Sympathetic and vascular effects of short-term passive smoke exposure in healthy nonsmokers

The physiological effects of cigarette smoking have been widely studied; however, little is known about the effects of acute exposure to sidestream smoke (passive smoking). We examined the effects of sidestream smoke on muscle sympathetic nerve activity (MSNA) and forearm vascular resistance (FVR) a...

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Veröffentlicht in:Circulation (New York, N.Y.) N.Y.), 1997-07, Vol.96 (1), p.282-287
Hauptverfasser: HAUSBERG, M, MARK, A. L, WINNIFORD, M. D, BROWN, R. E, SOMERS, V. K
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container_issue 1
container_start_page 282
container_title Circulation (New York, N.Y.)
container_volume 96
creator HAUSBERG, M
MARK, A. L
WINNIFORD, M. D
BROWN, R. E
SOMERS, V. K
description The physiological effects of cigarette smoking have been widely studied; however, little is known about the effects of acute exposure to sidestream smoke (passive smoking). We examined the effects of sidestream smoke on muscle sympathetic nerve activity (MSNA) and forearm vascular resistance (FVR) at rest and during stressful stimuli, including the cold pressor test (CPT), sustained handgrip (SHG), and mental stress (MS). In 17 healthy nonsmokers, blood pressure (BP), heart rate (HR), forearm blood flow (venous occlusion plethysmography), FVR, and MSNA (obtained through direct intraneural recordings) were measured before and during inhalation of sidestream smoke in one session (n = 16) and before and during vehicle (air) inhalation in another session (n = 17) on a separate day. The order of sessions was randomized between subjects. Responses to CPT, SHG, and MS were measured before and after inhalation of smoke or vehicle (ie, twice during each session). After 15 minutes' exposure to sidestream smoke, plasma nicotine and carboxyhemoglobin levels increased to 0.77 +/- 0.11 ng/mL and 0.36 +/- 0.04% (mean +/- SEM, P < .05), respectively. Sidestream smoke, but not vehicle inhalation, increased resting MSNA from 23 +/- 2 to 28 +/- 2 bursts/min (P < .05). FVR increased with passive smoking, but this increase was not significantly different from the change in FVR with vehicle. Plasma norepinephrine and epinephrine, BP, and HR were not changed significantly by sidestream smoke. The responses of MSNNA, BP, HR, and FVR to the stressful stimuli were not potentiated by sidestream smoke, except for an increased BP response to the CPT (P < .05). Acute short-term passive (sidestream) smoke exposure elicits a modest increase in MSNA in healthy non-smokers but does not change HR, BP, or FVR.
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L ; WINNIFORD, M. D ; BROWN, R. E ; SOMERS, V. K</creator><creatorcontrib>HAUSBERG, M ; MARK, A. L ; WINNIFORD, M. D ; BROWN, R. E ; SOMERS, V. K</creatorcontrib><description>The physiological effects of cigarette smoking have been widely studied; however, little is known about the effects of acute exposure to sidestream smoke (passive smoking). We examined the effects of sidestream smoke on muscle sympathetic nerve activity (MSNA) and forearm vascular resistance (FVR) at rest and during stressful stimuli, including the cold pressor test (CPT), sustained handgrip (SHG), and mental stress (MS). In 17 healthy nonsmokers, blood pressure (BP), heart rate (HR), forearm blood flow (venous occlusion plethysmography), FVR, and MSNA (obtained through direct intraneural recordings) were measured before and during inhalation of sidestream smoke in one session (n = 16) and before and during vehicle (air) inhalation in another session (n = 17) on a separate day. The order of sessions was randomized between subjects. Responses to CPT, SHG, and MS were measured before and after inhalation of smoke or vehicle (ie, twice during each session). After 15 minutes' exposure to sidestream smoke, plasma nicotine and carboxyhemoglobin levels increased to 0.77 +/- 0.11 ng/mL and 0.36 +/- 0.04% (mean +/- SEM, P &lt; .05), respectively. Sidestream smoke, but not vehicle inhalation, increased resting MSNA from 23 +/- 2 to 28 +/- 2 bursts/min (P &lt; .05). FVR increased with passive smoking, but this increase was not significantly different from the change in FVR with vehicle. Plasma norepinephrine and epinephrine, BP, and HR were not changed significantly by sidestream smoke. The responses of MSNNA, BP, HR, and FVR to the stressful stimuli were not potentiated by sidestream smoke, except for an increased BP response to the CPT (P &lt; .05). 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K</creatorcontrib><title>Sympathetic and vascular effects of short-term passive smoke exposure in healthy nonsmokers</title><title>Circulation (New York, N.Y.)</title><addtitle>Circulation</addtitle><description>The physiological effects of cigarette smoking have been widely studied; however, little is known about the effects of acute exposure to sidestream smoke (passive smoking). We examined the effects of sidestream smoke on muscle sympathetic nerve activity (MSNA) and forearm vascular resistance (FVR) at rest and during stressful stimuli, including the cold pressor test (CPT), sustained handgrip (SHG), and mental stress (MS). In 17 healthy nonsmokers, blood pressure (BP), heart rate (HR), forearm blood flow (venous occlusion plethysmography), FVR, and MSNA (obtained through direct intraneural recordings) were measured before and during inhalation of sidestream smoke in one session (n = 16) and before and during vehicle (air) inhalation in another session (n = 17) on a separate day. The order of sessions was randomized between subjects. Responses to CPT, SHG, and MS were measured before and after inhalation of smoke or vehicle (ie, twice during each session). After 15 minutes' exposure to sidestream smoke, plasma nicotine and carboxyhemoglobin levels increased to 0.77 +/- 0.11 ng/mL and 0.36 +/- 0.04% (mean +/- SEM, P &lt; .05), respectively. Sidestream smoke, but not vehicle inhalation, increased resting MSNA from 23 +/- 2 to 28 +/- 2 bursts/min (P &lt; .05). FVR increased with passive smoking, but this increase was not significantly different from the change in FVR with vehicle. Plasma norepinephrine and epinephrine, BP, and HR were not changed significantly by sidestream smoke. The responses of MSNNA, BP, HR, and FVR to the stressful stimuli were not potentiated by sidestream smoke, except for an increased BP response to the CPT (P &lt; .05). 