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Coronary Leukotriene Levels and Myocardial Ischemia

  • Robert E. Goldstein
  • Giora Feuerstein
  • David Ezra
  • Gordon Letts
  • Peter W. Ram-Well
Part of the GWUMC Department of Biochemistry Annual Spring Symposia book series (GWUN)

Abstract

Potential for Involvement of Cysteinyl Leukotrienes in Myocardial Infarction Several lines of evidence suggest that leukotrienes might be involved in the path-ogenesis of myocardial infarction. Cysteinyl leukotrienes released by inflammatory cells have a potent capacity to cause vasoconstriction and edema formation. Administration of cysteinyl leukotrienes to blood-perfused, in situ hearts can produce profound coronary constriction accompanied by electrocardiographic evidence of myocardial ischemia, depression of myocardial contractility, and ventricular arrhythmias (Michelassi et al., 1982; Woodman and Dusting, 1983; Ezra et al., 1983). Figure 1 illustrates the influence of leukotriene C4 as observed in our laboratory. In this example, a l-μg bolus of leukotriene C4, given directly into the left anterior descending coronary artery of a pig, caused transient arrest of regional blood flow and ST segment elevation characteristic of myocardial ischemia on a local surface electrocardiogram. Left ventricular end-diatolic pressure is not altered in this example. In other experiments, however, regional wall motion, recorded by epicardial sonomicrometers in myocardium supplied by the left anterior descending coronary artery, demonstrated transient, severe reduction in myocardial shortening in conjunction with marked leukotriene-induced coronary flow decrement (Mich-elassi et al., 1982; Ezra et al., 1984). Thus, release of cysteinyl leukotrienes within the heart might have substantial deleterious consequences for coronary and myocardial function.

Keywords

Myocardial Ischemia Left Anterior Descend Coronary Flow Coronary Blood Flow Coronary Occlusion 
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 Science+Business Media New York 1985

Authors and Affiliations

  • Robert E. Goldstein
    • 1
  • Giora Feuerstein
    • 1
  • David Ezra
    • 1
  • Gordon Letts
    • 2
  • Peter W. Ram-Well
    • 3
  1. 1.Neurobiology Research Unit, Divisions of Cardiology and Clinical Pharmacology, Departments of Medicine and PharmacologyUniformed Services University of the Health SciencesBethesdaMarylandUSA
  2. 2.Merck Frosst, Inc.DorvalCanada
  3. 3.Department of Physiology and BiophysicsGeorgetown University Medical CenterUSA

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