EJCTS Click here to locate an Ethicon representative
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to Personal Folders
Right arrow Download to citation manager
Right arrow Permission Requests
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Misthos, P.
Right arrow Articles by Skottis, I.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Misthos, P.
Right arrow Articles by Skottis, I.
Related Collections
Right arrow Lung - basic science

Eur J Cardiothorac Surg 2005;27:379-383
© 2005 Elsevier Science NL

Postresectional pulmonary oxidative stress in lung cancer patients. The role of one-lung ventilation

P. Misthosb,*, S. Katsaragakisa, N. Milingosa, S. Kakarisb, E. Sepsasa, K. Athanassiadib, D. Theodoroua, I. Skottisb

a University of Athens Medical School, First Propaedeutic Surgical Department, Athens, Greece
b First Thoracic Surgical Department, ‘SOTIRIA’ General Hospital for Chest Diseases, 7 P. Dimitrakopoulou Street, 11141 Athens, Greece

Received 5 September 2004; received in revised form 13 December 2004; accepted 17 December 2004.

* Corresponding author. Tel./fax: +30 210 252 9048. (E-mail: pamnisthos{at}yahoo.gr).


   Abstract
Top
 Abstract
1. Introduction
 2. Material and methods
 3. Results
 4. Comment
 Appendix A. Conference...
 References
 
Objective: The authors conducted a prospective analysis in order to investigate through lipid peroxidation metabolites the generation of oxygen free radicals after one-lung ventilation (OLV). Methods: From 2001 to 2003, 212 patients were prospectively studied for lung reexpansion/reperfusion injury. They were classified in six groups. Group A, non-OLV lobectomy group; B, OLV pneumonectomy group; C–E, OLV lobectomy of 60, 90, and 120min duration, respectively; F, normal subjects as baseline group. Preoperative, intraoperative and postoperative strict blood sampling protocol was followed. Malondialdehyde (MDA) plasma levels were measured. The recorded values were analyzed and statistically compared between groups and within each one. Results: Comparison of groups C–E (OLV) to all other documented significant (P<0.001) increase of MDA levels during lung reexpansion and for the following 12h. The magnitude of oxidative stress was related to OLV duration (group E>D>C, all P<0.001). The removal of cancer-associated parenchyma led to MDA level decrease postoperatively (P<0.001) especially after pneumonectomy (A vs. B, P<0.001). Conclusions: (1) Lung reexpansion provoked severe oxidative stress. (2) The degree of the amount of generated oxygen free radicals was associated to the duration of OLV. (3) Patients with lung cancer had a higher production of oxygen free radicals than normal population. (4)Tumor resection removes a large oxidative burden from the organism. (5) Mechanical ventilation and surgical trauma are weak free radical generators. (6) Manipulated lung tissue is also a source of oxygen free radicals, not only intraoperatively but also for several hours later.

Key Words: Oxidative stress • Lung reexpansion • Lung reperfusion


   1. Introduction
Top
 Abstract
 1. Introduction
2. Material and methods
 3. Results
 4. Comment
 Appendix A. Conference...
 References
 
Oxygen deprivation from ischemia or nonventilation leads to cellular hypoxic injury. Paradoxically, reperfusion of hypoxic tissues may result in further cellular damage. There is now abundant evidence that reperfusion injury is the structural damage caused by the interaction of free radicals, endothelial factors and neutrophils [1]. Lung is a critical organ in oxidative stress process of either systematic or pulmonary origin [2,3]. Pulmonary parenchyma is one of the largest reservoirs for neutrofils, monocytes and macrophages. Moreover atelectasis leads to hypoxic vasoconstriction. Reexpansion along with oxygen reentrance through the airways causes reactive pulmonary vascular dilatation commencing reperfusion of the lung. Ischemia-reperfusion sequence develops oxygen-free radicals. These are highly reactive species due to the unpaired electrons they contain to their outer orbits. They interact with cellular structural molecules provoking dysfunction mostly to endothelial cells. Lipid peroxidation is one of the most important metabolic consequences of oxidative stress. Under normal circumstances these events are counteracted by the action of endogenous antioxidant defense mechanisms [4]. This balance is disturbed during reperfusion. A tremendous cascade of events develops extremely reactive molecules that outnumber the reserves of antioxidant systems.

