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Ann Thorac Surg 1996;62:184-190
© 1996 The Society of Thoracic Surgeons
Department of Thoracic and Cardiovascular Surgerya, Institute of Clinical Chemistry and Laboratory Medicineb, Department of Anesthesiology and Surgical Intensive Carec, Institute of Arteriosclerosis Researchd, Muenster University Hospital, Muenster, Germany
Accepted for publication March 11, 1996.
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Abstract |
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 TopFootnotes Abstract IntroductionMaterial and MethodsResultsCommentAcknowledgmentsReferences |
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Methods. We compared arterial and mixed venous levels of interleukin-6, tumor necrosis factor-
, soluble interleukin-2 receptor, and interleukin-2 at 10 points in time (24 hours before until 48 hours after extracorporeal circulation) in 21 patients with an ejection fraction of less than 0.45 (study group) to 15 patients with an ejection fraction of more than 0.55 (control group) undergoing elective coronary artery bypass grafting. The study and control group differed with regard to left ventricular ejection fraction (0.37 ± 0.05 versus 0.66 ± 0.11, p < 0.05) and reperfusion time (35 ± 42 minutes versus 18 ± 4 minutes, p = 0.07), but not age, sex, vessel involvement, number of grafts performed, cross-clamp time, extracorporeal circulation time, core temperature, and duration of ventilation.
Results. Six patients in the study group required mechanical support and 1 died. There were no complications in the control group. In the study group, there were higher preoperative interleukin-2 and tumor necrosis factor- levels and a higher maximum cytokine response to extracorporeal circulation for interleukin-2, soluble interleukin-2 receptor, interleukin-6, and tumor necrosis factor- (all p < 0.05). Interleukin-6 correlated with duration of extracorporeal circulation, dose of norepinephrine and epinephrine support, pulmonary capillary wedge pressure, mean pulmonary arterial pressure, right atrial pressure, heart rate, cardiac index, and inversely with systemic vascular resistance. Interleukin-6 was highest in patients with complications. Arterial and venous cytokine levels correlated closely.
Conclusions. Preoperative left ventricular dysfunction is associated with a higher degree of proinflammatory cytokine release during elective coronary artery bypass grafting. This response is associated with impaired hemodynamics and a higher incidence of perioperative complications.
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Introduction |
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(TNF-) [8, 11, 12, 14–16] and interferon-
[9]. IL-2, IL-6, and TNF- exert a negative inotropic effect on the myocardium in the hamster model, probably mediated by the inducible nitric oxide synthase [17] and inhibition of cardiac myocyte ß-adrenergic responsiveness [18]. They have been implicated in cardiac dysfunction in sepsis [19], severe heart failure [20], cardiac transplantation [21], cancer therapy [22], and antiviral therapy [23]. We were interested in the association between preoperative left ventricular dysfunction, cytokine release, and hemodynamic alterations after ECC because data are scarce in this cohort [24]. The specific aim of this study was to test the hypothesis that patients with preoperative left ventricular dysfunction undergoing bypass grafting would have more pronounced alterations in cytokine release and associated impairment of hemodynamics and clinical outcome than a control group with normal left ventricular function undergoing bypass grafting. |
Material and Methods |
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Medication, Technique of Anesthesia, Extracorporeal Circulation, and Cardioplegia
