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Changes in Vascular Capacity in Awake Dogs in Response to Carotid Sinus Occlusion and Administration of Catecholamines
Changes in cardiac filling pressure (central venous pressure) were measured following carotid occlusion and infusions of catecholamines in awake dogs while cardiac output was held constant. After carotid occlusion in dogs with vagi blocked, central venous pressure increased about 0.8 mm Hg (an estim...
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Published in: | Circulation research 1984-10, Vol.55 (4), p.440-453 |
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description | Changes in cardiac filling pressure (central venous pressure) were measured following carotid occlusion and infusions of catecholamines in awake dogs while cardiac output was held constant. After carotid occlusion in dogs with vagi blocked, central venous pressure increased about 0.8 mm Hg (an estimated decrease in vascular capacity of 2.4 ml/kg). Carotid occlusion before vagal block or following vagal block and β-adrenergic block with propranolol caused no significant changes in central venous pressure. Phenylephrine (0.1–2.0 μg/min per kg) caused dose-dependent increases in arterial pressure, but changed central venous pressure (ca. 2.5 mm Hg) only at the highest doses. Epinephrine in doses (0.03–0.51 μg/min per kg) that caused little change in arterial pressure increased central venous pressure up to 5.3 mm Hg (an estimated decrease in vascular capacity of 12.0 ml/kg); this response was attenuated about 50% by propranolol. Isoproterenol (0.01–0.40 μg/min per kg) decreased arterial pressure and caused changes in central venous pressure similar to those seen with epinephrine. These responses were abolished by propranolol. Vascular compliance, determined from the change in central venous pressure following known changes in vascular blood volume, averaged 3.0 ± 0.6 ml/mm Hg per kg. In the conscious, resting dog, both α- and β-adrenergic receptors are involved in the reflex control of cardiac filling pressure. The β-adrenergic responses predominate. |
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After carotid occlusion in dogs with vagi blocked, central venous pressure increased about 0.8 mm Hg (an estimated decrease in vascular capacity of 2.4 ml/kg). Carotid occlusion before vagal block or following vagal block and β-adrenergic block with propranolol caused no significant changes in central venous pressure. Phenylephrine (0.1–2.0 μg/min per kg) caused dose-dependent increases in arterial pressure, but changed central venous pressure (ca. 2.5 mm Hg) only at the highest doses. Epinephrine in doses (0.03–0.51 μg/min per kg) that caused little change in arterial pressure increased central venous pressure up to 5.3 mm Hg (an estimated decrease in vascular capacity of 12.0 ml/kg); this response was attenuated about 50% by propranolol. Isoproterenol (0.01–0.40 μg/min per kg) decreased arterial pressure and caused changes in central venous pressure similar to those seen with epinephrine. These responses were abolished by propranolol. Vascular compliance, determined from the change in central venous pressure following known changes in vascular blood volume, averaged 3.0 ± 0.6 ml/mm Hg per kg. In the conscious, resting dog, both α- and β-adrenergic receptors are involved in the reflex control of cardiac filling pressure. The β-adrenergic responses predominate.</description><identifier>ISSN: 0009-7330</identifier><identifier>EISSN: 1524-4571</identifier><identifier>DOI: 10.1161/01.RES.55.4.440</identifier><identifier>PMID: 6478550</identifier><identifier>CODEN: CIRUAL</identifier><language>eng</language><publisher>Hagerstown, MD: American Heart Association, Inc</publisher><subject>Animals ; Biological and medical sciences ; Blood Pressure - drug effects ; Blood Vessels - drug effects ; Blood Vessels - physiology ; Blood vessels and receptors ; Blood Volume ; Cardiac Output ; Carotid Sinus - physiology ; Catecholamines - pharmacology ; Central Venous Pressure - drug effects ; Constriction ; Dogs ; Epinephrine - pharmacology ; Fundamental and applied biological sciences. Psychology ; Heart Rate - drug effects ; Isoproterenol - pharmacology ; Phenylephrine - pharmacology ; Stroke Volume - drug effects ; Vagus Nerve - physiology ; Vasoconstriction - drug effects ; Vertebrates: cardiovascular system</subject><ispartof>Circulation research, 1984-10, Vol.55 (4), p.440-453</ispartof><rights>1984 American Heart Association, Inc.