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K</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-p262t-6624d2893555c9ee008f42744ff3ff9860fcb0b5f4a57b445269eef8064c3d353</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1997</creationdate><topic>Adult</topic><topic>Biological and medical sciences</topic><topic>Blood Pressure - physiology</topic><topic>Carbon Monoxide - blood</topic><topic>Electrocardiography</topic><topic>Female</topic><topic>Forearm - blood supply</topic><topic>Hand Strength - physiology</topic><topic>Heart Rate - physiology</topic><topic>Humans</topic><topic>Isometric Contraction - physiology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Mental Processes - physiology</topic><topic>Muscle, Skeletal - blood supply</topic><topic>Muscle, Skeletal - innervation</topic><topic>Nicotine - blood</topic><topic>Oxygen Consumption - physiology</topic><topic>Pressoreceptors - physiology</topic><topic>Reference Values</topic><topic>Stress, Physiological - physiopathology</topic><topic>Sympathetic Nervous System - physiopathology</topic><topic>Tobacco Smoke Pollution - adverse effects</topic><topic>Tobacco, tobacco smoking</topic><topic>Toxicology</topic><topic>Vascular Resistance - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>HAUSBERG, M</creatorcontrib><creatorcontrib>MARK, A. L</creatorcontrib><creatorcontrib>WINNIFORD, M. D</creatorcontrib><creatorcontrib>BROWN, R. E</creatorcontrib><creatorcontrib>SOMERS, V. K</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>ProQuest Health &amp; Medical Complete (Alumni)</collection><collection>Nursing &amp; Allied Health Premium</collection><jtitle>Circulation (New York, N.Y.)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>HAUSBERG, M</au><au>MARK, A. L</au><au>WINNIFORD, M. D</au><au>BROWN, R. E</au><au>SOMERS, V. K</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Sympathetic and vascular effects of short-term passive smoke exposure in healthy nonsmokers</atitle><jtitle>Circulation (New York, N.Y.)</jtitle><addtitle>Circulation</addtitle><date>1997-07-01</date><risdate>1997</risdate><volume>96</volume><issue>1</issue><spage>282</spage><epage>287</epage><pages>282-287</pages><issn>0009-7322</issn><eissn>1524-4539</eissn><coden>CIRCAZ</coden><abstract>The physiological effects of cigarette smoking have been widely studied; however, little is known about the effects of acute exposure to sidestream smoke (passive smoking). We examined the effects of sidestream smoke on muscle sympathetic nerve activity (MSNA) and forearm vascular resistance (FVR) at rest and during stressful stimuli, including the cold pressor test (CPT), sustained handgrip (SHG), and mental stress (MS). In 17 healthy nonsmokers, blood pressure (BP), heart rate (HR), forearm blood flow (venous occlusion plethysmography), FVR, and MSNA (obtained through direct intraneural recordings) were measured before and during inhalation of sidestream smoke in one session (n = 16) and before and during vehicle (air) inhalation in another session (n = 17) on a separate day. The order of sessions was randomized between subjects. Responses to CPT, SHG, and MS were measured before and after inhalation of smoke or vehicle (ie, twice during each session). After 15 minutes' exposure to sidestream smoke, plasma nicotine and carboxyhemoglobin levels increased to 0.77 +/- 0.11 ng/mL and 0.36 +/- 0.04% (mean +/- SEM, P &lt; .05), respectively. Sidestream smoke, but not vehicle inhalation, increased resting MSNA from 23 +/- 2 to 28 +/- 2 bursts/min (P &lt; .05). FVR increased with passive smoking, but this increase was not significantly different from the change in FVR with vehicle. Plasma norepinephrine and epinephrine, BP, and HR were not changed significantly by sidestream smoke. The responses of MSNNA, BP, HR, and FVR to the stressful stimuli were not potentiated by sidestream smoke, except for an increased BP response to the CPT (P &lt; .05). Acute short-term passive (sidestream) smoke exposure elicits a modest increase in MSNA in healthy non-smokers but does not change HR, BP, or FVR.</abstract><cop>Hagerstown, MD</cop><pub>Lippincott Williams &amp; Wilkins</pub><pmid>9236446</pmid><tpages>6</tpages></addata></record>
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ispartof Circulation (New York, N.Y.), 1997-07, Vol.96 (1), p.282-287
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source MEDLINE; EZB-FREE-00999 freely available EZB journals; American Heart Association; Journals@Ovid Complete
subjects Adult
Biological and medical sciences
Blood Pressure - physiology
Carbon Monoxide - blood
Electrocardiography
Female
Forearm - blood supply
Hand Strength - physiology
Heart Rate - physiology
Humans
Isometric Contraction - physiology
Male
Medical sciences
Mental Processes - physiology
Muscle, Skeletal - blood supply
Muscle, Skeletal - innervation
Nicotine - blood
Oxygen Consumption - physiology
Pressoreceptors - physiology
Reference Values
Stress, Physiological - physiopathology
Sympathetic Nervous System - physiopathology
Tobacco Smoke Pollution - adverse effects
Tobacco, tobacco smoking
Toxicology
Vascular Resistance - physiology
title Sympathetic and vascular effects of short-term passive smoke exposure in healthy nonsmokers
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