During one lung ventilation the operated lung remains completely atelectatic for a period of time. It is well known that non-ventilated lung is also hypoperfused due to hypoxic vasoconstriction [5]. Besides, the postresectional remaining pulmonary tissue has been subjected to considerable manipulation during the conducted lobectomy or segmentectomy. When bronchial block is ended the following immediate lung reexpansion along with tissue reperfusion might generate oxygen free radicals through a fairly well described mechanism [6–9]. Although lung is a resistant tissue to hypoxia because of its dual blood flow and the use of oxygen reserves in alveolar spaces reexpansion injury detected after pneumothorax management and reperfusion injury after lung transplantation are two examples for possible oxidative damage [10,11].

The authors conducted a prospective analysis in order to investigate the generation of oxygen free radicals through lipid peroxidation metabolites after one-lung ventilation (OLV) pulmonary resections.


   2. Material and methods
Top
 Abstract
 1. Introduction
 2. Material and methods
3. Results
 4. Comment
 Appendix A. Conference...
 References
 
From July 2001 to July 2003, 182 patients with NSCLC were prospectively studied for reexpansion/reperfusion lung injury. The study group included 126 men (69.2%) and 56 women (30.8%). Their age ranged from 44 to 78 years (mean 61.2 years). The side of the lesions was to the right in 114 cases (62.6%) and 68 (37.4%) to the left. All of them were ex-smokers with mild COPD, suffering from non-small cell lung cancer (NSCLC) without any prior exposure to chemotherapy or radiotherapy. The patients were grouped according to one lung ventilation use or not, to the duration of lung's atelectasis and to the kind of the resection. Moreover, 30 additional patients with minor blunt chest trauma were studied as baseline group. Specifically six groups (A–F) were designed weighted for their demographic characteristics (Table 1).


View this table:
[in this window]
[in a new window]
  		Table 1. Demographic data
 
Group A included patients with confirmed non-small cell lung cancer (NSCLC) who were subjected to lobectomy without one lung ventilation (single lumen endotracheal tube for intraoperative ventilation).

Group B included patients with documented NSCLC who were subjected to pneumonectomy with one lung ventilation. The aim of this group was to record malondialdehyde (MDA) plasma levels in cases of OLV but with the affected lung removed from the body so as to estimate the systematic effect of oxygen free radicals generated by other systems to serum MDA levels.

The next three groups were the actual study groups and included patients who were subjected to OLV lobectomy. These patients were grouped according to the duration of OLV. Group C included patients subjected to 60min OLV. Group D included patients subjected to 90min OLV. Group E included patients subjected to 120min OLV.

Chemotherapy, radiation, mechanical ventilation and infection are widely considered as free oxygen radicals generators [12–14]. Twelve patients that needed mechanical ventilation or were septic within the first 48h postoperatively were excluded from the study.

Finally patients, who were treated for minor chest trauma as outpatients participated in this study as baseline group after their rehabilitation (group F). All were ex-smokers, without COPD.

Serum MDA was measured. Plasma MDA levels were recorded in every patient following a fixed blood sampling protocol. Peripheral venous blood was aspirated to a amount of 5cm3 each time. The timing of blood sampling was the following: (a) 1 sample 24h preoperatively, (b) 1 sample 30min after the onset of operation for the control groups or 30min after the OLV onset for the study groups, and (c) 1 sample 5min after lung reoxygenation (groups C–E), after pneumonectomy completed (group B) and, after non-OLV lobectomy performed (group A), (d) 1 sample at 1, 6, 12, 24 and, 48h postoperatively for all patients.

Plasma MDA levels as an index of lipid peroxidation due to oxygen free radicals, were measured using high-performance liquid chromatography. A sensitive and easily reproduced method was used that was developed by Fukunaga and colleagues [15].

