The Journal of Thoracic and Cardiovascular Surgery
Volume 139, Issue 5 , Pages 1357-1358, May 2010

Hypoxemic reperfusion of ischemic states prevents myocardial injury, attenuating the oxidative and inflammatory response

3rd Department of Critical Care Medicine, University of Athens Medical School, Athens, Greece

Article Outline

CTSNet classification: 31.4, 38, 38.1

 

To the Editor:

We read with great interest the recent article by Abdel-Rahman and colleagues1 on the favorable effect of “hypoxic reoxygenation” in the attenuation of myocardial ischemia–reperfusion injury after cardioplegic arrest. The importance of progressive oxygen re-entry into ischemic tissues has been shown since 2001 in the brains of a porcine model of cardiac arrest.2, 3 The favorable effect of the strategy was documented through better overall neurological performance, less lipid peroxidation,2 and attenuation of the brain morphologic changes.3 Because of malondialdehyde (MDA) increase, oxidative stress has been theoretically implicated, thought not confirmed by the measurement of reactive oxygen species (ROS).

With regard to the current study, 3 comments are to be addressed. First, the authors deduced oxidative myocardial injury by determining MDA concentrations in coronary sinus blood without comparative reference MDA concentrations at the distal site. Nevertheless, ROS seem to be directly cardiotoxic, independent of the site of their production. In fact, normoxemic reperfusion of a distal ischemic organ (eg, the intestine) has been shown to cause myocardial injury that was prevented with progressive oxygen re-entry during reperfusion.4

Second, in the above studies, similarly to the current one, with the exception of MDA measurement, the favorable effect of hypoxemic reperfusion was not substantiated by direct indices of oxidative stress alterations, such as ROS measurement. ROS and cytokines were recently assessed in a model of hypoxemic resuscitation of hemorrhagic shock in rabbits and found to be particularly diminished compared with those seen in the standard resuscitation mode of clinical practice.5 The weakening effect on cytokine production is an additional important achievement of hypoxemic resuscitation because these mediators lead to post–ischemia–reperfusion inflammatory injury.

Third, the authors have repetitively used erroneously the term “hypoxic reoxygenation” instead of “hyperoxic reoxygenation” to describe Pao2 values of 250 to 350 mm Hg, which is usually applied in the clinical setting. Furthermore, we consider even more accurate the term “hyperoxemic” because it describes higher arterial oxygen content largely and easily modifiable by fraction of inspired oxygen changes; in contrast, the term “hyperoxic” describes tissue oxygen concentration dependent on addition to hemodynamic parameters. Correspondingly, the other treatment branch is represented by gradual reoxygenation by means of an initial “hypoxemic” instead of “hypoxic” period.

Our published data support the findings of Abdel-Rahman and colleagues1 regarding the principal idea of the strategy for the prevention of reperfusion injury,2, 3, 4 the restoration of hemodynamic parameters,4, 5 and the attenuation of oxidative stress.2, 3, 4, 5 Additionally, these data provide a further insight into the potentially protective role of this strategy through the attenuation of the inflammatory response during reperfusion.5

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References 

  1. Abdel-Rahman U, Risteski P, Tizi K, Kerscher S, Bejati S, Zwicker K, et al. Hypoxic reoxygenation during initial reperfusion attenuates cardiac dysfunction and limits ischemia–reperfusion injury after cardioplegic arrest in a porcine model. J Thorac Cardiovasc Surg. 2009;137:978–982
  2. Douzinas EE, Andrianakis I, Pitaridis MT, Karmpaliotis DJ, Kypriades EM, Betsou A, et al. The effect of hypoxemic reperfusion on cerebral protection after a severe global ischemic brain insult. Intensive Care Med. 2001;27:269–275
  3. Douzinas EE, Patsouris E, Kypriades E, Andrianakis I, Makris DJ, Korkolopoulou P, et al. Hypoxemic reperfusion ameliorates the histopathologic changes in the brain after a severe global cerebral ischemic insult. Intensive Care Med. 2001;27:905–910
  4. Douzinas EE, Pitaridis MT, Patsouris E, Kollias S, Boursinos V, Karmpaliotis DI, et al. Myocardial ischemia in intestinal postischemic shock: the effect of hypoxemic reperfusion. Crit Care Med. 2003;31:2183–2189
  5. Douzinas EE, Livaditi O, Andrianakis I, Prigouris P, Paneris P, Villiotou V, et al. The effect of hypoxemic resuscitation from hemorrhagic shock on blood pressure restoration and on oxidative and inflammatory responses. Intensive Care Med. 2008;34:1133–1141

PII: S0022-5223(10)00129-7

doi:10.1016/j.jtcvs.2009.04.069

Refers to article:

  • Hypoxic reoxygenation during initial reperfusion attenuates cardiac dysfunction and limits ischemia–reperfusion injury after cardioplegic arrest in a porcine model

    U. Abdel-Rahman, P. Risteski, K. Tizi, S. Kerscher, S. Bejati, K. Zwicker, M. Scholz, U. Brandt, A. Moritz
    The Journal of Thoracic and Cardiovascular Surgery April 2009 (Vol. 137, Issue 4, Pages 978-982)

The Journal of Thoracic and Cardiovascular Surgery
Volume 139, Issue 5 , Pages 1357-1358, May 2010

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