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Eur J Cardiothorac Surg 2006;30:569-570
© 2006 Elsevier Science NL

Letter to the Editor

Reply to Heerdt et al.

Panagiotis Misthos*

First Thoracic Surgical Department, ‘SOTIRIA’ General Hospital for Chest Diseases, Athens, Greece

Stylianos Katsaragakis

University of Athens Medical School, First Propaedeutic Surgical Department, Athens, Greece

Received 21 May 2006; accepted 29 May 2006.

* Corresponding author. Address: 16-18 Markou Avgeri Street, 15343 Agia Paraskevi, Athens, Greece. Tel.: +30 210 6080107; fax: +30 210 6080107. (Email: panmisthos{at}yahoo.gr).

Key Words: Oxidative stress • Lung re-expansion • Postresectional complications

We appreciate the comments of Heerdt et al. [1]. We are delighted that such a prominent group was interested in our study and their preliminary results are qualitatively consistent with ours.

We 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 and to define the contribution of the generated oxygen and nitrogen reactive species on postlobectomy morbidity and mortality [2,3].

The difference concerning the duration of postresectional oxidative stress (12 h vs 72 h) might be explained by the following thoughts: (1) Our results represent the total systematic level of oxidation as it is measured in peripheral blood samples and suggest a common internal antioxidative mechanism of oxygen-free radicals’ clearance and a constant counteraction by the endogenous antioxidant systems. Heerdt et al. reported their results from both the operated and non-operated lung and that is maybe different since they actually study the source of the oxidative stress (even from the contralateral healthy lung which sustained the effects of one-lung ventilation, is a local response) in contrast to our group that studied the net systematic effect which incorporates the action of more antioxidant mechanisms sited out of the thorax. That means that although there is an ongoing generation of free radicals within the chest, the oxidative products are effectively counteracted. The net result is the short-lived (12 h) systematic oxidative stress. (2) The postoperative medications (especially, for effective pain management) is another explanation. (3) Although we are not familiar with the swine model for the study of postresectional oxidative stress, one may ask if there are quantitative differences in the results that are recorded between animal and human studies.

We are looking forward to reading their final results, which would add a lot to our knowledge for the impact of lung oxidative stress on the cardiovascular system.

References

  1. Heerdt PM, Lane PB, Crabtree MJ, Park BJ. Systemic oxidative stress associated with lung resection during single lung ventilation. Eur J Cardiothorac Surg 2006;30(3):569-570.[Free Full Text]
  2. Misthos P, Katsaragakis S, Milingos N, Kakaris S, Sepsas E, Athanassiadi K, Theodorou D, Skottis I. Postresectional pulmonary oxidative stress in lung cancer patients. The role of one-lung ventilation. Eur J Cardiothorac Surg 2005;27(3):379-383.[Abstract/Free Full Text]
  3. Misthos P, Katsaragakis S, Theodorou D, Milingos N, Skottis I. The degree of oxidative stress is associated with major adverse effects after lung resection: a prospective study. Eur J Cardiothorac Surg 2006;29(4):591-595.[Abstract/Free Full Text]




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