Preoperatively, aspirin was stopped 10 days before the scheduled date of operation and antianginal substances were continued until the day before operation. There was no perioperative use of steroids. Premedication consisted of oral flunitrazepam (2 mg) as night sedation and another dose of 2 mg 90 minutes before induction of anesthesia. Routine monitoring in the perioperative period consisted of an electrocardiogram, a peripheral venous cannula, a pulmonary artery catheter positioned to obtain a reliable pulmonary capillary wedge pressure tracing during balloon inflation, and an intraarterial line in the left radial artery. Body temperature was continuously monitored. Anesthesia was induced with 2.5 to 5 mg of midazolam, 2 to 8 µg/kg of sufentanil, 0.2 mg/kg of etomidate, and 0.1 mg/kg of pancuronium while the patients inspired 100% oxygen. After endotracheal intubation, the patients were mechanically ventilated with oxygen and air (inspired oxygen fraction, 0.5). The ventilation was adjusted to maintain an arterial carbon dioxide tension of 35 to 40 mm Hg or an end-tidal carbon dioxide level of 4.5% to 5%. Just before sternotomy the patients received another dose of 2 to 8 µg/kg of sufentanil. Further boluses of 25 to 50 µg of sufentanil were injected as appropriate during the entire surgical procedure. The surgical and cardiopulmonary bypass management protocols were applied according to the standard in our institution using a centrifugal pump, membrane oxygenation, and identical priming solution. Bretschneider cardioplegia was used routinely. Cardiopulmonary bypass conditions were mildly hypothermic. Administration of heparin before cannulation and subsequent neutralization with protamine sulfate was performed in a standardized fashion. Postoperatively, pharmacologic support was instituted according to hemodynamic requirements. Low-dose dopamine (2.5 µg • kg-1 • min-1) and nitroglycerine (0.4 µg • kg-1 • min-1) was administered to virtually all patients of the study and control groups in the first 24-hour period postoperatively. In addition, dobutamine was administered as first-line drug when low-output syndrome with pulmonary hypertension predominated, epinephrine was given in situations refractory to dobutamine, and norepinephrine, when low-output syndrome with severe systemic hypotension persisted. The intraaortic balloon pump was initiated if patients were unresponsive to volume loading, afterload optimization, inotropic drugs, and pacing.
Sample Collection
Samples were drawn from the central venous and arterial line, respectively. Venous and arterial levels were measured simultaneously, because there is no information available regarding the correlation of the two sampling sites in patients with left ventricular dysfunction. The correlation is of interest because of the potential elimination of mediators in the extracorporeal circuit and the potential contribution of the pulmonary circulation to cytokine regulation [6, 24]. Blood samples were collected in glass tubes not containing any additives, allowed to clot at room temperature for 30 minutes, and centrifuged at 4°C with 3,000 rpm for 5 minutes. Serum was aliquoted into sterile tubes and stored at -70°C until measurement.
Cytokine Assay Technique
Analysis was performed with commercially available immunoenzymometric assay kits for IL-2, soluble IL-2 receptor, IL-6 (Immunotech, Hamburg, Germany) and TNF- (Quantikine High Sensitivity; R&D Systems, MN) according to the instructions of the manufacturers. All measurements were done in duplicate. For the purpose of data analysis, mean values of the two measurements were used. Intraassay and interassay variability according to the manufacturers' information were less than 3.4% and less than 10.1% for IL-2, less than 6.6% and less than 11.4% for soluble IL-2 receptor, less than 6.8% and less than 20.1% for IL-6, less than 10.0% and less than 13.5% for TNF-, respectively. Assay ranges (including sensitivity threshold) were 5 to 1,000 pg/mL for IL-2, 5 to 400 pmol/L for soluble IL-2 receptor, 2 to 1,000 pg/mL for IL-6, and 0.17 to 64 pg/mL for TNF-. The NIBSC/WHO TNF- international reference standard (87/650) was used for calibration of the TNF- immunoassay. Normal serum reference values are reported according to information provided by the manufacturers. Results were not corrected for hemodilution.
Hemodynamic Assessment
Ventricular performance was assessed by pulmonary artery catheterization with standard parameters including right atrial pressure, pulmonary arterial pressure, pulmonary capillary wedge pressure, and cardiac output. Artery pressure was measured in the radial artery. Cardiac index, pulmonary and systemic vascular resistance were calculated using standard formulas.
