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J Thorac Cardiovasc Surg 2006;132:513-518
© 2006 The American Association for Thoracic Surgery

General Thoracic Surgery

Oxidative stress during 1-lung ventilation

Ya-Jung Cheng, MD, PhDa, Kuang-Cheng Chan, MDa, Chiang-Ting Chien, PhDb, Wei-Zen Sun, MDa, Chen-Jung Lin, MDa,*

a Department of Anesthesiology, National Taiwan University Hospital, National Taiwan University, Taipei, Taiwan
b Office for Medical Research Administration, National Taiwan University Hospital, National Taiwan University, Taipei, Taiwan.

Received for publication November 3, 2005; revisions received February 7, 2006; accepted for publication March 21, 2006.

* Address for reprints: Chen-Jung Lin, MD, Department of Anesthesiology, National Taiwan University Hospital, National Taiwan University, No 7, Chung-Shan South Rd, Taipei, Taiwan 10016, Taiwan (Email: lincj{at}anesth.mc.ntu.edu.tw).


   Abstract
Top
 Abstract
Introduction
 Patients and Methods
 Results
 Discussion
 References
 
OBJECTIVES: Resuming 2-lung ventilation from 1-lung ventilation might induce a re-expansion and reoxygenation effect. The oxidative stress during 1-lung ventilation/2-lung ventilation has not been studied, although severe complications, such as re-expansion pulmonary edema, were reported. Reactive oxygen species production and total antioxidant status assay levels were measured in this study during 1-lung ventilation/2-lung ventilation. The effects on extravascular lung water, cardiac output, and intrathoracic blood volume were also studied by using the Pulsion PiCCO system.

METHODS: Twenty patients undergoing 1-lung ventilation/2-lung ventilation (>60 minutes) for video-assisted thoracoscopic surgery with minimal lung injuries were included in this study. Reactive oxygen species production was measured by means of lucigenin (detecting superoxide mainly) and luminol (detecting H2O2 and HOCl mainly) chemiluminescence. Reactive oxygen species production, total antioxidant status assay (by using the Randox TAS kit), extravascular lung water, cardiac output, and intrathoracic blood volume values were measured before 1-lung ventilation (T1), before resuming 2-lung ventilation (T2), 5 minutes after 2-lung ventilation (T3), and 30 minutes after 2-lung ventilation (T4).

RESULTS: One-lung ventilation time was 118 ± 33 minutes. Lucigenin chemiluminescence (but not luminol chemiluminescence) increased significantly at T3 and T4. Total antioxidant status decreased nonsignificantly. Extravascular lung water, intrathoracic blood volume, and permeability index values changed nonsignificantly after 2-lung ventilation. Cardiac output increased significantly at T4, and there is a negative correlation between cardiac output and extravascular lung water (r = –0.431, P < .005).

CONCLUSIONS: Resuming 2-lung ventilation induces a massive superoxide production. Comparable extravascular lung water and intrathoracic blood volume and a nonsignificant decrease of total antioxidant status indicate adequate antioxidant capacity to counteract it. Severe oxidative injuries after 1-lung ventilation/2-lung ventilation should be considered in patients without adequate antioxidative capacity, such as those with cancer and trauma.

Abbreviations and Acronyms CL = chemiluminescence; CO = cardiac output; CVP = central venous pressure; EVLW = extravascular lung water; FIO 2 = fraction of inspired oxygen; GEDV = global end-diastolic volume; ITBV = intrathoracic blood volume; MDA = malondialdehyde; OLV = 1-lung ventilation; ROS = reactive oxygen species; TAS = total antioxidant status; 2LV = 2-lung ventilation; VATS = video-assisted thoracoscopic surgery


   Introduction
Top
 Abstract
 Introduction
Patients and Methods
 Results
 Discussion
 References
 
One-lung ventilation (OLV) for thoracotomy or thoracoscopy is frequently applied for a clear operational field in thoracic surgery. During OLV, the nonventilated lung not only remains atelectatic but also hypoperfused because of hypoxic vasoconstriction. When resuming 2-lung ventilation (2LV), re-expansion, along with oxygen re-entry through the airways, causes reactive pulmonary vascular dilatation, commencing reperfusion of the lung, and thus excessive oxidative radicals might be released. Few experiments about oxidative stress caused by OLV-2LV manipulation were done because most patients tolerate OLV-2LV well, although some cases of re-expansion pulmonary edema were reported.1Go Re-expansion pulmonary edema was reported more after treatment of pneumothorax,2,3Go but the mechanisms and preventive methods need to be substantiated by stronger scientific evidence.4Go A previous study on lobectomy in patients with lung cancer showed that lung re-expansion from OLV provoked more severe oxidative injuries than surgical intervention by measuring malondialdehyde (MDA), a product of lipid peroxidation, but resection of lung cancer can also decrease MDA levels.5Go However, higher serial MDA levels were shown in patients with lung cancer, and the injuries on lung parenchyma cannot be excluded in lobectomy.