Statistical analysis was performed using Student's t-test (otherwise the Wilcoxon rank-sum test) and {chi}2 (Fisher's Exact test when needed) test where appropriate.


   3. Results
Top
 Abstract
 1. Introduction
 2. Material and methods
 3. Results
4. Comment
 Appendix A. Conference...
 References
 
The results from all samplings and the number of patients included in each group are fully described in Table 2. Patients without any malignancy (group F) presented with serum MDA of 1.28±3.7nmol/ml. On the other hand patients with lung cancer presented with serum MDA that ranged from 5.89±3.6 to 5.9±3.4nmol/ml. Statistical analysis revealed that the difference between F1 and A1–G1 was significant (P<0.001) while the comparison between the values of A1–E1 was not.


View this table:
[in this window]
[in a new window]
  		Table 2. Comparative results of MDA plasma levels (nmol/ml)a
 
Group A and B cases showed a pronounced elevation during thoracotomy and lung resection. Their peak of increase was detected intraoperatively (from 5.89±4.7 and 5.89±4.2 to 6.43±3.4 and 6.42±1.4nmol/ml, respectively). For both groups this increase was statistically significant (P<0.001). Group A showed a gradual return to lower levels (A3–A8). On the contrary in group B the decline of MDA levels was very steep after entire lung's removal (from 5.89±4.2nmol/ml preoperatively to 6.44±3.8nmol/ml (P<0.001) at the beginning of operation to 4.86±4.4nmol/ml (P<0.001) at the first postoperative hour). Statistical analysis disclosed that intraoperative values became significantly lower at 12h for group A (P<0.001) and at 1h for group B (P<0.001).

When OLV was used the oxidative stress proved to be the most severe. Groups C–E disclosed the same tendency. At the beginning of the operation all three groups showed a mild elevation of MDA levels like the first two groups. Comparison between A2–E2 did not revealed significant differences. But 5min after the end of OLV a notable increase of MDA levels was measured which overdoubled the figures. In group C raised from 6.44±3.6nmol/ml during OLV to 14.48±5.8nmol/ml (P<0.001) after reventilation. In groups D and E from 6.44±3.2 and 6.35±0.4nmol/ml raised to 15.71±4.0 (P<0.001) and 18.31±3.9nmol/ml (P<0.001), respectively, in minutes after the end of OLV. This increase was significantly more intense than the respective one in groups A and B (A3 and B3 vs. C3–E3, all P<0.001). Characteristically the raise of MDA serum levels was relevant to the duration of lung atelectasis. E3 was significantly higher than D3 (P<0.001) and D3 than C3 (P<0.001). The more prolonged OLV the more strengthful oxidative stress was developed. These high values were noted up to 1h postoperatively. After that a gradual decrease was detected (Table 2) to lower than preoperative levels (C1 vs. C8, D1 vs. D8 and E1 vs. E8 were all statistically significant, P<0.001).

In all groups, the oxidative stress gradually subsided after the first 6 postoperative hours. This was more pronounced after pneumonectomy (B4 vs C4–E4, P<0.001, respectively).

Besides, the malignancy itself produced increased lipid peroxidation compared to group F. Tumor removal led in a short time (48h) to decreased levels of MDA in comparison to preoperative measurements (A1–E1 vs. A8-E8, P<0.001). This was independent to the use or not of OLV (Table 2).


   4. Comment
Top
 Abstract
 1. Introduction
 2. Material and methods
 3. Results
 4. Comment
Appendix A. Conference...
 References
 
