Baroreflex Mediated Autonomic Modulation by Acute Pain and Orthostatic Stress

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dc.contributor.advisorJames Caffrey
dc.contributor.committeeMemberJoan Carroll
dc.contributor.committeeMemberRobert Mallet
dc.creatorRaven, Joseph Simon
dc.date.accessioned2019-08-22T21:30:32Z
dc.date.available2019-08-22T21:30:32Z
dc.date.issued2008-10-01
dc.date.submitted2013-09-30T06:24:05-07:00
dc.description.abstractRaven, Joseph Simon, Baroreflex Mediated Autonomic Modulation by Acute Pain and Orthostatic Stress. Doctor of Philosophy (Integrative Physiology), October 2008, 147 pp.; 23 figures; bibliography; 123 titles. Nociceptive and baroreceptor afferent neurons are implicated as the components responsible for carotid baroreceptor reflex (CBR) resetting. The purpose of this dissertation was to identify the effect of cold induced pain, and cardiopulmonary baroreceptor (CPBR) unloading accompanied by pain, on CBR resetting. First, the relationships between cold induced pain to cardiovascular responses, pain perception, and muscle sympathetic nerve activity (MSNA) were investigated. Questions were addressed through use of the cold pressor test (CPT), finger plethysmography, and microneurography. This study demonstrated perceived pain, MSNA, and blood pressure responses to a cold stimulus were reproducible. Furthermore, graded responses observed in mean arterial pressure (MAP) and MSNA directly correlated to the intensity of the pain stimulus. The next study examined cold induced pain on CBR gain and operational point resetting in healthy normotensive subjects. Using similar experimental methodologies to the previous study, the data demonstrated acute pain shifted the CBR operational point toward the lower limiting value of MSNA. These data also confirmed an upward-rightward shift and increased gain of the CBR function curve during pain. Finally, CBR gain and operational point resetting during simultaneous CPBR unloading and cold induced pain in healthy normotensive subjects was addressed. Using the previous experimental paradigm, this investigation revealed CPBR unloading during acute pain did not abolish the shift of the CBR operational point. Thus, the capacity for hypotensive buffering remained enhanced. This study also determined CPBR unloading during acute pain produced higher prevailing blood pressures compared to periods of CPBR unloading alone. In summary: 1)MSNA and cardiovascular responses were tightly coupled to pain. 2) The CPT was a reliable technique for producing repeated sympathoexcitation within a subject. 3) Acute pain increased CBR gain and induced a shift of the CBR operational point. 4) The CBR operational point shift remained in the presence of CPBR unloading, which precipitated increased MAP during hypotensive stimuli. These findings suggested pain improves blood pressure maintenance during central hypovolemic stress.
dc.format.mimetypeapplication/pdf
dc.identifier.urihttps://hdl.handle.net/20.500.12503/29384
dc.language.isoen
dc.provenance.legacyDownloads0
dc.subjectCardiovascular System
dc.subjectExercise Physiology
dc.subjectKinesiology
dc.subjectLife Sciences
dc.subjectMedical Physiology
dc.subjectMedicine and Health Sciences
dc.subjectNervous System
dc.subjectPhysiological Processes
dc.subjectPhysiology
dc.subjectPsychology of Movement
dc.subjectSystems and Integrative Physiology
dc.subjectBlood pressure maintenance
dc.subjectcentral hypovolemic stress
dc.subjectmuscle sympathetic nerve activity
dc.subjectcold pressor test
dc.subjectcarotid baroreceptor reflex
dc.subjectsympathoexcitation
dc.subjectpain
dc.subjectbaroreflex mediated autonomic modulation
dc.subjectacute pain
dc.subjectorthostatic stress
dc.titleBaroreflex Mediated Autonomic Modulation by Acute Pain and Orthostatic Stress
dc.typeDissertation
dc.type.materialtext
thesis.degree.departmentGraduate School of Biomedical Sciences
thesis.degree.disciplineIntegrative Physiology
thesis.degree.grantorUniversity of North Texas Health Science Center at Fort Worth
thesis.degree.nameDoctor of Philosophy

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