</rights><rights>1985 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4432-8f2400986b46716d8e358510e3ecb7a99310bb90d18221d3bc1c4d61a54c35ca3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=8917656$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/6478550$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Bennett, Tom D</creatorcontrib><creatorcontrib>Wyss, Craig R</creatorcontrib><creatorcontrib>Scher, Allen M</creatorcontrib><title>Changes in Vascular Capacity in Awake Dogs in Response to Carotid Sinus Occlusion and Administration of Catecholamines</title><title>Circulation research</title><addtitle>Circ Res</addtitle><description>Changes in cardiac filling pressure (central venous pressure) were measured following carotid occlusion and infusions of catecholamines in awake dogs while cardiac output was held constant. After carotid occlusion in dogs with vagi blocked, central venous pressure increased about 0.8 mm Hg (an estimated decrease in vascular capacity of 2.4 ml/kg). Carotid occlusion before vagal block or following vagal block and β-adrenergic block with propranolol caused no significant changes in central venous pressure. Phenylephrine (0.1–2.0 μg/min per kg) caused dose-dependent increases in arterial pressure, but changed central venous pressure (ca. 2.5 mm Hg) only at the highest doses. Epinephrine in doses (0.03–0.51 μg/min per kg) that caused little change in arterial pressure increased central venous pressure up to 5.3 mm Hg (an estimated decrease in vascular capacity of 12.0 ml/kg); this response was attenuated about 50% by propranolol. Isoproterenol (0.01–0.40 μg/min per kg) decreased arterial pressure and caused changes in central venous pressure similar to those seen with epinephrine. These responses were abolished by propranolol. Vascular compliance, determined from the change in central venous pressure following known changes in vascular blood volume, averaged 3.0 ± 0.6 ml/mm Hg per kg. In the conscious, resting dog, both α- and β-adrenergic receptors are involved in the reflex control of cardiac filling pressure. The β-adrenergic responses predominate.</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Blood Pressure - drug effects</subject><subject>Blood Vessels - drug effects</subject><subject>Blood Vessels - physiology</subject><subject>Blood vessels and receptors</subject><subject>Blood Volume</subject><subject>Cardiac Output</subject><subject>Carotid Sinus - physiology</subject><subject>Catecholamines - pharmacology</subject><subject>Central Venous Pressure - drug effects</subject><subject>Constriction</subject><subject>Dogs</subject><subject>Epinephrine - pharmacology</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Heart Rate - drug effects</subject><subject>Isoproterenol - pharmacology</subject><subject>Phenylephrine - pharmacology</subject><subject>Stroke Volume - drug effects</subject><subject>Vagus Nerve - physiology</subject><subject>Vasoconstriction - drug effects</subject><subject>Vertebrates: cardiovascular system</subject><issn>0009-7330</issn><issn>1524-4571</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1984</creationdate><recordtype>article</recordtype><recordid>eNo9kcFv2yAUh9G0qsu6nXea5MPUm12eAYOPUdZukypVartdEca4YSWQAV7U_354iXoB8X4fT48PhD4BbgA6uMLQ3F8_NIw1tKEUv0ErYC2tKePwFq0wxn3NCcHv0PuUfmMMlLT9OTrvKBeM4RX6u9kq_2RSZX31SyU9OxWrjdorbfPLUlwf1LOpvoan_8i9Sfvgk6lyKFQM2Y7Vg_Vzqu60dnOywVfKj9V63FlvU44qL6UwFTobvQ1OlcCkD-hsUi6Zj6f9Av28uX7cfK9v77792Kxva03LpLWYWlqeILqBdhy6URjCBANsiNEDV31PAA9Dj0cQbQsjGTRoOnagGNWEaUUu0OWx7z6GP7NJWe5s0sY55U2YkxTQEs44L-DVEdQxpBTNJPfR7lR8kYDlYlpikMW0ZExSWUyXG59PredhZ8ZX_qS25F9OedGq3BSV1za9YqIH3rGuYPSIHYLLJqZnNx9MlFujXN7K8oGYYGhr6AWF5VQvS0v-AdQRlXQ</recordid><startdate>198410</startdate><enddate>198410</enddate><creator>Bennett, Tom D</creator><creator>Wyss, Craig R</creator><creator>Scher, Allen M</creator><general>American Heart Association, Inc</general><general>Lippincott</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>198410</creationdate><title>Changes in Vascular Capacity in Awake Dogs in Response to Carotid Sinus Occlusion and Administration