Effect of pulmonary-generated reactive oxygen species on left-ventricular dysfunction associated with cardio-pulmonary ischemia-reperfusion injury.

The purpose of the present study was to demonstrate the contribution of pulmonary-generated reactive oxygen species (ROS) on cardiac dysfunction using a rat model of ischemia-reperfusion (IR) injury. Three groups of rats were subjected to regional IR injury in (i) lung, (ii) heart, (iii) lung + heart. A fourth (control) group of rats were instrumented using the same methods but without induction IR. Hemodynamic data were recorded in real time. Blood from the proximal aorta was sampled during baseline, ischemia, and reperfusion, mixed with α-phenyl-N-tert-butylnitrone (PBN) for measuring ROS by electron paramagnetic resonance spectrometry. Data were analyzed by a two-way analysis of variance. The results showed that the lung IR generated an increased burst of ROS that resulted in significant cardiac dysfunction, including hypotension and ECG changes. The results indicated that generation of ROS as a result of acute IR lung injury may be sufficiently large enough to cause direct cardiac dysfunction that is independent of injury caused to the myocardium as a result of regional myocardial IR injury alone.
AuthorsMahmood Khan, Mark E Brauner, Michael C Plewa, Vijay K Kutala, Mark Angelos, Periannan Kuppusamy
JournalCell biochemistry and biophysics (Cell Biochem Biophys) Vol. 67 Issue 2 Pg. 275-80 (Nov 2013) ISSN: 1559-0283 [Electronic] United States
PMID21947963 (Publication Type: Journal Article, Research Support, N.I.H., Extramural, Research Support, Non-U.S. Gov't)
Chemical References
  • Reactive Oxygen Species
  • Animals
  • Heart (physiopathology)
  • Lung (metabolism)
  • Male
  • Myocardial Reperfusion Injury (metabolism, physiopathology)
  • Rats
  • Rats, Sprague-Dawley
  • Reactive Oxygen Species (metabolism)
  • Reperfusion Injury (metabolism, physiopathology)
  • Ventricular Dysfunction, Left (metabolism)

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