Free radicals are constantly produced by normal aerobic metabolism. Oxidative stress is the result of an imbalance between radical-generating and radical-scavenging systems. Previous reports have focused on the effects of oxygen free radicals on lung parenchyma [16–24]. The authors used serum MDA measurement in order to evaluate the systematic effect of OLV. Comparing baseline serum MDA values (group F) with patients suffering from cancer (groups A–E), a significant increase in lipid peroxidation level was observed. This is in accordance with previous series supporting that the presence of tumor is accompanied with systematic and local inflammatory reaction. Moreover there are convincing data that cancerous tissue is a source of oxygen-free radicals and lipid peroxidation products [25]. Studying the results in group A, the authors noted a slight increase of MDA levels at the beginning of the operation. This represents the effect on free radicals generation of surgical stress/trauma and mechanical ventilation. Surgical trauma is associated with the release of inflammatory cytokines and consequently neutrophil chemoattraction, which are the source of large amounts of oxidants. During the operation the scavenging systems are unable to confront the oxidant outburst of the trauma itself, and oxidative stress is developed. Apart from surgical stress and mechanical ventilation, lung parenchyma manipulation strongly contributes to free radicals generation since no reperfusion/reexpansion took place. Moreover manipulated lung tissue continued to be a source of oxygen free radicals for a long period (almost for 12h) as it is suggested by the gradual return of MDA levels towards the preoperative levels and even lower finally in group A, probably because of lung cancer removal which is a free radical generator. Comparison between groups A and B disclosed that the removal of the operated lung in the latter group (pneumonectomy cases) led to rapid decrease of MDA levels almost immediately after the end of the operation, allowing us to conclude that total lung removal along with the malignancy left behind a smaller oxidative burden to be managed by the organism.

Severe oxidative stress is developed when one-lung ventilation is used, which is supported biochemically and pathophysiologically by the reexpansion/reperfusion syndrome. Comparative study of all groups reveals that after subtracting all the free radicals generating factors mentioned above, OLV produces severe oxidative burden to the organism a few minutes after reventilation of the atelectatic lung. The degree of the amount of generated oxygen free radicals was associated to the duration of OLV. The longer the atelectasis the more powerful the subsequent oxidative stress. A common pathway was observed in groups C–E: a steep rise of MDA serum levels immediately after reventilation which gradually returned to near preoperative levels in almost 12-h period. The significantly higher levels of MDA between group A and groups C–E at 6h postoperatively suggests that the reventilated remaining lobe has been suffered a much more severe oxidative stress than the manipulated non-atelectatic remaining lobe in group A. Furthermore the gradual decrease of MDA levels postoperatively suggests a common internal antioxidative mechanism of oxygen free radicals clearance and a constant counteraction by the endogenous antioxidant systems (glutathione, superoxide dismutase, etc).

Pneumonectomy group B represents a model of OLV without subsequent reperfusion/reoxygenation, in which the affected lung is removed. The lowest long-term postoperative MDA levels (B8) were observed. It is suggested that although OLV ischemia and surgical stress were responsible for a certain amount of oxidative stress, the lack of reexpansion/reperfusion effect led to the lowest MDA levels postoperatively. Consequently, lung reexpansion could be considered as the main contributor of free radicals generation, since it was the only factor altered in the comparison between groups A–E. Besides, the removal of the non-ventilated lung led to the greatest and fastest decrease of MDA levels postoperatively compared to groups A, C–E. This should not be attributed to the reversal of surgical stress or to tumor removal, but rather to the resection of the manipulated lung tissue. In that context is difficult to attribute postpneumonectomy pulmonary edema to the action of the generated oxygen free radicals.

Although oxidative stress after OLV was documented, the clinical implications remain still obscure. This intensifies the need for more studies in order to define the possible deleterious effects of oxidative stress to postoperative function of the lung and other organs. Also, different groups of patients should be studied such as with COPD, ischemic heart disease, in sepsis or long-term mechanically ventilated. In this future context we might have much more informations concerning the use of exogenous antioxidant factors in several situations such as lung transplantation, ARDS, radiation pneumonitis and even during lung resections.

From the comparative study of groups A–F one can conclude that: (1) Patients with NSCLC have a higher production level of oxygen free radicals than normal population. (2) Mechanical ventilation and surgical trauma are weak free radical generators. (3) Manipulated lung tissue is also a source of oxygen free radicals, not only intraoperatively but also for several hours later. (4) Tumor resection removes a large oxidative burden from the organism (5) Lung reexpansion provoked severe oxidative stress. (6) The degree of the amount of generated oxygen free radicals was associated to the duration of OLV.


