreton, C. Articles by Loisance, D. Y.