of Catecholamines</title><author>Bennett, Tom D ; Wyss, Craig R ; Scher, Allen M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4432-8f2400986b46716d8e358510e3ecb7a99310bb90d18221d3bc1c4d61a54c35ca3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1984</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Blood Pressure - drug effects</topic><topic>Blood Vessels - drug effects</topic><topic>Blood Vessels - physiology</topic><topic>Blood vessels and receptors</topic><topic>Blood Volume</topic><topic>Cardiac Output</topic><topic>Carotid Sinus - physiology</topic><topic>Catecholamines - pharmacology</topic><topic>Central Venous Pressure - drug effects</topic><topic>Constriction</topic><topic>Dogs</topic><topic>Epinephrine - pharmacology</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Heart Rate - drug effects</topic><topic>Isoproterenol - pharmacology</topic><topic>Phenylephrine - pharmacology</topic><topic>Stroke Volume - drug effects</topic><topic>Vagus Nerve - physiology</topic><topic>Vasoconstriction - drug effects</topic><topic>Vertebrates: cardiovascular system</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Bennett, Tom D</creatorcontrib><creatorcontrib>Wyss, Craig R</creatorcontrib><creatorcontrib>Scher, Allen M</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>Circulation research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Bennett, Tom D</au><au>Wyss, Craig R</au><au>Scher, Allen M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Changes in Vascular Capacity in Awake Dogs in Response to Carotid Sinus Occlusion and Administration of Catecholamines</atitle><jtitle>Circulation research</jtitle><addtitle>Circ Res</addtitle><date>1984-10</date><risdate>1984</risdate><volume>55</volume><issue>4</issue><spage>440</spage><epage>453</epage><pages>440-453</pages><issn>0009-7330</issn><eissn>1524-4571</eissn><coden>CIRUAL</coden><abstract>Changes in cardiac filling pressure (central venous pressure) were measured following carotid occlusion and infusions of catecholamines in awake dogs while cardiac output was held constant. After carotid occlusion in dogs with vagi blocked, central venous pressure increased about 0.8 mm Hg (an estimated decrease in vascular capacity of 2.4 ml/kg). Carotid occlusion before vagal block or following vagal block and β-adrenergic block with propranolol caused no significant changes in central venous pressure. Phenylephrine (0.1–2.0 μg/min per kg) caused dose-dependent increases in arterial pressure, but changed central venous pressure (ca. 2.5 mm Hg) only at the highest doses. Epinephrine in doses (0.03–0.51 μg/min per kg) that caused little change in arterial pressure increased central venous pressure up to 5.3 mm Hg (an estimated decrease in vascular capacity of 12.0 ml/kg); this response was attenuated about 50% by propranolol. Isoproterenol (0.01–0.40 μg/min per kg) decreased arterial pressure and caused changes in central venous pressure similar to those seen with epinephrine. These responses were abolished by propranolol. Vascular compliance, determined from the change in central venous pressure following known changes in vascular blood volume, averaged 3.0 ± 0.6 ml/mm Hg per kg. In the conscious, resting dog, both α- and β-adrenergic receptors are involved in the reflex control of cardiac filling pressure. The β-adrenergic responses predominate.</abstract><cop>Hagerstown, MD</cop><pub>American Heart Association, Inc</pub><pmid>6478550</pmid><doi>10.1161/01.RES.55.4.440</doi><tpages>14</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Animals Biological and medical sciences Blood Pressure - drug effects Blood Vessels - drug effects Blood Vessels - physiology Blood vessels and receptors Blood Volume Cardiac Output Carotid Sinus - physiology Catecholamines - pharmacology Central Venous Pressure - drug effects Constriction Dogs Epinephrine - pharmacology Fundamental and applied biological sciences. Psychology Heart Rate - drug effects Isoproterenol - pharmacology Phenylephrine - pharmacology Stroke Volume - drug effects Vagus Nerve - physiology Vasoconstriction - drug effects Vertebrates: cardiovascular system |
title | Changes in Vascular Capacity in Awake Dogs in Response to Carotid Sinus Occlusion and Administration of Catecholamines |
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