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Effects of calcium entry blockers on coronary constriction and myocardial ischemia due to leukotriene D4
Year:
1985
Authors :
Ezra, David
;
.
Volume :
233
Co-Authors:
Ezra, D., Division of Clinical Pharmacology, Department of Pharmacology, Uniformed Services University of the Health Sciences, Bethesda, MD 20814, United States
Boyd, L.M., Division of Clinical Pharmacology, Department of Pharmacology, Uniformed Services University of the Health Sciences, Bethesda, MD 20814, United States
Goldstein, R.E., Division of Clinical Pharmacology, Department of Pharmacology, Uniformed Services University of the Health Sciences, Bethesda, MD 20814, United States
Feuerstein, G., Division of Clinical Pharmacology, Department of Pharmacology, Uniformed Services University of the Health Sciences, Bethesda, MD 20814, United States
Facilitators :
From page:
229
To page:
234
(
Total pages:
6
)
Abstract:
Recent studies show that leukotrienes (LTs) produce profound coronary artery constriction. Although calcium 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 calcium entry blockers in the in situ, blood-perfused hearts of domestic pigs. Intravenous administration of verapamil (0.1-1.6 mg/kg), nifedipine (10 or 100 μg/kg) or diltiazem (0.6-2.0 mg/kg), sufficient to increase base-line coronary blood flow (CBF) and decrease mean arterial pressure, did not change decrement in CBF after LTD4. Infusion of verapamil (0.01-0.04 mg/min) into the left anterior descending coronary artery raised pre-LTD4 CBF 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 μg) during verapamil infusion into the same vessel caused dose-dependent decreases in CBF identical to those observed when LTD4 was injected during control infusion. ECGs showed myocardial ischemia during severe flow reduction after high dose intracoronary LTD4 (3.0 or 10.0 μg). When the same LTD4 doses were injected during intracoronary verapamil, electrocardiographic changes did not occur despite similar decreases in CBF. The capacity of verapamil to prevent LTD4-induced ischemia may be caused by higher residual CBF after LTD4 even though the magnitude of LTD4-induced CBF decrement was unaltered. LTD4-induced coronary constriction seems to be mediated by a mechanism unrelated to calcium entry channels blocked by verapamil, nifedipine or diltiazem.
Note:
Related Files :
Animal
animal experiment
Calcium Channel Blockers
Female
intravenous drug administration
Male
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More details
DOI :
Article number:
Affiliations:
Database:
Scopus
Publication Type:
article
;
.
Language:
English
Editors' remarks:
ID:
19908
Last updated date:
02/03/2022 17:27
Creation date:
16/04/2018 23:32
Scientific Publication
Effects of calcium entry blockers on coronary constriction and myocardial ischemia due to leukotriene D4
233
Ezra, D., Division of Clinical Pharmacology, Department of Pharmacology, Uniformed Services University of the Health Sciences, Bethesda, MD 20814, United States
Boyd, L.M., Division of Clinical Pharmacology, Department of Pharmacology, Uniformed Services University of the Health Sciences, Bethesda, MD 20814, United States
Goldstein, R.E., Division of Clinical Pharmacology, Department of Pharmacology, Uniformed Services University of the Health Sciences, Bethesda, MD 20814, United States
Feuerstein, G., Division of Clinical Pharmacology, Department of Pharmacology, Uniformed Services University of the Health Sciences, Bethesda, MD 20814, United States
Effects of calcium entry blockers on coronary constriction and myocardial ischemia due to leukotriene D4
Recent studies show that leukotrienes (LTs) produce profound coronary artery constriction. Although calcium 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 calcium entry blockers in the in situ, blood-perfused hearts of domestic pigs. Intravenous administration of verapamil (0.1-1.6 mg/kg), nifedipine (10 or 100 μg/kg) or diltiazem (0.6-2.0 mg/kg), sufficient to increase base-line coronary blood flow (CBF) and decrease mean arterial pressure, did not change decrement in CBF after LTD4. Infusion of verapamil (0.01-0.04 mg/min) into the left anterior descending coronary artery raised pre-LTD4 CBF 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 μg) during verapamil infusion into the same vessel caused dose-dependent decreases in CBF identical to those observed when LTD4 was injected during control infusion. ECGs showed myocardial ischemia during severe flow reduction after high dose intracoronary LTD4 (3.0 or 10.0 μg). When the same LTD4 doses were injected during intracoronary verapamil, electrocardiographic changes did not occur despite similar decreases in CBF. The capacity of verapamil to prevent LTD4-induced ischemia may be caused by higher residual CBF after LTD4 even though the magnitude of LTD4-induced CBF decrement was unaltered. LTD4-induced coronary constriction seems to be mediated by a mechanism unrelated to calcium entry channels blocked by verapamil, nifedipine or diltiazem.
Scientific Publication
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