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CARDIOVASCULAR ANESTHESIA

Neutrophil Number and Interleukin-8 and Elastase Concentrations in Bronchoalveolar Lavage Fluid Correlate with Decreased Arterial Oxygenation After Cardiopulmonary Bypass

Naoki Kotani, MD^*, Hiroshi Hashimoto, MD^*, Daniel I. Sessler, MD, Masatoshi Muraoka, MD^*, Jian-Sheng Wang, MD, Michael F. O’Connor, MD, and Akitomo Matsuki, MD^*

*Department of Anesthesiology, University of Hirosaki School of Medicine, Hirosaki, Japan; Department of Anesthesia and Perioperative Care, University of California–San Francisco, San Francisco, California; and Department of Anesthesia and Critical Care, University of Chicago, Chicago, Illinois

Address correspondence and reprint requests to Naoki Kotani, MD, Department of Anesthesiology, University of Hirosaki School of Medicine, Hirosaki 036-8562, Japan. Address e-mail to nao{at}cc.hirosaki-u.ac.jp

	Abstract

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Atelectasis is a major cause of decreased arterial oxygenation after cardiopulmonary bypass (CPB). There is a close relationship between atelectasis and inflammatory responses. We therefore tested the hypothesis that neutrophil number and the concentrations of proinflammatory cytokines and elastase in plasma and bronchoalveolar lavage fluid correlate with changes in arterial oxygenation. Bronchoalveolar lavage was performed just after the induction of anesthesia and at the end of surgery in 80 patients undergoing CPB. Peripheral blood was sampled simultaneously. Arterial oxygenation was quantified by PaO₂/fraction of inspired oxygen (FIO₂) and intrapulmonary shunt (Q_s/Q_t). PaO₂/FIO₂ and Q_s/Q_t decreased significantly at the end of surgery, whereas neutrophil number, interleukin (IL)-6, IL-8, tumor necrosis factor-, and elastase concentrations in the lavage fluid increased significantly. The increase in neutrophil count from the lavage fluid correlated significantly with the increases in IL-8 and elastase concentrations. The increase in neutrophil number and IL-8 and elastase concentrations in the lavage fluid correlated significantly with PaO₂/FIO₂ and Q_s/Q_t at the end of surgery. In contrast, none of the plasma values correlated with these variables. Significant correlation between immune mediators and decreased arterial oxygenation suggests that inflammatory responses in the distal airway are strongly related to a decrease in arterial oxygenation after CPB.

Implications: The increases in neutrophil number, interleukin-8, and elastase concentrations in bronchoalveolar lavage correlated significantly with decreases in arterial oxygenation. Our results suggest immunologic responses in the distal airway are closely related to pulmonary gas change.

	Introduction

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Reduced arterial oxygenation is a common complication in patients undergoing cardiopulmonary bypass (CPB). For example, intrapulmonary shunt is typically 25% of the cardiac output by the end of CPB (1,2). The major cause of decrease in arterial oxygenation is thought to be atelectasis (2,3). However, intrapulmonary shunt does not always correlate with atelectasis (4). At the very least, we speculate that various factors are related to development of atelectasis, which itself can induce an inflammatory reaction in the distal airway. Atelectasis lasting only 1 h facilitates production of proinflammatory cytokines by alveolar macrophages (5). These cytokines decrease the synthesis of surfactant protein, which in turn facilitates development of atelectasis (6).

CPB up-regulates neutrophil and endothelial adhesive molecule expression, promoting enhanced neutrophil-endothelial adherence (7). The increases in endothelial permeability induced by neutrophil-endothelial adherence and subsequent neutrophil accumulation cause parenchymal and interstitial edema, resulting in a decrease in arterial oxygenation (8). Neutrophils that migrate to the distal airway become activated and further damage bronchoalveolar architecture by secreting oxygen-free radicals and lysozomal enzymes.