Echocardiography
The degree of regional and global left ventricular dysfunction was determined by transesophageal (times 2, 6, 8) and transthoracic (time 9) echocardiography. Besides calculation of global function (left ventricular ejection fraction) by planimetry we assessed regional wall motion by minor modifications of a method that has been described recently [24]. Briefly, transesophageal and transgastric multiplane long- and short-axis views were recorded on video tape. Four regions (anterior wall, lateral wall, septal wall, posterior wall) were evaluated separately according to the following scoring system: 0 = normokinetic, 1 = mildly hypokinetic, 2 = severely hypokinetic, 3 = akinetic, and 4 = dyskinetic. The total wall motion impairment score (WMS) was calculated using the following equation: WMS = [
(anterior2) + (posterior2) + (lateral2) + (septal2)]1/2. To minimize interobserver variability, off-line scoring was performed by one experienced echocardiographer blinded to clinical data. Intraobserver variability was assessed by repeated scoring of all echocardiograms at least 2 weeks apart.
Study Protocol
The following ten points in time were selected for measurement:
Venous levels of IL-2, soluble IL-2 receptor, IL-6, and TNF- were assessed at time 1 to 10, arterial levels at time 2 to 9 (arterial sampling was not performed before operation), and hemodynamic/echocardiographic measurements at time 2, 6, 8, and 9.
Statistical Analysis
For statistical analysis, the Statistical Package for the Social Sciences (SPSS 5.0.2) was used. Because a normal distribution of cytokine levels could not be assumed, descriptive statistical analysis of cytokine levels was performed using the median and 25%/75% quartiles instead of mean values and standard deviation. Correlations between cytokine levels and hemodynamic, echocardiographic, procedural, and pharmacologic parameters as well as between arterial and venous cytokine levels were calculated using linear regression analysis. Differences between groups of patients were assessed by Mann-Whitney U-test for independent samples. Values of p of less than 0.05 were considered significant, p values between 0.05 and 0.10 were considered as trend. The distribution of cytokine levels at each point in time were illustrated using box plots that incorporated the median as well as 25% and 75% quartiles.
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Results |
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Hemodynamic Patterns
Cardiac index (p = 0.05), stroke volume (p = 0.0001), and ejection fraction (p = 0.0001) were lower, whereas heart rate (p = 0.0002) and wall motion impairment score (p = 0.04) were higher in the study group compared with control (Fig 1). Within the study group, pulmonary vascular resistance preoperatively and wall motion impairment scores 4 hours postoperatively were highest in the group with complications (p = 0.05 and p = 0.04, respectively, compared with the study group).
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levels (reference value, 0 to 5 pg/mL) and IL-2 levels (reference value, 0 to 5 pg/mL) in the study group were elevated (TNF-: 6.1 versus 0.7 pg/mL, p = 0.00001; IL-2: 405 versus 234 pg/mL, p = 0.028). The perioperative cytokine patterns are summarized in Figure 2. We found a more pronounced and prolonged response of IL-6 in the study group (study versus control group: 387(277/780) pg/mL versus 277(153/427) pg/mL 4 hours after ECC; p = 0.03). The highest levels were found in the group with weaning problems (937(381/1330) pg/mL versus 387(277/780) pg/mL compared with the study group as a whole 4 hours after ECC; p = 0.02). There was a more pronounced response of TNF- (study versus control group: 7.7(5.2/9.7) pg/mL versus 2.0(0.3/9.5) pg/mL 4 hours after ECC; p = 0.0002), soluble IL-2 receptor (study versus control group: 67(47/89) pmol/L versus 37(19/59) pmol/L 24 hours after ECC; p = 0.02) and of IL-2 (study versus control group: 332(232/535) pmol/L versus 209(101/288) pmol/L 4 hours after ECC; p = 0.03).
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levels 30 minutes after the start of ECC correlated with ECC duration, cross-clamp time, and reperfusion time (r = 0.60, p = 0.01; r = 0.57, p = 0.02; and r = 0.57, p = 0.02, respectively).
Relationship Between Cytokines and Doses of Pharmacologic Support
Mean doses (number of patients in the study group requiring the drug in parentheses) were epinephrine: 0.07 ± 0.14 µg • kg-1 • min-1 (n = 13), norepinephrine: 0.04 ± 0.07 µg • kg-1 • min-1 (n = 5), dopamine: 2.77 ± 1.75 µg • kg-1 • min-1 (n = 20), dobutamine: 5.62 ± 4.44 µg • kg-1 • min-1 (n = 10), enoximone: 5.26 ± 2.73 µg • kg-1 • min-1 (n = 2), and nitroglycerine: 0.39 ± 0.35 µg • kg-1 • min-1 (n = 20). In the control group, only low doses of dopamine and nitroglycerine had to be administered temporarily. In the study group, correlations were found between IL-6 and dose of norepinephrine (r = 0.74; p = 0.0001) as well as dose of epinephrine (r = 0.51; p = 0.0001).
