Intracerebroventricular propranolol prevented vascular resistance increases on arousal from sleep apnea

Sophia Zinkovska and Debra A. Kirby Children's Hospital, Harvard Medical School, Boston 02115; and Veterans Affairs Medical Center, West Roxbury, Massachusetts 02132 Received 19 July 1995; accepted in final form 19 November 1996. Zinkovska, Sophia, and Debra A. Kirby. Intracerebroventricular pr...

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Veröffentlicht in:Journal of applied physiology (1985) 1997-05, Vol.82 (5), p.1637-1643
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description Sophia Zinkovska and Debra A. Kirby Children's Hospital, Harvard Medical School, Boston 02115; and Veterans Affairs Medical Center, West Roxbury, Massachusetts 02132 Received 19 July 1995; accepted in final form 19 November 1996. Zinkovska, Sophia, and Debra A. Kirby. Intracerebroventricular propranolol prevented vascular resistance increases on arousal from sleep apnea. J. Appl. Physiol. 82(5): 1637-1643, 1997. Despite the increased risk of sudden cardiac death associated with sleep apnea, little is known about mechanisms controlling cardiovascular responses to sleep apnea and arousal. Chronically instrumented pigs were used to investigate the effects of airway obstruction (AO) during rapid-eye-movement (REM) and non-REM (NREM) sleep and arousal on mean arterial pressure (MAP), heart rate (HR), cardiac output (CO), and total peripheral resistance (TPR). A stainless steel cannula was implanted in the lateral cerebral ventricle. During REM sleep, HR was 133 ± 10 beats/min, MAP was 65 ± 3 mmHg, CO was 1,435 ± 69 ml/min, and TPR was 0.046 ± 0.004 mmHg · ml 1 · min. During AO, CO decreased by 90 ± 17 ml/min ( P  
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Kirby Children's Hospital, Harvard Medical School, Boston 02115; and Veterans Affairs Medical Center, West Roxbury, Massachusetts 02132 Received 19 July 1995; accepted in final form 19 November 1996. Zinkovska, Sophia, and Debra A. Kirby. Intracerebroventricular propranolol prevented vascular resistance increases on arousal from sleep apnea. J. Appl. Physiol. 82(5): 1637-1643, 1997. Despite the increased risk of sudden cardiac death associated with sleep apnea, little is known about mechanisms controlling cardiovascular responses to sleep apnea and arousal. Chronically instrumented pigs were used to investigate the effects of airway obstruction (AO) during rapid-eye-movement (REM) and non-REM (NREM) sleep and arousal on mean arterial pressure (MAP), heart rate (HR), cardiac output (CO), and total peripheral resistance (TPR). A stainless steel cannula was implanted in the lateral cerebral ventricle. During REM sleep, HR was 133 ± 10 beats/min, MAP was 65 ± 3 mmHg, CO was 1,435 ± 69 ml/min, and TPR was 0.046 ± 0.004 mmHg · ml 1 · min. During AO, CO decreased by 90 ± 17 ml/min ( P  &lt; 0.05). On arousal from AO, MAP increased by 15 ± 3 mmHg, HR increased by 10 ± 3 beats/min, and TPR increased by 0.008 ± 0.001 mmHg · ml 1 · min (all P  &lt; 0.05). Changes during NREM were similar but were more modest during AO. After the intracerebroventricular administration of propranolol (50 µg/kg; a -adrenoreceptor blocking agent), decreases in CO during AO and increases in HR during arousal were intact, but increases in MAP and TPR were no longer significant. 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Stomatology ; Propranolol - pharmacology ; Receptors, Adrenergic, beta - physiology ; Sleep Apnea Syndromes - physiopathology ; Sleep, REM - physiology ; Swine ; Upper respiratory tract, upper alimentary tract, paranasal sinuses, salivary glands: diseases, semeiology ; Vascular Resistance - drug effects ; Vasodilator Agents - pharmacology</subject><ispartof>Journal of applied physiology (1985), 1997-05, Vol.82 (5), p.1637-1643</ispartof><rights>1997 