   Appendix A. Conference discussion
Top
 Abstract
 1. Introduction
 2. Material and methods
 3. Results
 4. Comment
 Appendix A. Conference...
References
 
Dr S. Elia (Rome, Italy): I have one question and one suggestion. Were your patients in one-lung ventilation all intubated by double-lumen or did you use endobronchial blockers? It would be interesting to see if you have the same results with endobronchial blockers, which is a more physiological type of ventilation.

Dr Misthos: We have used only double-lumen endotracheal tubes. Since the main mechanism for one lung ventilation is common, one should not wait for different results.

Dr D. Van Raemdonck (Leuven, Belgium): I think it's a very interesting study, and I think it has a very important message—that we should avoid one-lung ventilation as often as possible. You stated that the lung was ischemic, but there is still bronchial circulation, so how can you say that the lung is ischemic?

Dr Misthos: Well, you mean reperfusion during one-lung ventilation. Actually, this is a relative matter. During lung preservation, as a graft, we can have a better model for that event. But at the clinical setting, I think we can assume that it is a reasonable factor. We know that atelectasis leads to pulmonary vasoconstriction. So there is a relative hypoxia. But I think that the main mechanism is alvelar hypoxic conditions followed by reoxygenation after reexpansion.

Dr S. Mattioli (Bologna, Italy): If I understood, you suggest that there are two sources of free radicals: the tumor itself and the excluded lung. In light of your results, would you suggest to inflate the excluded lung for short periods during the operation in order to reduce the pulmonary oxidative stress?

Dr Misthos: That reminds me of preconditioning of the lung tissue. Well, we have to study and measure our results to propose something like that. We wanted to see for the first time in a clinical setting whether oxidative stress happens or not after lung resection. Repeted atelectasis-reexpansion would increase the generated oxidation stress.

Dr P. van Schil (Edegem, Belgium): I think our anesthesiologists will be very pleased with your conclusions. They completely agree. Sometimes they put a low flow of oxygen on the collapsed lung by way of a catheter through the double lumen tube. Do you think this is a good idea, or do you have any other methods to propose to reduce the oxidative stress?

Dr Misthos: A continuous flow of oxygen to the lung tissue might protect to some extent. Maybe I'm being repetitive, but I think we should measure all these. I can't say it is better or worse. There are no clues. It is a quite new field. There is a lot of work to be done.


   Footnotes
 
☆ Presented at the joint 18th Annual Meeting of the European Association for Cardio-thoracic Surgery and the 12th Annual Meeting of the European Society of Thoracic Surgeons, Leipzig, Germany, September 12–15, 2004.


   References
Top
 Abstract
 1. Introduction
 2. Material and methods
 3. Results
 4. Comment
 Appendix A. Conference...
 References
 