Relationship Between Cytokines and Hemodynamics
In the study group, there were weak correlations between IL-6 and heart rate (r = 0.41; p = 0.00001), cardiac index (r = 0.24; p = 0.02), mean pulmonary arterial pressure (r = 0.32; p = 0.0008), pulmonary capillary wedge pressure (r = 0.28; p = 0.004), right atrial pressure (r = 0.36; p = 0.0002), as well as a negative correlation between IL-6 and systemic vascular resistance (r = -0.27; p = 0.005). There was a weak correlation between soluble IL-2 receptor and mean arterial pressure (r = 0.19; p = 0.05), mean pulmonary arterial pressure (r = 0.20; p = 0.04), pulmonary capillary wedge pressure (r = 0.23; p = 0.02), and wall motion impairment score (r = 0.27; p = 0.02). A negative correlation was found between soluble IL-2 receptor and ejection fraction (r = -0.35; p = 0.001). In the control group, there was a positive correlation between IL-6 and heart rate (r = 0.49; p < 0.05).
Arterial and Venous Cytokine Levels
There was a close correlation between arterial and venous levels for IL-6 (r = 0.99; p = 0.00001), TNF- (r = 0.97; p = 0.00001), soluble IL-2 receptor (r = 0.82; p = 0.00001), and IL-2 (r = 0.65; p = 0.00001).
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Comment |
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Extracorporeal Circulation and Cytokine Levels
The association between duration of ECC, cross-clamp time, and reperfusion time and levels of IL-6- and TNF- is in line with the well-known damaging effect of ECC on the organism [1, 2]. It was interesting to note that in our study TNF- release preceded IL-6 release, as has been described in other settings [25]. The use of essentially normothermic conditions during ECC in our institution may have contributed to a higher overall level of cytokine release, as compared with hypothermic conditions [12]. To what extent the use of membrane oxygenators (versus bubble oxygenators) may have affected cytokine release is an interesting question that remains to be elucidated.
Pharmacologic Support and Cytokine Levels
The correlation between IL-6 levels and dose of norepinephrine and epinephrine support is in line with other reports about a feedback relationship between proinflammatory cytokines and neuroendocrine systems [25]. In light of the potentially cardiodepressant effect of IL-6 on the myocardium [17], it is tempting to speculate that stimulation of cytokine release by catecholamines may constitute an intrinsic mechanism to limit myocardial oxygen expenditure in situations of exogenous application of catecholamines or sympathetic nervous system activation. Within this context, it is of great interest to further investigate the potentially reciprocal intracellular ß-adrenoceptor–cyclic adenosine monophosphate and IL-6 receptor–cyclic guanosine monophosphate signaling-pathways, respectively [17, 18].
Interleukin-6
The positive albeit weak correlation between IL-6 and heart rate, pulmonary capillary wedge pressure, and right atrial pressure and the negative correlation between IL-6 and systemic vascular resistance, which were paralleled by a positive correlation between IL-6 and cardiac index was an interesting finding of this study. To our knowledge this is the first clinical report in patients with impaired preoperative left ventricular function undergoing CABG in which the magnitude of IL-6 response is shown to be correlated positively to heart rate, left and right ventricular preload, and negatively to left ventricular afterload, with the result of augmented cardiac index. There are only few reports about a correlation between cytokine levels and hemodynamic variables [11, 12, 14, 24]. In one study [12], the arterial levels of IL-1ß, IL-6, and TNF- correlated with the need for pressor substances, suggesting a more pronounced vasodilation and reduction of systemic vascular resistance, respectively. Direct values for systemic vascular resistance were not reported in this study. Another report did not find a correlation between venous cytokine levels and hemodynamic variables, although a significant decrease in systemic vascular resistance and a corresponding increase in cardiac index was observed within the first 24 hours after ECC [11]. We reported an association between IL-6 and heart rate in a patient cohort with normal preoperative left ventricular function [14]. A hyperdynamic pattern similar to the one observed in our study has been described in the sepsis syndrome [26] and in patients with large complicated myocardial infarctions [27] in which the cytokine TNF- plays a major mediating role, probably through the Ca-independent inducible nitric oxide synthase. Within the clinical study setting it is difficult to assess separately the negative inotropic influence of IL-6 that has been demonstrated in the isolated hamster papillary muscle preparation [17].
