Sympathetic withdrawal and forearm vasodilation during vasovagal syncope in humans
Niki M. Dietz, John R. Halliwill, John M. Spielmann, Lori A. Lawler, Bettina G. Papouchado, Tamara J. Eickhoff, and Michael J. Joyner Departments of Anesthesiology and of Physiology and Biophysics, Mayo Clinic and Foundation, Rochester, Minnesota 55905 Received 15 August 1996; accepted in final form...
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| creator | Dietz, Niki M Halliwill, John R Spielmann, John M Lawler, Lori A Papouchado, Bettina G Eickhoff, Tamara J Joyner, Michael J |
| description | Niki M.
Dietz,
John R.
Halliwill,
John M.
Spielmann,
Lori A.
Lawler,
Bettina G.
Papouchado,
Tamara J.
Eickhoff, and
Michael J.
Joyner
Departments of Anesthesiology and of Physiology and Biophysics,
Mayo Clinic and Foundation, Rochester, Minnesota 55905
Received 15 August 1996; accepted in final form 5 February 1997.
Dietz, Niki M., John R. Halliwill, John M. Spielmann, Lori
A. Lawler, Bettina G. Papouchado, Tamara J. Eickhoff, and Michael J. Joyner. Sympathetic withdrawal and forearm vasodilation during
vasovagal syncope in humans. J. Appl.
Physiol. 82(6): 1785-1793, 1997. Our aim was to
determine whether sympathetic withdrawal alone can account for the
profound forearm vasodilation that occurs during syncope in humans. We
also determined whether either vasodilating 2 -adrenergic receptors or
nitric oxide (NO) contributes to this dilation. Forearm blood flow was
measured bilaterally in healthy volunteers
( n = 10) by using plethysmography
during two bouts of graded lower body negative pressure (LBNP) to
syncope. In one forearm, drugs were infused via a brachial artery
catheter while the other forearm served as a control. In the control
arm, forearm vascular resistance (FVR) increased from 77 ± 7 units
at baseline to 191 ± 36 units with 40 mmHg of LBNP
( P |
| doi_str_mv | 10.1152/jappl.1997.82.6.1785 |
| format | Article |
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Dietz,
John R.
Halliwill,
John M.
Spielmann,
Lori A.
Lawler,
Bettina G.
Papouchado,
Tamara J.
Eickhoff, and
Michael J.
Joyner
Departments of Anesthesiology and of Physiology and Biophysics,
Mayo Clinic and Foundation, Rochester, Minnesota 55905
Received 15 August 1996; accepted in final form 5 February 1997.
Dietz, Niki M., John R. Halliwill, John M. Spielmann, Lori
A. Lawler, Bettina G. Papouchado, Tamara J. Eickhoff, and Michael J. Joyner. Sympathetic withdrawal and forearm vasodilation during
vasovagal syncope in humans. J. Appl.
Physiol. 82(6): 1785-1793, 1997. Our aim was to
determine whether sympathetic withdrawal alone can account for the
profound forearm vasodilation that occurs during syncope in humans. We
also determined whether either vasodilating 2 -adrenergic receptors or
nitric oxide (NO) contributes to this dilation. Forearm blood flow was
measured bilaterally in healthy volunteers
( n = 10) by using plethysmography
during two bouts of graded lower body negative pressure (LBNP) to
syncope. In one forearm, drugs were infused via a brachial artery
catheter while the other forearm served as a control. In the control
arm, forearm vascular resistance (FVR) increased from 77 ± 7 units
at baseline to 191 ± 36 units with 40 mmHg of LBNP
( P < 0.05). Mean arterial pressure
fell from 94 ± 2 to 47 ± 4 mmHg just before syncope, and all
subjects demonstrated sudden bradycardia at the time of syncope. At the
onset of syncope, there was sudden vasodilation and FVR fell to 26 ± 6 units ( P < 0.05 vs. baseline). When the experimental forearm was treated with
bretylium, phentolamine, and propranolol, baseline FVR fell to 26 ± 2 units, the vasoconstriction during LBNP was absent, and FVR fell
further to 16 ± 1 units at syncope
( P < 0.05 vs. baseline). During the
second trial of LBNP, mean arterial pressure again fell to 47 ± 4 mmHg and bradycardia was again observed. Treatment of the experimental
forearm with the NO synthase inhibitor
N G -monomethyl- L -arginine in addition
to bretylium, phentolamine, and propranolol significantly increased
baseline FVR to 65 ± 5 units but did not prevent the marked forearm
vasodilation during syncope (FVR = 24 ± 4 vs. 29 ± 8 units in
the control forearm). These data suggest that the profound vasodilation
observed in the human forearm during syncope is not mediated solely by
sympathetic withdrawal and also suggest that neither
2 -adrenergic-receptor-mediated vasodilation nor NO is essential to observe this response.
