Browsing by Subject "mean arterial pressure"
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Item Effects of Endurance Training on Aortic and Carotid Baroreflex Function(1999-06-01) Smith, Scott Alan; Peter B. Raven; Michael Smith; Patricia A. GwirtzSmith, Scott Alan, Effects of Endurance Training on Aortic and Carotid Baroreflex Function. Doctor of Philosophy (Biomedical Sciences), June 1999; 122 pp; 8 tables; 10 figures; bibliography, 148 titles. Arterial bareflex control of cardiac function is dependent upon afferent input from both the aortic arch and carotid sinus bareceptors. Extensive research in animals has generated conflicting results as to the range of arterial pressures over which each baroreflex operates. Further, the complex integration of afferent signals within the medullary cardiovascular center, in reference to aortic and carotid baroreceptor input, has been characterized as additive, inhibitory, and facilitatory in nature. Such reports make it difficult to draw definitive conclusions about the behavior or central neural processing within the brainstem. In addition, these relationships have yet to be examined in humans. Therefore, the purpose of the investigations described herein, was to quantify the range of pressures over which the arterial aortic and carotid baroreflexes operate as well as to describe the interactive relationship between the aortic and carotid baroreceptors. In order to investigate these questions, we isolated the arterial, aortic, and carotid-cardiac baroreflexes in volunteer subjects generating sigmoidal stimulus-response curves for each reflex arc. Arterial and aortic baroreflex (ABR) control of heart rate (HR) was assessed by inducing graded increases and decreases in mean arterial pressure (MAP) by bolus infusion of the vasoactive agents phenylephrine (PE) and sodium nitroprusside (SN), respectively. Carotid baroreflex (CBR) function was determined utilizing ramped five second pulses of both pressure and suction applied to the carotid sinus via a neck chamber collar, independent of drug administration. The MAP at which the threshold and saturation were elicited did not differ among the reflexes examined indicating each reflex operated over a similar range of arterial pressures. Further, the simple sum of the independently driven HR response ranges of the CBR and ABR was significantly greater than that produced when both baroreceptor populations were concomitantly stimulated (i.e. arterial baroreflex) suggesting an inhibitory interaction. To investigate differential baroreflex control of HR in response to chronic endurance exercise training, a second investigation was designed implementing the reflex isolation techniques described previously. Stimulus-response relationships were compared between high fit (maximal oxygen uptake, VO2max [greater than] 60ml˖kg-1˖min-1) and average fit (VO2maxml˖kg-1˖min-1) individuals. Interestingly, neither the range of operating pressures for each reflex nor the integrative relationship between the ABR and CBR were altered as a result of aerobic training. However, the HR response range elicited from the aortic baroreceptors as a result of hypotensive and hypertensive insult was markedly attenuated in the aerobically trained population compared to their sedentary counterparts, exclusively causing a requisite reduction in arterial baroreflex sensitivity.Item Influence of the Carotid Baroreflex on Cerebral Blood Flow During Seated Upright Rest(2007-07-01) Eubank, Wendy L.; Peter B. Raven; Robert Mallet; James CaffreyEubank, Wendy L., Influence of Carotid Baroreflex on Cerebral Blood Flow During Seated Upright Rest. Master of Science (Integrative Physiology), July, 2007, 25 pp., 1 table, 4 illustrations, 34 references. This study tested the hypothesis that sympathetic activation via the carotid baroreflex directly influences cerebral vasomotion during seated upright test. This study also examined the effects of pulsatile neck pressure (NP) and neck suction (NS) during seated upright rest in healthy human subjects. Changes in mean arterial pressure (MAP) and mean middle cerebral arterial velocity (MCA V mean), were measured. The power spectral density (PSD) of MAP of 0.1Hz increased during pulsatile NP and NS. The PSD of MCA V mean at 0.1Hz was much greater during NP than that of NS. There were no significant differences between end-tidal CO2 between each condition. These findings suggest that cerebral vasoconstriction during NP was a result of the autoregulatory response to the NP mediated pulsatile changes in arterial pressure and the NP induced sympathetically mediated vasoconstriction.Item Neural Control of the Carotid Baroreflex During Exercise(2000-05-01) Gallagher, Kevin Matthew; Peter B. Raven; Stephen R. Grant; H. Fred DowneyGallagher, Kevin Matthew, Neural Control of the Carotid Baroreflex During Exercise. Doctor of Osteopathic Medicine/Doctor of Philosophy (Biomedical Sciences), May 2000; 151 pages; 13 tables; 19 figures; bibliography; 161 titles. Carotid baroreflex (CBR) function is reset upward and rightward to the prevailing blood pressure during dynamic and static exercise. Feedforward central neural inputs (central command) and negative feedback from skeletal muscle (exercise pressor reflex) both contribute to the resetting. The purpose of this investigation was to identify the individual roles of central command and the exercise pressor reflex in