  1. Grace P. Ischaemia-reperfusion injury. Br J Surg 1994;81:637-647.[Medline]
  2. Perrot de M, Liu M, Waddell TK, Keshavjee S. Ischemia-reperfusion-induced lung injury. Am J Respir Crit Care Med 2003;167:490-511.[Abstract/Free Full Text]
  3. Chow CW, Abreu MTH, Suzuki T, Downey GP. Oxidative stress and acute lung injury. Am J Respir Cell Mol Biol 2003;29:427-431.[Free Full Text]
  4. Li C, Jackson RM. Reactive species mechanisms of cellular hypoxia-reoxygenation injury. Am J Physiol Cell Physiol 2002;282:C227-C241.[Abstract/Free Full Text]
  5. Sylvester JT. Hypoxic pulmonary vasoconstriction: a radical view. Circ Res 2001;88:1259-1266.[Abstract/Free Full Text]
  6. Fukanoshi T, Ishibe Y, Okazaki N, Miura K, Liu R, Nagai S, Minami Y. Effect of re-expansion after short-period lung collapse on pulmonary capillary permeability and pro-inflammatory cytokine gene expression in isolated rabbit lungs. Br J Anaesth 2004;92:558-563.[Abstract/Free Full Text]
  7. Tarver RD, Broderick LS, Conces Jr DJ. Reexpansion pulmonary edema. J Thorac Imaging 1996;11:198-209.[Medline]
  8. Wilkinson PD, Keegan J, Davies SW, Bailey J, Rudd RM. Changes in pulmonary microvascular permeability accompanying re-expansion oedema: evidence from dual isotope scintigraphy. Thorax 1990;45:456-459.[Abstract]
  9. Iqbal M, Multz AS, Rossoff LJ, lackner RP. Reexpansion pulmonary edema after VATS successfully treated with continuous positive airway pressure. Ann Thorac Surg 2000;70:669-671.[Abstract/Free Full Text]
  10. Lang JD, McArdle J, O'Reilly PJ, Matalon S. Oxidant–antioxidant balance in acute lung injury. Chest 2002;122:314S-320S.[Abstract/Free Full Text]
  11. Comhair SAA, Erzurum SC. Antioxidant responses to oxidant-mediated lung diseases. Am J Physiol Lung Cell Mol Physiol 2002;283:L246-255.[Abstract/Free Full Text]
  12. Look MP, Musch E. Lipid peroxides in the polychemotherapy of cancer patients. Chemotherapy 1994;40:8-15.
  13. Jack CI, Cottier B, Jackson MJ, Cassapi L, fraser WD, Hind CR. Indicators of free radical activity in patients developing radiation pneumonitis. Int J Radiat Oncol Biol Phys 1996;34:149-154.[CrossRef][Medline]
  14. Duflo F, debon R, Goudable J, Chassard D, Allaouchiche B. Alveolar and seroum oxidative stress in ventilator-associated pneumonia. Br J Anaesth 2002;89:231-236.[Abstract/Free Full Text]
  15. Fukunaga K, Yoshida M, Nakazono N. A simple, rapid, highly sensitive and reproducible quantification method for plasma malondialdehyde by high-performance liquid chromatography. Biomed Chromatogr 1998;12:300-303.[CrossRef][Medline]
  16. Lases EC, Duurkens VAM, Gerritsen WBM, Haas FJLM. Oxidative stress after lung resection therapy. A pilot study. Chest 2000;117:999-1003.
  17. Slinger PD. Acute lung injury after pulmonary resection: more pieces of the puzzle. Anesth Analg 2003;97:1555-1557.[Free Full Text]
  18. Bigatello LM, Allain R, Gaissert HA. Acute lung injury after pulmonary resection. Minerva Anesthesiol 2004;70:159-166.
  19. Sivrikoz MC, Tuncozgur B, Cekmen M, Bakir K, Meram I, Kocer E, Cengiz B, Elbeyli L. The role of tissue reperfusion in the reexpansion injury of the lungs. Eur J Cardiothorac Surg 2002;22:721-727.[Abstract/Free Full Text]
  20. Kutlu CA, Williams EA, Evans TW, Pastorino U, Goldstraw P. Acute lung injury and acute respiratory distress syndrome after pulmonary resection. Ann Thorac Surg 2000;69:376-380.[Abstract/Free Full Text]
  21. Jordan S, Mitchell JA, Quinlan GJ, Goldstraw P. The pathogenesis of lung injury following pulmonary resection. Eur Respir J 2000;15:790-799.[Abstract]
  22. Ruffini E, Parola A, Papalia E, Filoso PL, Mancuso M, Oliario A, Actis-Dato G, Maggi G. Frequency and mortality of acute lung injury and acute respiratory distress after pulmonary resection for bronchogenic carcinoma. Eur J Cardiothorac Surg 2001;20:30-37.[Abstract/Free Full Text]
  23. Pfitzer J, Ishikawa S, Nakazawa K, Makita M. Acute lung injury following one-lung anaesthesia. Br J Anaesth 2003;91:153-154.[Free Full Text]
  24. Williams EA, Evans TW, Goldstraw P. Acute lung injury following lung resection: is one lung anaesthesia to blame?. Thorax 1996;51:114-116.[Abstract]
  25. Zieba M, Suwalski M, Kwiatkowska S, Piaceska G, Grzelewska-Rzymowska I, Stolarek R, Nowak D. Comparison of hydrogen peroxide generation and the content of lipid peroxidation products in lung cancer tissue and pulmonary parenchyma. Respir Med 2000;94:800.[CrossRef][Medline]