nitric oxide; 2 -adrenergic
receptors; humans
0161-7567/97 $5.00
Copyright © 1997 the American Physiological Society</description><identifier>ISSN: 8750-7587</identifier><identifier>EISSN: 1522-1601</identifier><identifier>DOI: 10.1152/jappl.1997.82.6.1785</identifier><identifier>PMID: 9173942</identifier><identifier>CODEN: JAPHEV</identifier><language>eng</language><publisher>Bethesda, MD: Am Physiological Soc</publisher><subject>Acetylcholine - pharmacology ; Adult ; Biological and medical sciences ; Blood Pressure ; Female ; Forearm - blood supply ; Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy ; Heart Rate ; Humans ; Male ; Medical sciences ; Nervous system (semeiology, syndromes) ; Neurology ; Nitroprusside - pharmacology ; Posture ; Skin - blood supply ; Space life sciences ; Stress, Physiological - physiopathology ; Sympathetic Nervous System - physiopathology ; Syncope, Vasovagal - physiopathology ; Vasodilation - drug effects ; Vasodilator Agents - pharmacology</subject><ispartof>Journal of applied physiology (1985), 1997-06, Vol.82 (6), p.1785-1793</ispartof><rights>1997 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c475t-cbd45b796913e551474a18bc1ac5eca27fe2604e7c839a3b961bef7a1e1694c53</citedby><cites>FETCH-LOGICAL-c475t-cbd45b796913e551474a18bc1ac5eca27fe2604e7c839a3b961bef7a1e1694c53</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,3025,27903,27904</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=2704935$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9173942$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Dietz, Niki M</creatorcontrib><creatorcontrib>Halliwill, John R</creatorcontrib><creatorcontrib>Spielmann, John M</creatorcontrib><creatorcontrib>Lawler, Lori A</creatorcontrib><creatorcontrib>Papouchado, Bettina G</creatorcontrib><creatorcontrib>Eickhoff, Tamara J</creatorcontrib><creatorcontrib>Joyner, Michael J</creatorcontrib><title>Sympathetic withdrawal and forearm vasodilation during vasovagal syncope in humans</title><title>Journal of applied physiology (1985)</title><addtitle>J Appl Physiol (1985)</addtitle><description>Niki M.
Dietz,
John R.
Halliwill,
John M.
Spielmann,
Lori A.
Lawler,
Bettina G.
Papouchado,
Tamara J.
Eickhoff, and
Michael J.
Joyner
Departments of Anesthesiology and of Physiology and Biophysics,
Mayo Clinic and Foundation, Rochester, Minnesota 55905
Received 15 August 1996; accepted in final form 5 February 1997.
Dietz, Niki M., John R. Halliwill, John M. Spielmann, Lori
A. Lawler, Bettina G. Papouchado, Tamara J. Eickhoff, and Michael J. Joyner. Sympathetic withdrawal and forearm vasodilation during
vasovagal syncope in humans. J. Appl.
Physiol. 82(6): 1785-1793, 1997. Our aim was to
determine whether sympathetic withdrawal alone can account for the
profound forearm vasodilation that occurs during syncope in humans. We
also determined whether either vasodilating 2 -adrenergic receptors or
nitric oxide (NO) contributes to this dilation. Forearm blood flow was
measured bilaterally in healthy volunteers
( n = 10) by using plethysmography
during two bouts of graded lower body negative pressure (LBNP) to
syncope. In one forearm, drugs were infused via a brachial artery
catheter while the other forearm served as a control. In the control
arm, forearm vascular resistance (FVR) increased from 77 ± 7 units
at baseline to 191 ± 36 units with 40 mmHg of LBNP
( P < 0.05). Mean arterial pressure
fell from 94 ± 2 to 47 ± 4 mmHg just before syncope, and all
subjects demonstrated sudden bradycardia at the time of syncope. At the
onset of syncope, there was sudden vasodilation and FVR fell to 26 ± 6 units ( P < 0.05 vs. baseline). When the experimental forearm was treated with
bretylium, phentolamine, and propranolol, baseline FVR fell to 26 ± 2 units, the vasoconstriction during LBNP was absent, and FVR fell
further to 16 ± 1 units at syncope
( P < 0.05 vs. baseline). During the
second trial of LBNP, mean arterial pressure again fell to 47 ± 4 mmHg and bradycardia was again observed. Treatment of the experimental
forearm with the NO synthase inhibitor
N G -monomethyl- L -arginine in addition
to bretylium, phentolamine, and propranolol significantly increased
baseline FVR to 65 ± 5 units but did not prevent the marked forearm
vasodilation during syncope (FVR = 24 ± 4 vs. 29 ± 8 units in
the control forearm). These data suggest that the profound vasodilation
observed in the human forearm during syncope is not mediated solely by
sympathetic withdrawal and also suggest that neither
2 -adrenergic-receptor-mediated vasodilation nor NO is essential to observe this response.