Alveolar leukocytes, more than 90% of which are macrophages, have a critical role in pulmonary insult. We reported inflammatory responses in alveolar leukocytes during general surgery (9–12). Although some studies showed increases in neutrophil influx and cytokine production during CPB (13,14), the extent to which increases in systemic and pulmonary immune components correlate with observed decreases in arterial oxygenation remains unknown. We therefore tested the hypothesis that neutrophil number and concentrations of proinflammatory cytokines and elastase in plasma and bronchoalveolar lavage fluid correlate with decrease in arterial oxygenation after CPB.

	Methods

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The protocol for this study was approved by the institutional review board at the University of Hirosaki, and written, informed consent was obtained from all the patients. We studied 80 patients scheduled to undergo cardiac surgery using CPB.

Inclusion and exclusion criteria were described in the accompanying study (15). Anesthetic method and the CPB apparatus were also described in the accompanying study (15). Briefly, anesthesia was maintained with fentanyl, isoflurane, and vecuronium. Patients’ lungs were mechanically ventilated throughout anesthesia (PaCO₂ 35–45 mm Hg), except during total bypass; tidal volume was maintained at 10 mL/kg with 100% oxygen. Immediately after termination of total bypass, the lungs were inflated manually for 10 s to 40 cm H₂O five times to reduce the severity of atelectasis; mechanical ventilation was then resumed.

Postbypass management was described in our accompanying paper (15). From the end of surgery, attempts were made to reduce the concentration of inhaled oxygen and to wean patients from mechanical ventilation after core temperature stabilized (rectal temperature >36°C). Patients demonstrated hemodynamic stability without excessive blood loss and were able to breathe spontaneously with satisfactory arterial blood gas tension values.

We quantified the degree of arterial oxygenation by PaO₂/fraction of inspired oxygen (FIO₂) and intrapulmonary shunt (Q_s/Q_t). As FIO₂ was 1.0 in our patients, PaO₂/FIO₂ equals PaO₂. Furthermore, SaO₂ was nearly 100% because PaO₂ exceeded 150 mm Hg. Q_s/Q_t was therefore simply calculated as follows:

Bronchoalveolar lavage was performed based on a previously described method (9,10,12), immediately after the induction of anesthesia (Beginning) and at the end of surgery (End). A flexible fiberoptic bronchoscope (Olympus BF-B3^TM; Olympus Co., Tokyo, Japan) was introduced through the endotracheal tube. The tip of the bronchoscope was wedged randomly into a subsegment of the left or right middle lobe of the lungs, and 20 mL of sterile buffered saline solution (pH 7.4) was instilled through the bronchoscope. The lavage fluid was aspirated by gentle suction. This procedure was repeated five times with instillation of 20 mL of buffered saline solution each time. The lavage position was different between two points. After gauze filtration, the lavage fluid was centrifuged immediately, and the cell-free supernatant was stored at -80°C for subsequent analysis of interleukin (IL)-8 and elastase.

Blood for determination of white blood cell number and plasma IL-8 and elastase concentrations was sampled from the radial artery catheter 5 min before each bronchoalveolar lavage. Differential white blood cell analysis was performed by an automated counter on blood anticoagulated with EDTA. For determination of IL-8 and elastase concentrations, blood (also anticoagulated with EDTA) was centrifuged immediately, and plasma samples were stored at -80°C until analysis.

Tumor necrosis factor- (TNF-), IL-6, and IL-8 in bronchoalveolar lavage fluid; plasma; and culture supernatant were measured in duplicate by using a commercial ELISA assay kit^TM (TFB, Tokyo, Japan). The minimum detection levels of TNF-, IL-6, and IL-8 were 0.7, 1.0, and 1.0 pg/mL, respectively. The maximum intra- and interassay coefficients of variation were less than 5% and 8%, respectively.