Other Cytokines
The suppression of IL-2 levels during ECC has been described before [14] and may be attributed to an immunosuppressive effect of ECC [9, 13]. Because IL-2 is a key mediator of cellular immunity that is required for initiating and sustaining T-cell maturation and differentiation, our results are compatible with the notion of an immunosuppressive effect of ECC. The increase of soluble IL-2 receptor level in the study group, as compared with the control group, which could be demonstrated starting 24 hours preoperatively suggests-by potentially the same mechanism as the one responsible for IL-2 elevation preoperatively-an immunoaugmentatory effect of left ventricular dysfunction in the situation of anticipation of ECC. It is of interest to note the preoperative elevation of TNF- in the group with left ventricular dysfunction in contrast to the control group. This finding underlines reports in the chronic heart failure population [20]. The published data concerning TNF- release during ECC are conflicting [7, 8, 11, 12, 14–16]. Our results suggest only a very modest increase in TNF- levels in a high-risk patient cohort after ECC, compared with the considerable TNF- release in septic conditions [19, 26].
Potential Mechanisms of Impaired Weaning
The subgroup with complications had higher preoperative pulmonary vascular resistance levels than the other study group patients, a trend toward longer reperfusion times, and higher levels of postoperative IL-6 release, whereas IL-6 release was associated with a higher degree of hemodynamic impairment. These observations are consistent with the hypothesis of a multifactorial chain of events in which preoperative impairment of left ventricular function causes longer reperfusion times and a higher IL-6 release that, in turn, might play a role to impair weaning by its negative inotropic action [17].
Arterial and Venous Cytokine Patterns
The essentially identical cytokine level is an important finding as some groups have reported their results measuring arterial cytokine levels [8, 12, 16] whereas others have reported venous cytokine levels [11, 15] or coronary sinus levels [10]. These findings suggest that there was no detectable elimination of cytokines during ECC in the extracorporeal circuit and no significant production or elimination of cytokines in the pulmonary circulation after termination of ECC in the cohort of patients with preoperatively impaired left ventricular function.
Limitations
The cytokine assays applied have an inherent sensitivity limit. Because cytokines are characterized by tight gene control, short duration of action, and an autocrine or paracrine rather than an endocrine mode of action as opposed to hormones, thus affecting only the immediate environment, all studies based on systemic venous or arterial blood sampling may yield a lower sensitivity of detection than studies examining intracellular cytokine production or cytokine mRNA transcription levels in appropriate target tissues. As cytokines are acting in minute quantities, we might have missed some regulatory movements below the detection threshold. Another study limitation is the small sample size that may have kept differences in ECC duration and ventilation time in the study versus control group from becoming significant.
Conclusions
Patients with impaired left ventricular function undergoing elective CABG experience longer reperfusion times, a more pronounced response of proinflammatory cytokines, and more weaning problems. Although from these data no inferences can be drawn as to whether impaired hemodynamics caused cytokine release, or whether cytokines caused impaired hemodynamics, clearly an association is present. Ongoing experiments will have to shed light on the important issue of a cause and effect relationship.