The oxidative injuries are started from an excessive free radical production that cannot be counteracted by the action of endogenous antioxidant defense. Our preliminary data showed an abrupt increase of reactive oxygen species (ROS) production after resuming 2LV from OLV. On the other hand, antioxidants were reported to be decreased in pulmonary edema fluids in acute lung injury.6Go To investigate the effects on oxidant-antioxidant balance of OLV-2LV, total antioxidant status (TAS) assay levels were measured, as was ROS production. Free radicals have been reported involved in pulmonary reperfusion injuries, including superoxide7Go and H2O2,8Go and thus lucigenin9Go and luminol10Go chemiluminescence (CL) were used in this study to obtain a more specific detection of superoxide, HOCl, and H2O2.

The hallmark of oxidative lung injury is endothelial cell damage, which is reflected in increased pulmonary vascular permeability. In an animal study re-expansion of the atelectatic lung causes a significant increase in permeability and pulmonary hypertension,11Go with subsequent edema formation and hypoxemia.12Go Reperfusion-induced vascular leakage was reported to peak at 30 minutes in rat blood-perfused lungs,13Go and superoxide dismutase was shown to prevent it completely.14Go Concerning a previous clinical study, albumin permeability was frequently applied through lavage, but it is difficult to evaluate the extent of pulmonary vascular leakage, especially in patchy edema. In this study the PiCCO system (Pulsion Medical Systems, Munich, Germany) was applied to measure extravascular lung water (EVLW), cardiac output (CO), and intrathoracic blood volume (ITBV) levels by means of the transpulmonary indicator dilution technique because it has been proved effective in preload, EVLW measurement,15Go and pulmonary permeability index deterination,16Go including in patients undergoing lung transplantation.17Go

The goals of this study were (1) to measure ROS production, as well as TAS levels, during OLV-2LV with minimal pulmonary injury in video-assisted thoracoscopic surgery (VATS) and (2) to explore the effects of OLV-2LV on EVLW, CO, and ITBV by using the Pulsion PiCCO system.


   Patients and Methods
Top
 Abstract
 Introduction
 Patients and Methods
Results
 Discussion
 References
 
With ethics committee approval and written informed consent, 20 adult patients (American Society of Anesthesiologists [ASA] physical status class I-II, 25-60 years old) scheduled for VATS that involved a long period of intraoperative OLV (>60 minutes) with minimal lung trauma were studied. Patients with recent vitamin ingestion were excluded. Anesthesia was induced with thiopental (3-5 mg/kg), fentanyl (3 ug/kg), and pancuronium (0.1 mg/kg). After induction of anesthesia, an appropriate size of left bronchial catheter (Broncho-Cath, Mallinckrodt) was intubated and adjusted by using a fiberoptic bronchoscope before and after turning to the lateral decubitus position. Incremental doses of pancuronium were added for muscle relaxation. Isoflurane (1%-2%) was used to maintain the anesthesia. Intermittent positive ventilation was performed with a volumetric ventilator (Fabius GS, Dräger). A 4F fiberoptic thermistor (Pulsiocath, Pulsion Medical Systems) was advanced into the descending aorta through a femoral artery and connected to the integrated fiberoptic monitoring system. A central venous line was inserted through the right internal jugular vein, and another arterial line was inserted through the right radial artery for monitoring and blood gas analysis. Systolic arterial blood pressure, diastolic arterial blood pressure through the arterial line, heart rate, central venous pressure (CVP), electrocardiography, pulse oximetry, body temperature, urine output, and peak airway pressure were monitored continuously. Intravenous crystalloid and fentanyl were titrated to maintain the systolic blood pressure within 15% of preinduction values. Ventilation was delivered mechanically. When OLV was started, the nondependent lung was collapsed and opened to air with suction if necessary, and the dependent lung was ventilated at a fraction of inspired oxygen (FIO 2) of 1, a tidal volume of 8 to 10 mL/kg, a respiratory rate of 12 to 16 breaths/min adjusted to maintain the arterial carbon dioxide between 35 and 45 mm Hg, and an inspiration:expiration ratio of 1:2. The concentrations of inspiratory and expiratory gas mixture (FIO 2, end-tidal CO2, fraction of inspired isoflurane, and end-tidal isoflurane) were continuously monitored (Capnomac Datex). Direct observation of the collapsed lung was monitored in the operative hemithorax.

