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Coronary Artery Occlusion in the Conscious Dog
Author(s) -
Eldon R. Smith,
David R. Redwood,
William E. McCarron,
Stephen E. Epstein
Publication year - 1973
Publication title -
circulation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.795
H-Index - 607
eISSN - 1524-4539
pISSN - 0009-7322
DOI - 10.1161/01.cir.47.1.51
Subject(s) - medicine , cardiology , anesthesia , tachycardia , blood pressure , heart rate , coronary occlusion , ischemia , mean arterial pressure , methoxamine , coronary perfusion pressure , artery , myocardial infarction , resuscitation , cardiopulmonary resuscitation , receptor , agonist
Nitroglycerin is generally believed to be contraindicated during acute myocardial infarction because the resultant decrease in coronary perfusion pressure and reflex tachycardia might extend the area of ischemia. To determine the effects of nitroglycerin and alterations in arterial pressure on the degree of myocardial ischemia, the left anterior descending coronary artery was occluded for repeated 15-min periods in closed-chest conscious dogs. The degree of myocardial ischemia was estimated by summating the S-T segment elevation (∑ST) recorded from 12 myocardial electrodes. Although heart rate increased and arterial pressure decreased, ∑ST after 15 min of coronary occlusion was 14 ± 3 mv (P < 0.02) less during nitroglycerin therapy than during control occlusions. When the same alteration in arterial pressure was produced by venous hemorrhage, ∑ST tended to be greater than during control occlusions (+14 ± 7 mv, NS); the difference between the nitroglycerin and hemorrhage interventions was highly significant (28 ± 9 mv, P < 0.02). ∑ST was also less than control when phenylephrine was administered in doses sufficient to increase arterial pressure 25 mm Hg (−16 ± 3 mv, P < 0.005) and 50 mm Hg (−15 ± 2 mv, P < 0.001). When the decrease in arterial pressure and reflex tachycardia induced by nitroglycerin were reversed by simultaneous infusion of methoxamine, ∑ST was greatly reduced from control (−50 ± 16 mv, P < 0.02) and was significantly less than that occurring during nitroglycerin alone (−25 ± 5 mv, P < 0.001). We conclude that nitroglycerin may be a useful agent during acute myocardial infarction, particularly when the fall in coronary perfusion pressure and increase in heart rate are prevented by the simultaneous administration of an alpha-adrenergic agonist.

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