Elastase in the plasma and lavage fluid was measured in duplicate by a commercial immunoenzymatic assay kit (Esterase EIA^TM; Sanwa Chemistry Co., Nagoya, Japan) that detects both free elastase and monometric complexes of elastase and ₁-antitrypsin. The minimum detection level was 5 pg/mL. The maximum intra- and interassay coefficients of variation were less than 5%. A single investigator who was blinded to pulmonary function measured cytokines and elastase.

We used parametric or rank-sums statistics, depending on the distribution of the data. The data of neutrophils, cytokines, and elastase between beginning and end time points were analyzed by Wilcoxon’s signed rank test. We analyzed these data between plasma and alveolar cells by using the Mann-Whitney U-test. Other time-dependent data and data between plasma and alveolar cells were analyzed by using two-tailed paired and unpaired t-test, respectively. Regression analysis was used to determine the correlation of measured variables to PaO₂/FIO₂ and Q_s/Q_t. Data were expressed as means ± SD; differences were considered significant when P < 0.05.

	Results

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Morphometric and demographic characteristics, preoperative cardiopulmonary function, duration of surgery, CPB, and aortic cross-clamping results are shown in the accompanying article (15), along with changes in cardiorespiratory variables. PaO₂/FIO₂ decreased and Q_s/Q_t increased significantly at the end of surgery. Total number of neutrophils and IL-6, IL-8, TNF-, and elastase concentrations in the bronchoalveolar lavage fluid also increased significantly at the end of surgery (Table 1).

View larger version (23K): [in this window] [in a new window]   Figure 1. The intraoperative (End–Beginning) increase in total polymorphonuclear neutrophil count in bronchoalveolar lavage fluid correlated with intraoperative (End–Beginning) concentration of interleukin-8 (IL-8) and neutrophil-derived elastase-1-anti-trypsin complex (elastase) in the bronchoalveolar lavage fluid of patients undergoing cardiopulmonary bypass.

View larger version (23K): [in this window] [in a new window]   Figure 2. PaO2/fraction of inspired oxygen (FIO2) at the end of cardiac surgery correlated with intraoperative (End–Beginning) polymorphonuclear neutrophil counts, concentration of interleukin-8 (IL-8), and neutrophil-derived elastase-1-antitrypsin complex (elastase) in the bronchoalveolar lavage fluid of patients undergoing cardiopulmonary bypass.

View larger version (22K): [in this window] [in a new window]   Figure 3. Qs/Qt at the end of cardiac surgery correlated with intraoperative (End–Beginning) polymorphonuclear neutrophil counts, concentration of interleukin-8 (IL-8), and neutrophil-derived elastase-1-antitrypsin complex (elastase) in the bronchoalveolar lavage fluid of patients undergoing cardiopulmonary bypass.

	Discussion

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Some studies, for example, conclude that atelectasis is a major cause of postbypass decrease in arterial oxygenation (1,2) and that manual hyperinflation of the lungs at the end of CPB can prevent the atelectasis (2,3). Although we included this precaution in our protocol, most of our patients experienced either mild or moderate decreases in arterial oxygenation. Our most notable finding is that the neutrophil influx and IL-8 and elastase concentrations from the lavage fluid correlated significantly with the changes in PaO₂/FIO₂ and Q_s/Q_t. This is consistent with previous reports indicating that increases in neutrophils and concentrations of IL-8, and elastase in the lavage fluid correlate with the degree of pulmonary inflammation in nonsurgical patients (16,17). These data suggest (but do not prove) that inflammation is an important factor modulating decrease in arterial oxygenation.