PiCCO Monitoring
The CO and volumetric variables were obtained through the transpulmonary indicator dilution technique. The mean of 3 subsequent CO measurements were obtained. Fifteen milliliters of cold saline (<8°C) was injected through the distal port of the CVP. CO was calculated by using the thermodilution curve through the embedded thermistor in a femoral arterial catheter. ITBV and EVLW were calculated by using the mean transit time methods, as described previously.18Go

Experimental Protocol
Arterial blood gases were monitored 10 and 30 minutes after OLV to avoid hypoxemia during the operation. Six-milliliter blood samples were drawn from the arterial line after stabilization in the decubitus position after induction and before starting OLV as a baseline (T1), after surgical incision and at the end of OLV immediately before resuming 2LV (T2), and 5 minutes (T3) and 30 minutes (T4) after resuming 2LV for measurement of ROS production and TAS assay. One-milliliter blood samples were immediately wrapped in aluminum foil and kept on ice until CL measurement for ROS production determination within 2 hours.19Go Five-milliliter blood samples were placed into tubes containing ethylenediamine tetraacetic acid. Sera were separated (at 2000 rpm for 10 minutes) immediately after sampling and were stored at –80°C until determination of TAS was done within 4 weeks.

CL measurement for ROS production
Immediately before CL measurement, 0.1 mL of phosphate-buffered saline buffer (pH 7.4) was added to a 0.2-mL blood sample. The CL was measured in a completely dark chamber of the CL analyzing system. After 100-second background level determination, 1.0 mL of 0.1 mmol/L lucigenin or 1.0 mL of 0.1 mmol/L luminol in phosphate-buffered saline (pH 7.4) was injected into the sample. The CL was continuously monitored for an additional 600 seconds; integrating the area under the curve and subtracting it from the background level was used to calculate the total amount of CL. The assay was performed in duplicate for each sample and was expressed as CL counts per 10 seconds for whole-blood CL.

TAS assay
The total antioxidant status in 20 µL of plasma or distilled water (as a blank) was measured with a TAS kit (catalog no. NX2332, Randox), according to the manufacturer's instructions.20Go

Measurement of CO, EVLW, ITBV, and global end-diastolic volume
At T1, T2, T3, and T4, a thermodilution curve was recorded in the aorta with the thermistor-tipped fiberoptic catheter. CO was continuously shown after calibration. EVLW and ITBV were determined by using the thermal dilution curve from 3 successive measurements.21Go The permeability index was calculated as follows: EVLW/(ITBV – GEDV), where GEDV is the global end-diastolic volume.

Statistical Analysis
Values are expressed as means ± standard deviation. Means ± standard error are shown in figures. Significant differences between groups were analyzed with the 1-way analysis of variance test. Pearson product moment correlation was used to clarify the relation between lucigenin CL and EVLW, GEDV and ITBV, and CO and EVLW.


   Results
Top
 Abstract
 Introduction
 Patients and Methods
 Results
Discussion
 References
 
Changes in Hemodynamics, Oxygenation, CO, EVLW, ITBV, and GEDV
The characteristics of the patients undergoing VATS were as follows: 12 patients for a thymus tumor (5 with myasthenia gravis) and the other 8 patients for esophagectomy (5 with esophageal reconstruction), age of 40 ± 15 years, 13 male and 7 female patients, and OLV time of 118 ± 33 minutes. As shown in Table 1, hemodynamic data during OLV and 2LV, including systolic arterial blood pressure, diastolic arterial blood pressure, heart rate, and CVP, did not change significantly during the study. The PO 2 values decreased significantly after OLV and were comparable (nonsignificantly lower) to baseline values after 2LV. Positive end-expiratory pressure was not added in our patients because of satisfactory oxygenation during OLV. GEDV and ITBV changed nonsignificantly, and EVLW increased nonsignificantly. CO increased nonsignificantly at 5 minutes after 2LV but increased significantly at 30 minutes after 2LV. The permeability index was statistically nonsignificant.


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  		TABLE 1. Changes of hemodynamic data, extravascular lung water, intrathoracic blood volume, global end-diastolic volume, and cardiac output during 1-lung ventilation/2-lung ventilation
 
ROS Production by Means of Luminol and Lucigenin CL and TAS Assay During OLV and 2LV
The baseline of ROS production was as follows: lucigenin CL, 11,678 ± 5897 (counts/per 600 seconds); luminol CL, 43,905 ± 28,149 (counts/per 600 seconds). As shown in Figure 1, lucigenin CL increased significantly at 5 and 30 minutes after resuming 2LV (P < .001). Lucigenin CL increased to 5 times at T3 and 11 times at T4 compared with the data from T1. Luminol CL increased nonsignificantly about 2 times at T3 and 1.5 times at T4 compared with the data from T1. TAS increased at T2 and decreased at T3 and T4 nonsignificantly.