nitric oxide; 2 -adrenergic
receptors; humans
0161-7567/97 $5.00
Copyright © 1997 the American Physiological Society</description><subject>Acetylcholine - pharmacology</subject><subject>Adult</subject><subject>Biological and medical sciences</subject><subject>Blood Pressure</subject><subject>Female</subject><subject>Forearm - blood supply</subject><subject>Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy</subject><subject>Heart Rate</subject><subject>Humans</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Nervous system (semeiology, syndromes)</subject><subject>Neurology</subject><subject>Nitroprusside - pharmacology</subject><subject>Posture</subject><subject>Skin - blood supply</subject><subject>Space life sciences</subject><subject>Stress, Physiological - physiopathology</subject><subject>Sympathetic Nervous System - physiopathology</subject><subject>Syncope, Vasovagal - physiopathology</subject><subject>Vasodilation - drug effects</subject><subject>Vasodilator Agents - pharmacology</subject><issn>8750-7587</issn><issn>1522-1601</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1997</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kEGL1TAUhYMo43P0Hyh0ITKb1t40aZqlDDOjMCDouA63afqaIW1q0s6z_9523uOBC1eBnO-cCx8h7yHPADj9_Ijj6DKQUmQVzcoMRMVfkN0a0RTKHF6SXSV4ngpeidfkTYyPeQ6McbggFxJEIRndkR8_l37EqTOT1cnBTl0T8IAuwaFJWh8Mhj55wugb63CyfkiaOdhh__z3hPuVjMug_WgSOyTd3OMQ35JXLbpo3p3eS_Lr9ubh-mt6__3u2_WX-1QzwadU1w3jtZClhMJwDkwwhKrWgJobjVS0hpY5M0JXhcSiliXUphUIBkrJNC8uyafj7hj879nESfU2auMcDsbPUQkJecFpuYLsCOrgYwymVWOwPYZFQa42lepZpdpUqoqqUm0q19qH0_5c96Y5l07u1vzjKceo0bUBB23jGaMiZ7LYZq6OWGf33cEGo8ZuidY7v1-2w_9cZP9Hb2fnHsyfaeucK2ps2uIvLrigdQ</recordid><startdate>19970601</startdate><enddate>19970601</enddate><creator>Dietz, Niki M</creator><creator>Halliwill, John R</creator><creator>Spielmann, John M</creator><creator>Lawler, Lori A</creator><creator>Papouchado, Bettina G</creator><creator>Eickhoff, Tamara J</creator><creator>Joyner, Michael J</creator><general>Am Physiological Soc</general><general>American Physiological Society</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>19970601</creationdate><title>Sympathetic withdrawal and forearm vasodilation during vasovagal syncope in humans</title><author>Dietz, Niki M ; Halliwill, John R ; Spielmann, John M ; Lawler, Lori A ; Papouchado, Bettina G ; Eickhoff, Tamara J ; Joyner, Michael J</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c475t-cbd45b796913e551474a18bc1ac5eca27fe2604e7c839a3b961bef7a1e1694c53</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1997</creationdate><topic>Acetylcholine - pharmacology</topic><topic>Adult</topic><topic>Biological and medical sciences</topic><topic>Blood Pressure</topic><topic>Female</topic><topic>Forearm - blood supply</topic><topic>Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy</topic><topic>Heart Rate</topic><topic>Humans</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Nervous system (semeiology, syndromes)</topic><topic>Neurology</topic><topic>Nitroprusside - pharmacology</topic><topic>Posture</topic><topic>Skin - blood supply</topic><topic>Space life sciences</topic><topic>Stress, Physiological - physiopathology</topic><topic>Sympathetic Nervous System - physiopathology</topic><topic>Syncope, Vasovagal - physiopathology</topic><topic>Vasodilation - drug effects</topic><topic>Vasodilator Agents - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Dietz, Niki M</creatorcontrib><creatorcontrib>Halliwill, John R</creatorcontrib><creatorcontrib>Spielmann, John M</creatorcontrib><creatorcontrib>Lawler, Lori A</creatorcontrib><creatorcontrib>Papouchado, Bettina G</creatorcontrib><creatorcontrib>Eickhoff, Tamara J</creatorcontrib><creatorcontrib>Joyner, Michael J</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Journal of applied physiology (1985)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Dietz, Niki M</au><au>Halliwill, John R</au><au>Spielmann, John M</au><au>Lawler, Lori A</au><au>Papouchado, Bettina G</au><au>Eickhoff, Tamara J</au><au>Joyner, Michael J</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Sympathetic withdrawal and forearm vasodilation during vasovagal syncope in humans</atitle><jtitle>Journal of applied physiology (1985)</jtitle><addtitle>J Appl Physiol (1985)</addtitle><date>1997-06-01</date><risdate>1997</risdate><volume>82</volume><issue>6</issue><spage>1785</spage><epage>1793</epage><pages>1785-1793</pages><issn>8750-7587</issn><eissn>1522-1601</eissn><coden>JAPHEV</coden><abstract>Niki M.