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c455t-e558db165de3c692a49814d1effc758bcd0ad86034ba52a74de97e48dddd9e0f3</citedby><cites>FETCH-LOGICAL-c455t-e558db165de3c692a49814d1effc758bcd0ad86034ba52a74de97e48dddd9e0f3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,3039,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&amp;idt=2670079$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9134914$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Zinkovska, Sophia</creatorcontrib><creatorcontrib>Kirby, Debra A</creatorcontrib><title>Intracerebroventricular propranolol prevented vascular resistance increases on arousal from sleep apnea</title><title>Journal of applied physiology (1985)</title><addtitle>J Appl Physiol (1985)</addtitle><description>Sophia Zinkovska and Debra A. Kirby Children's Hospital, Harvard Medical School, Boston 02115; and Veterans Affairs Medical Center, West Roxbury, Massachusetts 02132 Received 19 July 1995; accepted in final form 19 November 1996. Zinkovska, Sophia, and Debra A. Kirby. Intracerebroventricular propranolol prevented vascular resistance increases on arousal from sleep apnea. J. Appl. Physiol. 82(5): 1637-1643, 1997. Despite the increased risk of sudden cardiac death associated with sleep apnea, little is known about mechanisms controlling cardiovascular responses to sleep apnea and arousal. Chronically instrumented pigs were used to investigate the effects of airway obstruction (AO) during rapid-eye-movement (REM) and non-REM (NREM) sleep and arousal on mean arterial pressure (MAP), heart rate (HR), cardiac output (CO), and total peripheral resistance (TPR). A stainless steel cannula was implanted in the lateral cerebral ventricle. During REM sleep, HR was 133 ± 10 beats/min, MAP was 65 ± 3 mmHg, CO was 1,435 ± 69 ml/min, and TPR was 0.046 ± 0.004 mmHg · ml 1 · min. During AO, CO decreased by 90 ± 17 ml/min ( P  &lt; 0.05). On arousal from AO, MAP increased by 15 ± 3 mmHg, HR increased by 10 ± 3 beats/min, and TPR increased by 0.008 ± 0.001 mmHg · ml 1 · min (all P  &lt; 0.05). Changes during NREM were similar but were more modest during AO. After the intracerebroventricular administration of propranolol (50 µg/kg; a -adrenoreceptor blocking agent), decreases in CO during AO and increases in HR during arousal were intact, but increases in MAP and TPR were no longer significant. 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Stomatology</subject><subject>Propranolol - pharmacology</subject><subject>Receptors, Adrenergic, beta - physiology</subject><subject>Sleep Apnea Syndromes - physiopathology</subject><subject>Sleep, REM - physiology</subject><subject>Swine</subject><subject>Upper respiratory tract, upper alimentary tract, paranasal sinuses, salivary glands: diseases, semeiology</subject><subject>Vascular Resistance - 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>eNp1kEFv1DAQhS1EVZbCPwApB4S4JLUTO7aPqKJQqRKX9mxN7MluKm9i7KSw_x6nu1qJA77Yo_fezPgj5AOjFWOivn6CEHzFtJaVqitRsbaRr8gmS3XJWspek42SgpZSKPmGvE3piVLGuWCX5FKzhmvGN2R7N84RLEbs4vSMuRjs4iEWIU4hwjj5yec3rhK64hnSUY6YhjTDaLEYRhsREqZiGguI05LAF32c9kXyiKGAMCK8Ixc9-ITvT_cVebz99nDzo7z_-f3u5ut9abkQc4lCKNexVjhsbKtr4Fox7hj2vc3_6Kyj4FRLG96BqEFyh1oiVy4fjbRvrsjnY9-8_68F02z2Q7LoPYyYNzNSUyUEF9nIj0Ybp5Qi9ibEYQ_xYBg1K1_zwtesfI2qjTAr3xz7eOq_dHt059AJaNY_nfRMCnyfEdohnW11KymVOtu-HG27Ybv7PUQ0YXdIQ6a9PayD_5nI_2-9Xbx_wD_zmjlHTHB98xfiJ6nR</recordid><startdate>19970501</startdate><enddate>19970501</enddate><creator>Zinkovska, Sophia</creator><creator>Kirby, Debra A</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>19970501</creationdate><title>Intracerebroventricular propranolol prevented vascular resistance increases on arousal from sleep apnea</title><author>Zinkovska, Sophia ; Kirby, Debra A</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c455t-e558db165de3c692a49814d1effc758bcd0ad86034ba52a74de97e48dddd9e0f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1997</creationdate><topic>Adrenergic beta-Antagonists - pharmacology</topic><topic>Airway Obstruction - physiopathology</topic><topic>Animals</topic><topic>Arousal - physiology</topic><topic>Biological and medical sciences</topic><topic>Endothelium, Vascular - chemistry</topic><topic>Endothelium, Vascular - physiology</topic><topic>Hemodynamics - physiology</topic><topic>Injections, Intraventricular</topic><topic>Medical