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40
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Text
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URL Address
<a href="http://doi.org/10.1152/ajpheart.1997.273.3.H1606" target="_blank" rel="noreferrer noopener">http://doi.org/10.1152/ajpheart.1997.273.3.H1606</a>
Pages
H1606–1610
Issue
3
Volume
273
Dublin Core
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
Title
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Daily exercise attenuates the sympathetic nerve response to exercise by enhancing cardiac afferents.
Publisher
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The American journal of physiology
Date
A point or period of time associated with an event in the lifecycle of the resource
1997
1997-09
Subject
The topic of the resource
Afferent Pathways; Animal/*physiology; Animals; Baroreflex; Blood Pressure; Femoral Artery/physiology; Femoral Vein/physiology; Heart Rate; Heart/innervation/*physiology; Kidney/innervation; Physical Conditioning; Rabbits; Sympathetic Nervous System/*physiology
Creator
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DiCarlo S E; Stahl L K; Bishop V S
Description
An account of the resource
"Central command" may initiate the sympathoexcitatory responses at the onset of exercise by shifting the operating point of the arterial baroreflex toward higher pressures. Daily exercise (DE) attenuates the sympathoexcitatory responses to submaximal exercise. This DE-induced adaptation may be due, in part, to an enhanced inhibitory influence of cardiac afferents. This is suggested because cardiac afferents exert a tonic inhibitory influence on the arterial baroreflex which is enhanced by DE. Therefore, the influence of cardiac afferents on the regulation of renal sympathetic nerve activity (RSNA) during exercise was examined in a group of sedentary and age-matched DE rabbits. The rabbits were instrumented with a Silastic catheter inserted into the pericardial sac, electrodes around the renal sympathetic nerves, and catheters in the femoral artery and vein. In the sedentary rabbits, treadmill exercise (12 m/min, 20% grade) significantly increased mean arterial pressure (delta 18 +/- 3 mmHg), heart rate (delta 36 +/- 3 beats/min), and RSNA (delta 295 +/- 23%). More importantly, cardiac afferent blockade (2% intrapericardial procainamide) did not significantly alter the RSNA response to exercise in the sedentary rabbits. DE did not alter the mean arterial pressure (delta 15 +/- 1 mmHg) or heart rate (delta 55 +/- 8 beats/min) response to exercise; however, RSNA (delta 252 +/- 9%) was significantly reduced. In contrast to the sedentary rabbits, cardiac afferent blockade in the DE rabbits significantly increased the RSNA response to exercise (delta 417 +/- 30%). These results suggest that DE attenuates the RSNA response to dynamic exercise due, in part, to an enhanced inhibitory influence of cardiac afferents.
Identifier
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1152/ajpheart.1997.273.3.H1606" target="_blank" rel="noreferrer noopener">10.1152/ajpheart.1997.273.3.H1606</a>
Rights
Information about rights held in and over the resource
Article information provided for research and reference use only. All rights are retained by the journal listed under publisher and/or the creator(s).
1997
Afferent Pathways
Animal/*physiology
Animals
Baroreflex
Bishop V S
Blood Pressure
DiCarlo S E
Femoral Artery/physiology
Femoral Vein/physiology
Heart Rate
Heart/innervation/*physiology
Kidney/innervation
Physical Conditioning
Rabbits
Stahl L K
Sympathetic Nervous System/*physiology
The American journal of physiology
-
Text
A resource consisting primarily of words for reading. Examples include books, letters, dissertations, poems, newspapers, articles, archives of mailing lists. Note that facsimiles or images of texts are still of the genre Text.
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
The Dublin Core metadata element set is common to all Omeka records, including items, files, and collections. For more information see, http://dublincore.org/documents/dces/.
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
A point or period of time associated with an event in the lifecycle of the resource
2002
2002-02
Subject
The topic of the resource
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
An account of the resource
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
An unambiguous reference to the resource within a given context
<a href="http://doi.org/10.1177/153537020222700207" target="_blank" rel="noreferrer noopener">10.1177/153537020222700207</a>
Rights
Information about rights held in and over the resource
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