Dietz,
John R.
Halliwill,
John M.
Spielmann,
Lori A.
Lawler,
Bettina G.
Papouchado,
Tamara J.
Eickhoff, and
Michael J.
Joyner
Departments of Anesthesiology and of Physiology and Biophysics,
Mayo Clinic and Foundation, Rochester, Minnesota 55905
Received 15 August 1996; accepted in final form 5 February 1997.
Dietz, Niki M., John R. Halliwill, John M. Spielmann, Lori
A. Lawler, Bettina G. Papouchado, Tamara J. Eickhoff, and Michael J. Joyner. Sympathetic withdrawal and forearm vasodilation during
vasovagal syncope in humans. J. Appl.
Physiol. 82(6): 1785-1793, 1997. Our aim was to
determine whether sympathetic withdrawal alone can account for the
profound forearm vasodilation that occurs during syncope in humans. We
also determined whether either vasodilating 2 -adrenergic receptors or
nitric oxide (NO) contributes to this dilation. Forearm blood flow was
measured bilaterally in healthy volunteers
( n = 10) by using plethysmography
during two bouts of graded lower body negative pressure (LBNP) to
syncope. In one forearm, drugs were infused via a brachial artery
catheter while the other forearm served as a control. In the control
arm, forearm vascular resistance (FVR) increased from 77 ± 7 units
at baseline to 191 ± 36 units with 40 mmHg of LBNP
( P < 0.05). Mean arterial pressure
fell from 94 ± 2 to 47 ± 4 mmHg just before syncope, and all
subjects demonstrated sudden bradycardia at the time of syncope. At the
onset of syncope, there was sudden vasodilation and FVR fell to 26 ± 6 units ( P < 0.05 vs. baseline). When the experimental forearm was treated with
bretylium, phentolamine, and propranolol, baseline FVR fell to 26 ± 2 units, the vasoconstriction during LBNP was absent, and FVR fell
further to 16 ± 1 units at syncope
( P < 0.05 vs. baseline). During the
second trial of LBNP, mean arterial pressure again fell to 47 ± 4 mmHg and bradycardia was again observed. Treatment of the experimental
forearm with the NO synthase inhibitor
N G -monomethyl- L -arginine in addition
to bretylium, phentolamine, and propranolol significantly increased
baseline FVR to 65 ± 5 units but did not prevent the marked forearm
vasodilation during syncope (FVR = 24 ± 4 vs. 29 ± 8 units in
the control forearm). These data suggest that the profound vasodilation
observed in the human forearm during syncope is not mediated solely by
sympathetic withdrawal and also suggest that neither
2 -adrenergic-receptor-mediated vasodilation nor NO is essential to observe this response.
nitric oxide; 2 -adrenergic
receptors; humans
0161-7567/97 $5.00
Copyright © 1997 the American Physiological Society</abstract><cop>Bethesda, MD</cop><pub>Am Physiological Soc</pub><pmid>9173942</pmid><doi>10.1152/jappl.1997.82.6.1785</doi><tpages>9</tpages></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 8750-7587 |
| ispartof | Journal of applied physiology (1985), 1997-06, Vol.82 (6), p.1785-1793 |
| issn | 8750-7587 1522-1601 |
| language | eng |
| recordid | cdi_proquest_miscellaneous_79103526 |
| source | MEDLINE; American Physiological Society Paid; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | Acetylcholine - pharmacology Adult Biological and medical sciences Blood Pressure Female Forearm - blood supply Headache. Facial pains. Syncopes. Epilepsia. Intracranial hypertension. Brain oedema. Cerebral palsy Heart Rate Humans Male Medical sciences Nervous system (semeiology, syndromes) Neurology Nitroprusside - pharmacology Posture Skin - blood supply Space life sciences Stress, Physiological - physiopathology Sympathetic Nervous System - physiopathology Syncope, Vasovagal - physiopathology Vasodilation - drug effects Vasodilator Agents - pharmacology |
| title | Sympathetic withdrawal and forearm vasodilation during vasovagal syncope in humans |
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