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Text
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URL Address
<a href="http://doi.org/10.1177/153537020222700207" target="_blank" rel="noreferrer noopener">http://doi.org/10.1177/153537020222700207</a>
Pages
125–132
Issue
2
Volume
227
Dublin Core
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Title
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Effect of massive sympathetic nervous system activation on coronary blood flow and myocardial energy pool.
Publisher
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Experimental biology and medicine (Maywood, N.J.)
Date
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2002
2002-02
Subject
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Animals; Coronary Circulation/*physiology; Energy Metabolism; Female; Heart/innervation/*physiology; Male; Rabbits; Sympathetic Nervous System/drug effects/*physiology; Veratrine/pharmacology
Creator
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Smith Jennifer M; Pilati Charles F
Description
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Our previous work indicates that myocardial ischemia could be the mechanism responsible for the left ventricular (LV) dysfunction that frequently develops after massive sympathetic nervous system (SNS) activation. In this study, coronary blood flow (CBF) and myocardial ATP, creatine phosphate, and lactate concentrations were measured after massively activating the SNS of anesthetized rabbits with an intracisternal injection of veratrine. CBF was measured at time 0 (baseline), and at 2, 10, and 20 min after SNS activation in one group, and at 0, 45, 90, and 150 min in a second group. Myocardial ATP, creatine phosphate, and lactate were measured at 0, 2, 10, 20, 90, and 150 min in separate groups of rabbits. SNS activation caused LV dysfunction in approximately 60% of the rabbits. SNS-related increases in CBF kept pace with the increases in myocardial energy demand as determined from the systolic pressure-heart rate product. The subendocardial-to-subepicardial blood flow ratio did not change significantly. Myocardial creatine phosphate concentration was depressed 2 min after SNS activation and remained depressed for at least 20 min. ATP fell continuously and was significantly lower than baseline by 20 min. Tissue lactate concentration was elevated at this time. By 90 min, the concentrations of all three metabolites had recovered. These results indicate that myocardial high-energy phosphate compounds fall after massive SNS activation, but ischemia does not appear to be the underlying mechanism.
Identifier
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<a href="http://doi.org/10.1177/153537020222700207" target="_blank" rel="noreferrer noopener">10.1177/153537020222700207</a>
Rights
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Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
2002
Animals
Coronary Circulation/*physiology
Energy Metabolism
Experimental biology and medicine (Maywood, N.J.)
Female
Heart/innervation/*physiology
Male
Pilati Charles F
Rabbits
Smith Jennifer M
Sympathetic Nervous System/drug effects/*physiology
Veratrine/pharmacology