Early accumulation of the terminal complement-complex in the ischaemic myocardium after reperfusion

D Mathey1, J Schofer, H J Schäfer

  • 1Department of Cardiology, University Hospital Eppendorf, Hamburg, Germany.

Insights

Complement complex C5b-9 accumulates late in infarcted myocardium without reperfusion. With reperfusion, C5b-9 deposition occurs rapidly, suggesting a role in myocardial reperfusion injury.

Area of Science:

  • Cardiovascular Research
  • Immunology
  • Pathology

Background:

  • The terminal complement complex C5b-9 (also known as the membrane attack complex) is implicated in tissue damage.
  • Its accumulation in infarcted myocardium suggests a role in myocardial infarction pathogenesis.

Purpose of the Study:

  • To investigate the time course of C5b-9 deposition in experimental myocardial infarction.
  • To determine the influence of reperfusion on C5b-9 accumulation in the infarcted heart.

Main Methods:

  • Experimental myocardial infarction was induced in rabbits by coronary artery occlusion.
  • Groups were subjected to either prolonged occlusion without reperfusion or shorter occlusion followed by reperfusion.
  • C5b-9 deposition was quantified using immunohistochemistry and ELISA on myocardial biopsies.

Main Results:

  • In the absence of reperfusion, C5b-9 accumulation was a late event, observed after 5-6 hours of ischemia.
  • In the presence of reperfusion, significant C5b-9 deposition was detected as early as 30 minutes after ischemia onset.
  • This indicates reperfusion accelerates C5b-9 deposition in ischemic myocardium.

Conclusions:

  • C5b-9 accumulation occurs late in myocardial infarction when tissue is largely necrotic if reperfusion is absent.
  • Rapid C5b-9 deposition during ischemia-reperfusion suggests the complement system activation plays a significant role in reperfusion injury.
  • These findings highlight the complement system's involvement in the pathophysiology of myocardial infarction and reperfusion injury.

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