Effects of XXXX entry blockers on coronary constriction and @entity741 due to leukotriene D4.

@entity12526 @entity301 @entity63 @entity1855 @entity450 @entity3988 @entity15490 @entity460 @entity594 @entity741
Recent studies show that leukotrienes ( @entity15490 ) produce profound coronary artery constriction. Although @entity460 entry blockers are commonly used to remedy coronary vasospasm, their capacity to interfere with LT-mediated coronary constriction is unknown. Therefore, we compared effects of intracoronary LTD4 before and during treatment with @entity460 entry blockers in the in situ, blood-perfused hearts of @entity12526 . Intravenous administration of @entity1855 (0.1-1.6 mg/kg), @entity594 (10 or 100 micrograms/kg) or @entity3988 (0.6-2.0 mg/kg) sufficient to increase base-line @entity301 ( @entity301 ) and decrease mean arterial pressure did not change decrement in @entity301 after LTD4. Infusion of @entity1855 (0.01-0.04 mg/min) into the left anterior descending coronary artery raised pre-LTD4 @entity301 almost 2-fold without alteration in mean arterial pressure, heart rate or left ventricular end-diastolic pressure. Intracoronary boluses of LTD4 (0.3, 1.0 and 3.0 micrograms) during @entity1855 infusion into the same vessel caused dose-dependent decreases in @entity301 identical to those observed when LTD4 was injected during control infusion. ECGs showed @entity741 during severe @entity450 after high dose intracoronary LTD4 (3.0 or 10.0 micrograms). When the same LTD4 doses were injected during intracoronary @entity1855 , electrocardiographic changes did not occur despite similar decreases in @entity301 . The capacity of @entity1855 to prevent LTD4-induced @entity63 may be caused by higher residual @entity301 after LTD4 even though the magnitude of LTD4-induced @entity301 decrement was unaltered. LTD4-induced coronary constriction seems to be mediated by a mechanism unrelated to @entity460 entry channels blocked by @entity1855 , @entity594 or @entity3988 .