This article has been cited by other articles:


Home page
 Eur. J. Cardiothorac. Surg.Home page
V. Matzi, J. Lindenmann, A. Muench, J. Greilberger, H. Juan, R. Wintersteiger, A. Maier, and F. M. Smolle-Juettner
The impact of preoperative micronutrient supplementation in lung surgery. A prospective randomized trial of oral supplementation of combined {alpha}-ketoglutaric acid and 5-hydroxymethylfurfural
Eur. J. Cardiothorac. Surg., November 1, 2007; 32(5): 776 - 782.
[Abstract] [Full Text] [PDF]

Home page
 J. Thorac. Cardiovasc. Surg.Home page
C. Tekinbas, H. Ulusoy, E. Yulug, M. Muharrem Erol, A. Alver, E. Yenilmez, S. Geze, and M. Topbas
One-lung ventilation: For how long?
J. Thorac. Cardiovasc. Surg., August 1, 2007; 134(2): 405 - 410.
[Abstract] [Full Text] [PDF]

Home page
 Eur. J. Cardiothorac. Surg.Home page
P. Misthos and S. Katsaragakis
Reply to Heerdt et al.
Eur. J. Cardiothorac. Surg., September 1, 2006; 30(3): 569 - 570.
[Full Text] [PDF]

Home page
 J. Thorac. Cardiovasc. Surg.Home page
Y.-J. Cheng, K.-C. Chan, C.-T. Chien, W.-Z. Sun, and C.-J. Lin
Oxidative stress during 1-lung ventilation.
J. Thorac. Cardiovasc. Surg., September 1, 2006; 132(3): 513 - 518.
[Abstract] [Full Text] [PDF]

Home page
 Eur. J. Cardiothorac. Surg.Home page
P. M. Heerdt, P. B. Lane, M. J. Crabtree, and B. J. Park
Systemic oxidative stress associated with lung resection during single lung ventilation.
Eur. J. Cardiothorac. Surg., September 1, 2006; 30(3): 568 - 569.
[Full Text] [PDF]

Home page
 Eur. J. Cardiothorac. Surg.Home page
P. Misthos and S. Katsaragakis
Reply to birdas.
Eur. J. Cardiothorac. Surg., August 1, 2006; 30(2): 413 - 413.
[Full Text] [PDF]

Home page
 Anesth. Analg.Home page
P. Slinger
Pro: low tidal volume is indicated during one-lung ventilation.
Anesth. Analg., August 1, 2006; 103(2): 268 - 270.
[Full Text] [PDF]

Home page
 Eur. J. Cardiothorac. Surg.Home page
P. Misthos, S. Katsaragakis, D. Theodorou, N. Milingos, and I. Skottis
The degree of oxidative stress is associated with major adverse effects after lung resection: A prospective study.
Eur. J. Cardiothorac. Surg., April 1, 2006; 29(4): 591 - 595.
[Abstract] [Full Text] [PDF]

This Article
Right arrow Abstract Freely available
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Add to Personal Folders
Right arrow Download to citation manager
Right arrow Permission Requests
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Misthos, P.
Right arrow Articles by Skottis, I.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Misthos, P.
Right arrow Articles by Skottis, I.
Related Collections
Right arrow Lung - basic science

HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
ANN THORAC SURG ASIAN CARDIOVASC THORAC ANN EUR J CARDIOTHORAC SURG
J THORAC CARDIOVASC SURG ICVTS ALL CTSNet JOURNALS