We observed significant increases in IL-6 and TNF- concentrations in the lavage fluid. The increase in concentrations of IL-6 and TNF- in lavage fluid, however, failed to correlate with changes in neutrophil influx, PaO₂/FIO₂, and Q_s/Q_t. The lack of correlation of lavage IL-6 levels to PaO₂/FIO₂ and Q_s/Q_t is consistent with the results of Hauser et al. (18). These results suggest that neutrophil-related pulmonary inflammation is an important contributing factor. IL-6 and TNF- can be produced by other pulmonary cells, such as alveolar macrophages (15) and pulmonary epithelial cells (19). In addition, neutrophils, IL-8, and elastase are closely related. Neutrophils that migrate to the distal airway become activated and release elastase that damages alveolar architecture (20,21). Elastase, in turn, stimulates release of IL-8 from neutrophils in the distal airways (20,21), which attracts additional neutrophils, completing a vicious cycle (20,21).

Although cytokine concentrations in the pulmonary epithelial lining fluid were considerably diluted by 100 mL of saline, concentrations in the lavage fluid were similar to those in plasma. Average IL-6 concentrations, corrected for the estimated volume of epithelial lining fluid, are up to 25 times greater than those in plasma (18). Despite considerable dilution, TNF- could be detected in lavage fluid, but was undetectable in the plasma. These results were comparable with our accompanying study, which shows that alveolar macrophages produced a greater amount of IL-6 and TNF- than plasma monocytes, both with and without lipopolysaccharide stimulation (15).

Increases in the plasma concentrations of elastase and IL-8 did not correlate with decreases in arterial oxygenation. One possible explanation is that IL-8 in the lungs is not related to IL-8 in the plasma. Sankary et al. (22) demonstrated that plasma IL-8 is not derived from pulmonary endothelial and epithelial membranes in patients suffering from ARDS. Also, it is possible that plasma IL-8 has a different pharmacologic action from pulmonary IL-8. For example, plasma IL-8 inhibits adhesion of neutrophils (23), whereas IL-8 secreted by pulmonary fibroblasts and epithelial cells facilitates adhesion of neutrophils in lung vessels. The poor correlation between plasma elastase concentration and pulmonary function is comparable with a previous study by Suter et al. (24), who reported that plasma levels of elastase do not correlate with severity of ARDS.

The plasma concentrations of IL-6 and IL-8 increase during CPB and peak several hours after surgery concludes (25). Given the limited duration of our study, we thus cannot definitively conclude that plasma IL-6 and IL-8 do not correlate with arterial oxygenation. We performed the second bronchoalveolar lavage at the end of surgery because postoperative management could not be standardized. For example, there were numerous postoperative factors likely to influence immunologic functions, including transfusion of blood and blood products (none were transfused before the second lavage), administration of other ß-agonists, analgesics, steroids, antiproteases, and varying concentrations of inhaled oxygen (13,14).

Free elastase is rapidly neutralized by ₁-antitrypsin, which is plentiful in the lavage fluid. We therefore measured total elastase in the form of elastase-₁-antitrypsin because this complex reflects the total amount of elastase released from the neutrophils into the lavage fluid. A similar strategy has been used in studies of pulmonary immune responses during pneumonia (16) and ARDS (24).

In summary, various inflammatory mediators in bronchoalveolar lavage fluid and plasma increased significantly during CPB. The increase in the lavage fluid neutrophil number correlated significantly with the increases in IL-8 and elastase concentrations. Furthermore, increases in the number of neutrophils and IL-8 and elastase concentrations in bronchoalveolar lavage fluid correlated significantly with changes in PaO₂/FIO₂ and Q_s/Q_t. In contrast, there was no correlation between immune variables in the plasma and the respiratory variables. Marked increases in pulmonary immunologic mediators and significant correlation between these immune mediators and decrease in arterial oxygenation suggest that CPB provokes far greater pulmonary than systemic inflammatory responses, and that inflammatory responses in the distal airway are related to decreases in arterial oxygenation.

	Acknowledgments

 
This study was supported by Grant-in-aid for Scientific Research No. 08457399 (Department of Education, Japan), NIH Grant GM58273 (Bethesda, MD), the Joseph Drown Foundation (Los Angeles, CA), and the Fonds zur Förderung der wissenschaftlichen Forschung (Vienna, Austria).

	References

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