Frederick E. Kuhn
Georgetown University Medical Center
5 Papers
217 Citations
Frederick E. Kuhn is an academic researcher from Georgetown University Medical Center. The author has contributed to research in topics: Mean arterial pressure & Vasoconstriction. The author has an hindex of 5, co-authored 5 publications.
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Papers
Coronary Artery Disease in Women: Risk Factors, Evaluation, Treatment, and Prevention
TL;DR: The risk factors, methods of identification, and treatment of coronary artery disease in women, as well as the potential benefits of postmenopausal estrogen are reviewed.
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Effect of cocaine on the coronary circulation and systemic hemodynamics in dogs.
TL;DR: In this canine preparation with normal coronary arteries, cocaine produced vasoconstriction of both epicardial and coronary resistance vessels that was not associated with evidence of myocardial ischemia, suggesting that epinephrine (rather than norepinephrine) is primarily responsible for the peripheral vascular actions of cocaine.
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Additive myocardial depressant effects of cocaine and ethanol.
Ronald T. Uszenski,Ronald T. Uszenski,Richard A. Gillis,Gary L. Schaer,Ali R. Analouei,Frederick E. Kuhn +5 more
TL;DR: Failure of ethanol to enhance cocaine-induced coronary vasoconstriction suggests that the additive myocardial depressant effect of this combination is not related to ischemia but rather to a direct toxic effect of these drugs.
35
Cocaine-induced cardiovascular effects: lack of evidence for a central nervous system site of action based on hemodynamic studies with cocaine methiodide.
Linda W. Dickerson,David J. Rodak,Frederick E. Kuhn,Svea K. Wahlstrom,Richard E. Tessel,Marc S. Visner,Gary L. Schaer,Richard A. Gillis +7 more
TL;DR: The data suggest that the cardiovascular effects of cocaine result primarily from a peripheral site of action, and opiate sedation potentially might have attenuated central sympathetic outflow.
19
Cocaine produces coronary artery vasoconstriction independent of an intact endothelium.
TL;DR: Failure of endothelial injury to potentiate the coronary vasoconstrictive effect by cocaine suggests that factors other than endothelial dysfunction may be important in pathogenesis of cocaine-associated myocardial infarction.
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