Figure 1
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  		Figure 1. ROS production and TAS levels during OLV and 2LV. ROS, reactive oxygen species; TAS, total antioxidant status; OLV, 1-lung ventilation; 2LV, 2-lung ventilation.

 
Relationships Between Lucigenin CL and EVLW, GEDV and ITBV, and CO and EVLW
There is no significant relationship between ROS production by lucigenin CL and EVLW. As shown in Figure 2, there is a positive correlation between GEDV and ITBV (r = 0.997, P < .05). There is a negative correlation between CO and EVLW (r = –0.431, r2 = 0.168, P < .005, power of performed test: {alpha} = .05: 0.93). EVLW tends to decrease while CO increases.


Figure 2
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  		Figure 2. Relationships between EVLW and CO, GEDV and ITBV. EVLW, extravascular lung water; CO, cardiac output; GEDV, global end-diastolic volume; ITBV, intrathoracic blood volume.

 

   Discussion
Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Discussion
References
 
Our results revealed that OLV-2LV manipulation induces a massive ROS production, even with minimal pulmonary injury. This is the first report about ROS production but not oxidative metabolites during OLV-2LV. Detection of ROS in vivo is technically more difficult because of their rapid reactivity and short lifespan. However, it might be more important to measure ROS production than lipid hydroperoxides because some critically ill patients were reported to have decreased total antioxidant capacity with normal lipid peroxidation. It was shown in our study that superoxide production was more pronounced than HOCl and H2O2 production. It is also reported that superoxide induces reperfusion oxidative injuries in a previous animal study.14Go

TAS levels were slightly decreased but still well maintained after resuming 2LV, with a nonsignificant decrease of PO 2/FIO 2. The baseline TAS level in this study was also comparable with that of healthy patients.22Go Our data confirmed that OLV-2LV manipulation in VATS, as well as in lobectomy, can induce a massive superoxide production, but the well-maintained TAS data also elucidate why most patients tolerate OLV-2LV without complications. However, the magnitude of ROS production should not be ignored because when antioxidant capacity is compromised, a massive ROS production leads to severe oxidative injuries on DNAs, proteins, and lipids. Most previous case reports of severe re-expansion pulmonary edema were cases of pneumothorax. Re-expansion of collapsed lung for pneumothorax might induce more oxidative injuries because of a longer collapse time, a lower TAS level in emergency operations, and a stronger hypoxic vasoconstriction in collapsed lung than that during anesthesia. The effects on EVLW during OLV-2LV in this study were also milder than those in lung transplantation23Go because the transplanted lung is nonventilated and nonperfused, but in patients undergoing VATS, atelectatic lungs were still hypoperfused.

Lucigenin CL, luminol CL, and TAS data were comparable between T1 and T2. They reveal that with adequate anesthesia, surgical stimulation and mechanical ventilation would not induce a significant ROS production or decrease the antioxidant capacity.

The mechanisms of re-expansion pulmonary edema include the hydrostatic mechanisms and permeability mechanisms. A significant increase of CO on T4 was shown in our study and might have resulted from reactive vasodilatation of resuming 2LV. Although EVLW in a lung undergoing re-expansion could be underestimated in this experiment because PiCCO cannot measure the water content in each lung, the negative correlation of EVLW and CO shown in our results did not agree with the hydrostatic mechanisms. CO was also increased in our study, but the data of EVLW stands in contrast to that in Tan's report in pneumothorax.24Go However, there were very few patients studied concerning the pathogenesis of re-expansion pulmonary edema.25,26Go Despite previous research of alveolar barrier properties, the mechanisms that promote the alveolar entry of large quantities of liquid remain inadequately understood, especially on the alveolo-capillary barrier.27Go

As in a previous report, GEDV and ITBV correlated well with each other in this study. ITBV was shown to be more sensitive and responsive to fluid loading than pulmonary capillary wedge pressure.28Go In the pre-edematous condition fluid management remains an important but difficult issue. In clinical practice concerning impending pulmonary edema, the PiCCO Pulsion system provides a closer and beneficial monitor on balancing the preload and EVLW compared with the conventional chest radiographic examination.

We concluded that adequate antioxidant capacity to capture the significant ROS production might explain why re-expansion pulmonary edema remains rare in OLV-2LV. However, a massive superoxide production after resuming 2LV might result in a catastrophic pulmonary reperfusion in the cases of inadequate antioxidant capacity, such as severe trauma, sepsis, and emergency operations.


   Footnotes
 
Supported by National science council NSC92-2314-B-002-259.


   References
Top
 Abstract
 Introduction
 Patients and Methods
 Results
 Discussion
 References
 

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