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TopFootnotesAbstractIntroductionMaterial and MethodsResultsCommentAcknowledgmentsReferences |
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, IL-2, and IL-2-receptor-levels to cellular rejection, allograft dysfunction and mortality early after cardiac transplantation. Transplantation 1995;60:1118–24.[Medline]
. Circ Res 1990;67:68–77. (cachectin) in myocardial infarction. J Intern Med 1989;225:333–6.[Medline]This article has been cited by other articles:
|
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 |
|
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|
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|
|
 |
|
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|
|
|
|
 |
|
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|
|
|
|
 |
|
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|
|
|
|
 |
|
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|
|
|
|
|
|
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|
|
|
|
 |
|
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|
|
|
|
 |
|
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|
|
|
|
 |
|
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|
|
|
|
|
|
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|
|
|
|
 |
|
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|
|
|
|
|
|
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|
|
|
|
|
|
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|
|
|
|
|
|
P. Menasche and L. H. Edmunds Jr. Extracorporeal Circulation: The Inflammatory Response Card. Surg. Adult, January 1, 2003; 2(2003): 349 - 360. [Full Text]
|
|
|
|
|
|
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|
|
|
|
 |
|
 D J Brull, J Sanders, A Rumley, G D Lowe, S E Humphries, and H E Montgomery Impact of angiotensin converting enzyme inhibition on post-coronary artery bypass interleukin 6 release Heart, March 1, 2002; 87(3): 252 - 255. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
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|
|
|
|
 |
|
 G. E. Hill The Inflammatory Response to Cardiopulmonary Bypass-- Should It Be Treated? Seminars in Cardiothoracic and Vascular Anesthesia, September 1, 2001; 5(3): 229 - 235. [Abstract] [PDF]
|
|
|
|
 |
|
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|
|
|
|
 |
|
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|
|
|
|
 |
|
 A Sablotzki, J Muhling, M G Dehne, B Zickmann, R E Silber, and I Friedrich Treatment of sepsis in cardiac surgery: role of immunoglobulins Perfusion, March 1, 2001; 16(2): 113 - 120. [Abstract] [PDF]
|
|
|
|
|
|
H. Aebert, S. Kirchner, A. Keyser, D. E. Birnbaum, E. Holler, R. Andreesen, and G. Eissner Endothelial apoptosis is induced by serum of patients after cardiopulmonary bypass Eur J Cardiothorac Surg, November 1, 2000; 18(5): 589 - 593. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
V. Gulielmos, M. Menschikowski, H.-M. Dill, M. Eller, S. Thiele, S. M. Tugtekin, W. Jaross, and S. Schueler Interleukin-1, interleukin-6 and myocardial enzyme response after coronary artery bypass grafting - a prospective randomized comparison of the conventional and three minimally invasive surgical techniques Eur J Cardiothorac Surg, November 1, 2000; 18(5): 594 - 601. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
J.-O. Defraigne, J. Pincemail, R. Larbuisson, F. Blaffart, and R. Limet Cytokine release and neutrophil activation are not prevented by heparin-coated circuits and aprotinin administration Ann. Thorac. Surg., April 1, 2000; 69(4): 1084 - 1091. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 M. Azzawi and P. Hasleton Tumour necrosis factor alpha and the cardiovascular system: its role in cardiac allograft rejection and heart disease Cardiovasc Res, September 1, 1999; 43(4): 850 - 859. [Full Text] [PDF]
|
|
|
|
|
|
S. Wan and A. P. C. Yim Cytokines in myocardial injury: impact on cardiac surgical approach Eur J Cardiothorac Surg, September 1, 1999; 16(Supplement_1): S107 - S111. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
A. Alonso, C. W. Whitten, and G. E. Hill Pump prime only aprotinin inhibits cardiopulmonary bypass-induced neutrophil CD11b up-regulation Ann. Thorac. Surg., February 1, 1999; 67(2): 392 - 395. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
G. E. Cimochowski, M. D. Harostock, and P. J. Foldes MINIMAL OPERATIVE MORTALITY IN PATIENTS UNDERGOING CORONARY ARTERY BYPASS WITH SIGNIFICANT LEFT VENTRICULAR DYSFUNCTION BY MAXIMIZATION OF METABOLIC AND MECHANICAL SUPPORT J. Thorac. Cardiovasc. Surg., April 1, 1997; 113(4): 655 - 666. [Abstract] [Full Text]
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