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Ischaemia-Reperfusion in Sepsis

  • C. Adembri
  • A. R. De Gaudio
  • G. P. Novelli
Conference paper

Abstract

It has been over 20 years since Hearse described the “oxygen paradox” and the “calcium paradox” in hearts undergoing ischaemia-reperfusion (I-R) [1]. The concept that it is reperfusion itself that increases and potentiates ischaemia-induced damage has progressively gained ground, and it is now one of the main factors taken into account in the treatment of various pathological states, from crush injury to transplantation [2, 3] . Even when reperfusion itself is the goal of therapy, such as during thrombolysis for infarcted myocardium, reperfusion-associated dysfunctions, which range from arrhythmias to stunning, must be considered as they significantly affect morbidity and mortality rates [4, 5]. Regardless of the cause and the modality that have provoked it, the sequence of ischaemia and reperfusion actually induces a typical inflammatory response which is not restricted to the injured tissue but frequently has a systemic recoil [6].

Keywords

Nitric Oxide Multiple Organ Failure Bacterial Translocation Human Skeletal Muscle Xanthine Dehydrogenase 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.

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Copyright information

© Springer-Verlag Italia 2000

Authors and Affiliations

  • C. Adembri
  • A. R. De Gaudio
  • G. P. Novelli

There are no affiliations available

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