the resetting of the CBR during dynamic and static exercise. First, it was necessary to determine which receptor group that comprises the exercise pressor reflex, chemically-sensitive (chemoreceptors) or mechanically-sensitive (mechanoreceptors) receptors, was primarily involved in the regulation of the cardiovascular system. We observed the cardiovascular responses during exercise to individual action of the chemoreceptors and the mechanoreceptors. We demonstrated an increased mean arterial pressure (MAP) response to mechanoreceptor activation that was not identified during chemoreceptor stimulation. This finding suggested that the mechanoreflex was the primary exercise pressor mediated of arterial blood pressure during exercise. To identify the role of central command on CBR resetting, a second investigation increased central command by partial neuromuscular blockade during dynamic and static exercise. Resetting of CBR control of heart rate (carotid-cardiac; CSP-HR) and MAP (carodtid-vasomotor; CSP-MAP) during control exercise was further reset upward and rightward by increased central command without alterations in sensitivity. In conclusion, central command, a feedforward mechanism, was actively involved in the resetting of the CBR during exercise. To investigate the role of the exercise pressor reflex on CBR function, a third investigation activated by the exercise pressor reflex with the application of medical anti-shock trousers (MAS) during dynamic and static exercise. From control exercise, carotid-vasomotor function was further reset upward and rightward by the application of MAS trousers while CSP-HR function was only reset rightward. Sensitivity of the CSP-MAP and CSP-HR function curves were unaltered. The negative feedback mechanism of exercise pressor reflex, primarily mediated by mechanoreceptors, appeared to act as a modulator of CBR resetting during exercise.Item Resetting of the Carotid Arterial Baroreflex during Dynamic Exercise(1997-08-01) Bryant, Kristin Hannah Norton; Peter B. Raven; James Caffrey; Thomas YorioByrant, Kristin, Resetting of the Carotid Arterial Baroreflex during Dynamic Exercise Doctor of Philosophy (Biomedical Sciences), August, 1997; 121 pp; 8 tables; 20 figures, bibliography, 82 titles. Following the initial response to the onset of dynamic exercise, prolonged exercise at a constant workload is characterized by a progressive decrease in stroke volume (SV) and mean arterial pressure (MAP) and concomitant rise in heart rate (HR). These data raise the question as to whether there is a loss of baroreflex regulation of arterial blood pressure during prolonged dynamic exercise. However, we propose that the carotid barareflex (CBR) is continually reset during prolonged exercise, with the operating point being shifted toward the reflex threshold, in relation to a progressive increase in central command activity as motor fibers are recruited in response to muscle fatigue. Therefore, the baroreflex is unresponsive to the fall in MAP. In order to investigate the hypothesis, volunteer subjects performed one hour of dynamic leg cycling exercise at 65% of maximal oxygen uptake (VO2max) with: I) no intervention; and ii) maintenance of cardiac filling volume via continuous infusion of a 6% dextran in saline solution to counteract the fall in SV. At 10 and 50 minutes of exercise, CBR stimulous-response curves were generated using the neck pressure/neck suction technique. The maintenance of cardiac filling volume and thus SV resulted in a diminished drift in MAP. However, indices of central command such as HR, VO2 and ratings of perceived exertion (RPE) increased to the same extent regardless of exercise condition. Furthermore, there was augmented resetting of the CBR at 50 minutes of exercise as compared to 10 minutes under both exercise conditions. In order to further investigate the effects of central command on baroreflex control of blood pressure, a second investigation was designed to demonstrate the effects of exercise type and intensity on CBR function. Stimulus-response relationships were compared during dynamic exercise at a wide range of exercise intensities performed with either leg exercise alone or leg exercise combined with arm exercise. Increases in exercise intensity to maximal exercise resulted in increases in indices of central command such as HR and VO2 as well as an augmentation of the magnitude of the lateral shift in the CBR stimulus-response curve (with the operating point being shifted further toward the threshold of the reflex) relative to the activation of central command. In addition, the performance of combined arm and leg exercise elicited an augmented shift in the carotid-vasomotor stimulus-response relationship as compared to leg exercise alone at the same exercise intensity. As arm exercise compared to leg exercise performed at the same absolute VO2 results in an increased lactate accumulation in the venous system, the augmented resetting of the CBR is likely due to a disproportionate activation of the muscle metaboreflex component of the muscle pressor reflex. Therefore we propose that the central command is the primary mechanism by which the CBR is reset at the onset of dynamic exercise through feed-forward control. However, additional, feed-back modulation can be exerted by the muscle pressor reflex upon the development of mechanical or chemical error signals in the exercising muscle.