sciences</topic><topic>Non tumoral diseases</topic><topic>Otorhinolaryngology. Stomatology</topic><topic>Propranolol - pharmacology</topic><topic>Receptors, Adrenergic, beta - physiology</topic><topic>Sleep Apnea Syndromes - physiopathology</topic><topic>Sleep, REM - physiology</topic><topic>Swine</topic><topic>Upper respiratory tract, upper alimentary tract, paranasal sinuses, salivary glands: diseases, semeiology</topic><topic>Vascular Resistance - drug effects</topic><topic>Vasodilator Agents - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Zinkovska, Sophia</creatorcontrib><creatorcontrib>Kirby, Debra A</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>Zinkovska, Sophia</au><au>Kirby, Debra A</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Intracerebroventricular propranolol prevented vascular resistance increases on arousal from sleep apnea</atitle><jtitle>Journal of applied physiology (1985)</jtitle><addtitle>J Appl Physiol (1985)</addtitle><date>1997-05-01</date><risdate>1997</risdate><volume>82</volume><issue>5</issue><spage>1637</spage><epage>1643</epage><pages>1637-1643</pages><issn>8750-7587</issn><eissn>1522-1601</eissn><coden>JAPHEV</coden><abstract>Sophia Zinkovska and Debra A. Kirby Children's Hospital, Harvard Medical School, Boston 02115; and Veterans Affairs Medical Center, West Roxbury, Massachusetts 02132 Received 19 July 1995; accepted in final form 19 November 1996. Zinkovska, Sophia, and Debra A. Kirby. Intracerebroventricular propranolol prevented vascular resistance increases on arousal from sleep apnea. J. Appl. Physiol. 82(5): 1637-1643, 1997. Despite the increased risk of sudden cardiac death associated with sleep apnea, little is known about mechanisms controlling cardiovascular responses to sleep apnea and arousal. Chronically instrumented pigs were used to investigate the effects of airway obstruction (AO) during rapid-eye-movement (REM) and non-REM (NREM) sleep and arousal on mean arterial pressure (MAP), heart rate (HR), cardiac output (CO), and total peripheral resistance (TPR). A stainless steel cannula was implanted in the lateral cerebral ventricle. During REM sleep, HR was 133 ± 10 beats/min, MAP was 65 ± 3 mmHg, CO was 1,435 ± 69 ml/min, and TPR was 0.046 ± 0.004 mmHg · ml 1 · min. During AO, CO decreased by 90 ± 17 ml/min ( P  &lt; 0.05). On arousal from AO, MAP increased by 15 ± 3 mmHg, HR increased by 10 ± 3 beats/min, and TPR increased by 0.008 ± 0.001 mmHg · ml 1 · min (all P  &lt; 0.05). Changes during NREM were similar but were more modest during AO. After the intracerebroventricular administration of propranolol (50 µg/kg; a -adrenoreceptor blocking agent), decreases in CO during AO and increases in HR during arousal were intact, but increases in MAP and TPR were no longer significant. These data suggest that vascular responses to AO during sleep may be regulated in part by -adrenergic receptors in the central nervous system. brain; -adrenoreceptor; pig 0161-7567/97 $5.00 Copyright © 1997 the American Physiological Society</abstract><cop>Bethesda, MD</cop><pub>Am Physiological Soc</pub><pmid>9134914</pmid><doi>10.1152/jappl.1997.82.5.1637</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record>
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subjects Adrenergic beta-Antagonists - pharmacology
Airway Obstruction - physiopathology
Animals
Arousal - physiology
Biological and medical sciences
Endothelium, Vascular - chemistry
Endothelium, Vascular - physiology
Hemodynamics - physiology
Injections, Intraventricular
Medical sciences
Non tumoral diseases
Otorhinolaryngology. Stomatology
Propranolol - pharmacology
Receptors, Adrenergic, beta - physiology
Sleep Apnea Syndromes - physiopathology
Sleep, REM - physiology
Swine
Upper respiratory tract, upper alimentary tract, paranasal sinuses, salivary glands: diseases, semeiology
Vascular Resistance - drug effects
Vasodilator Agents - pharmacology
title Intracerebroventricular propranolol prevented vascular resistance increases on arousal from sleep apnea
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