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Concentration decrease of nitric oxide in the postischemic muscle is not only caused by the generation of O2-.

Felix Stoffels1, Felix Lohöfener, Moritz Beisenhirtz

  • 1Universitätsklinikum für Allgemein-, Viszeral-, Gefäss- und Thoraxchirurgie, Charité, Berlin, Germany.

Microsurgery
|August 21, 2007
PubMed
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Epigallocatechin-3-gallate (EGCG) reduces harmful superoxide levels in rat skeletal muscle during reperfusion after ischemia. This radical scavenger protects muscle from injury without significantly altering nitric oxide (NO) levels.

Area of Science:

  • Biochemistry
  • Physiology
  • Pharmacology

Background:

  • Ischemic skeletal muscle reperfusion alters superoxide (O(2)(-)) and nitric oxide (NO) concentrations.
  • Radical scavengers may modulate these changes during reperfusion injury.

Purpose of the Study:

  • To investigate the effect of epigallocatechin-3-gallate (EGCG) on O(2)(-) and NO balance in rat skeletal muscle during reperfusion.
  • To determine if EGCG protects against ischemia-reperfusion (I/R) injury.

Main Methods:

  • Wistar rats underwent 2-hour hind limb ischemia, followed by reperfusion.
  • Seven rats received EGCG infusion before reperfusion; controls did not.
  • Online measurements of O(2)(-), NO, and temperature were performed during reperfusion.

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Main Results:

  • EGCG significantly reduced O(2)(-) concentrations from 156.5 to 72.2 nmol/l (P=0.01).
  • NO levels decreased in both groups, with no significant difference between EGCG-treated and control rats (-175 vs. -227 nmol/l; P=0.33).
  • The observed changes suggest O(2)(-) and NO interactions are not solely responsible for NO decrease during reperfusion.

Conclusions:

  • EGCG demonstrates a protective effect on skeletal muscle against I/R injury.
  • EGCG effectively scavenges superoxide radicals without substantially altering the nitric oxide profile during reperfusion.