Coronary Leukotriene Levels and Myocardial Ischemia
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.
KeywordsMyocardial Ischemia Left Anterior Descend Coronary Flow Coronary Blood Flow Coronary Occlusion
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