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Evidence of a sympathetically mediated cardio-contractile arm of the baroreflex in anesthetized rats Stewart, Liam
Abstract
Contemporary discussion of the baroreflex includes the efferent vascular-sympathetic and cardio-vagal arms. Because sympathetic pre/post-ganglionic neurons innervate the LV, however, the heart may also undergo sympathetically mediated increases in cardiac contractility during baroreceptor unloading, but this has not been adequately investigated using a load-independent index of contractility. We aimed to a) determine whether left-ventricular (LV) contractility increases in response to baroreceptor unloading, and b) parse out whether the increase in contractility is mediated via the sympathetic or parasympathetic nervous system. 10 male rats were anesthetized (1.9 ± 0.4 g/kg urethane) and instrumented with arterial and LV pressure-volume catheters to measure mean arterial pressure (MAP) and contractility [maximal rate of pressure normalized to end-diastolic volume (dP/dtmax–EDV mmHg/s/µl)], respectively, and placed in a servo-controlled lower-body negative pressure (LBNP) chamber to reduce MAP by 10% to mechanically unload baroreceptors. LBNP was repeated in each animal following infusions of esmolol (beta-blocker which blocks cardiac sympathetic transmission), atropine (blocks cardiac parasympathetic transmission), and esmolol + atropine (full cardiac autonomic blockade). Under control conditions, dP/dtmax–EDV increased during baroreceptor unloading (26 ± 6 vs 31 ± 9 mmHg/s/µl, p=0.031) Blocking cardiac sympathetic transmission abolished this response (11 ± 2 vs. 12 ± 2 mmHg/s/µl, p=0.125). In contrast, contractility increased during baroreceptor unloading when blocking cardiac parasympathetic transmission (26 ± 6 vs. 31 ± 9 mmHg/s/µl, p=0.019), suggesting sympathetic activation, not parasympathetic withdrawal, is the key regulator of the contractile response to baroreceptor unloading. Full cardiac autonomic was associated with statistically significant increase in LV contractility (12 ± 3 vs. 15 ± 4 mmHg/s/µl, p=0.046), but the magnitude of which may be of limited functional relevance. The results of this study provide evidence of a sympathetically mediated cardio-contractile arm of the baroreflex in anesthetized rats.
Item Metadata
Title |
Evidence of a sympathetically mediated cardio-contractile arm of the baroreflex in anesthetized rats
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Creator | |
Supervisor | |
Publisher |
University of British Columbia
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Date Issued |
2022
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Description |
Contemporary discussion of the baroreflex includes the efferent vascular-sympathetic and cardio-vagal arms. Because sympathetic pre/post-ganglionic neurons innervate the LV, however, the heart may also undergo sympathetically mediated increases in cardiac contractility during baroreceptor unloading, but this has not been adequately investigated using a load-independent index of contractility. We aimed to a) determine whether left-ventricular (LV) contractility increases in response to baroreceptor unloading, and b) parse out whether the increase in contractility is mediated via the sympathetic or parasympathetic nervous system. 10 male rats were anesthetized (1.9 ± 0.4 g/kg urethane) and instrumented with arterial and LV pressure-volume catheters to measure mean arterial pressure (MAP) and contractility [maximal rate of pressure normalized to end-diastolic volume (dP/dtmax–EDV mmHg/s/µl)], respectively, and placed in a servo-controlled lower-body negative pressure (LBNP) chamber to reduce MAP by 10% to mechanically unload baroreceptors. LBNP was repeated in each animal following infusions of esmolol (beta-blocker which blocks cardiac sympathetic transmission), atropine (blocks cardiac parasympathetic transmission), and esmolol + atropine (full cardiac autonomic blockade). Under control conditions, dP/dtmax–EDV increased during baroreceptor unloading (26 ± 6 vs 31 ± 9 mmHg/s/µl, p=0.031) Blocking cardiac sympathetic transmission abolished this response (11 ± 2 vs. 12 ± 2 mmHg/s/µl, p=0.125). In contrast, contractility increased during baroreceptor unloading when blocking cardiac parasympathetic transmission (26 ± 6 vs. 31 ± 9 mmHg/s/µl, p=0.019), suggesting sympathetic activation, not parasympathetic withdrawal, is the key regulator of the contractile response to baroreceptor unloading. Full cardiac autonomic was associated with statistically significant increase in LV contractility (12 ± 3 vs. 15 ± 4 mmHg/s/µl, p=0.046), but the magnitude of which may be of limited functional relevance. The results of this study provide evidence of a sympathetically mediated cardio-contractile arm of the baroreflex in anesthetized rats.
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Genre | |
Type | |
Language |
eng
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Date Available |
2022-08-24
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Provider |
Vancouver : University of British Columbia Library
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Rights |
Attribution-NonCommercial-NoDerivatives 4.0 International
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DOI |
10.14288/1.0417539
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URI | |
Degree | |
Program | |
Affiliation | |
Degree Grantor |
University of British Columbia
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Graduation Date |
2022-11
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Campus | |
Scholarly Level |
Graduate
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Rights
Attribution-NonCommercial-NoDerivatives 4.0 International