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Polymorphonuclear granulocytes induce myocardial dysfunction during ischemia and in later reperfusion of hearts

C Seligmann1, A Bock, T Leitsch

  • 1Department of Cardiology, University Hospital Benjamin Franklin, Free University of Berlin, D-12200 Berlin, Germany. cseligmann@talknet.de

Journal of Leukocyte Biology
|May 19, 2001
PubMed

Insights

Polymorphonuclear granulocytes (PMNs) significantly impair heart function during low-flow ischemia and reperfusion. These white blood cells caused cardiac damage when introduced during ischemia or reperfusion, highlighting their role in myocardial injury.

Area of Science:

  • Cardiovascular Research
  • Hematology
  • Ischemia-Reperfusion Injury

Background:

  • Polymorphonuclear granulocytes (PMNs) are implicated in cardiac reperfusion injury.
  • The specific impact of PMNs on myocardial function during low-flow ischemia and their temporal effects during ischemia/reperfusion remain unclear.

Purpose of the Study:

  • To determine if PMNs compromise myocardial function in hearts subjected to low-flow ischemia.
  • To investigate the deleterious effects of PMNs at different time points during ischemia and reperfusion.

Main Methods:

  • Isolated, working guinea pig hearts underwent 30 minutes of low-flow ischemia and reperfusion.
  • Homologous PMNs were administered during ischemia or early reperfusion with thrombin.
  • External heart work recovery (REHW) and PMN retention (PMNR) were measured.
  • The effect of superoxide dismutase (SOD) was evaluated.

Main Results:

  • PMN application significantly reduced myocardial function (REHW) regardless of administration timing.
  • Intracoronary PMN retention (PMNR) was elevated compared to controls.
  • Superoxide dismutase (SOD) significantly improved REHW but did not alter PMNR.

Conclusions:

  • Thrombin-stimulated PMNs significantly impair cardiac function in low-flow ischemic conditions.
  • PMNs contribute to myocardial dysfunction during both ischemic and reperfusion phases.
  • Antioxidant therapy with SOD shows potential in mitigating PMN-induced cardiac damage.

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