The Effects of Increasing Plasma Concentrations of Dexmedetomidine in Humans

This study determined the responses to increasing plasma concentrations of dexmedetomidine in humans. Ten healthy men (20-27 yr) provided informed consent and were monitored (underwent electrocardiography, measured arterial, central venous [CVP] and pulmonary artery [PAP] pressures, cardiac output,...

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Published in	Anesthesiology (Philadelphia) Vol. 93; no. 2; pp. 382 - 394
Main Authors	Ebert, Thomas J., Hall, Judith E., Barney, Jill A., Uhrich, Toni D., Colinco, Maelynn D.
Format	Journal Article
Language	English
Published	Hagerstown, MD Lippincott 01.08.2000
Subjects	Adrenergic alpha-Agonists - administration & dosage Adrenergic alpha-Agonists - blood Adrenergic alpha-Agonists - pharmacology Adult Biological and medical sciences Conscious Sedation Dexmedetomidine - administration & dosage Dexmedetomidine - blood Dexmedetomidine - pharmacology Dose-Response Relationship, Drug Drug Synergism Epinephrine - blood Gas Chromatography-Mass Spectrometry Hemodynamics - drug effects Humans Hypnotics. Sedatives Infusions, Intravenous Male Medical sciences Mental Recall - drug effects Neuropharmacology Norepinephrine - blood Pharmacology. Drug treatments Phenylephrine - pharmacology Pressoreceptors - drug effects Psychology. Psychoanalysis. Psychiatry Psychometrics Psychopharmacology Regression Analysis Human α2-Adrenergic receptor Agonist Intravenous administration Healthy subject Sedation Dose activity relation Analgesia Analgesic Activity concentration relation Perfusion Autonomic nervous system Baroreflex Dexmedetomidine Hemodynamics Sedative
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Abstract	This study determined the responses to increasing plasma concentrations of dexmedetomidine in humans. Ten healthy men (20-27 yr) provided informed consent and were monitored (underwent electrocardiography, measured arterial, central venous [CVP] and pulmonary artery [PAP] pressures, cardiac output, oxygen saturation, end-tidal carbon dioxide [ETCO2], respiration, blood gas, and catecholamines). Hemodynamic measurements, blood sampling, and psychometric, cold pressor, and baroreflex tests were performed at rest and during sequential 40-min intravenous target infusions of dexmedetomidine (0.5, 0.8, 1.2, 2.0, 3.2, 5.0, and 8.0 ng/ml; baroreflex testing only at 0.5 and 0.8 ng/ml). The initial dose of dexmedetomidine decreased catecholamines 45-76% and eliminated the norepinephrine increase that was seen during the cold pressor test. Catecholamine suppression persisted in subsequent infusions. The first two doses of dexmedetomidine increased sedation 38 and 65%, and lowered mean arterial pressure by 13%, but did not change central venous pressure or pulmonary artery pressure. Subsequent higher doses increased sedation, all pressures, and calculated vascular resistance, and resulted in significant decreases in heart rate, cardiac output, and stroke volume. Recall and recognition decreased at a dose of more than 0.7 ng/ml. The pain rating and mean arterial pressure increase to cold pressor test progressively diminished as the dexmedetomidine dose increased. The baroreflex heart rate slowing as a result of phenylephrine challenge was potentiated at both doses of dexmedetomidine. Respiratory variables were minimally changed during infusions, whereas acid-base was unchanged. Increasing concentrations of dexmedetomidine in humans resulted in progressive increases in sedation and analgesia, decreases in heart rate, cardiac output, and memory. A biphasic (low, then high) dose-response relation for mean arterial pressure, pulmonary arterial pressure, and vascular resistances, and an attenuation of the cold pressor response also were observed.
AbstractList	This study determined the responses to increasing plasma concentrations of dexmedetomidine in humans. Ten healthy men (20-27 yr) provided informed consent and were monitored (underwent electrocardiography, measured arterial, central venous [CVP] and pulmonary artery [PAP] pressures, cardiac output, oxygen saturation, end-tidal carbon dioxide [ETCO2], respiration, blood gas, and catecholamines). Hemodynamic measurements, blood sampling, and psychometric, cold pressor, and baroreflex tests were performed at rest and during sequential 40-min intravenous target infusions of dexmedetomidine (0.5, 0.8, 1.2, 2.0, 3.2, 5.0, and 8.0 ng/ml; baroreflex testing only at 0.5 and 0.8 ng/ml). The initial dose of dexmedetomidine decreased catecholamines 45-76% and eliminated the norepinephrine increase that was seen during the cold pressor test. Catecholamine suppression persisted in subsequent infusions. The first two doses of dexmedetomidine increased sedation 38 and 65%, and lowered mean arterial pressure by 13%, but did not change central venous pressure or pulmonary artery pressure. Subsequent higher doses increased sedation, all pressures, and calculated vascular resistance, and resulted in significant decreases in heart rate, cardiac output, and stroke volume. Recall and recognition decreased at a dose of more than 0.7 ng/ml. The pain rating and mean arterial pressure increase to cold pressor test progressively diminished as the dexmedetomidine dose increased. The baroreflex heart rate slowing as a result of phenylephrine challenge was potentiated at both doses of dexmedetomidine. Respiratory variables were minimally changed during infusions, whereas acid-base was unchanged. Increasing concentrations of dexmedetomidine in humans resulted in progressive increases in sedation and analgesia, decreases in heart rate, cardiac output, and memory. A biphasic (low, then high) dose-response relation for mean arterial pressure, pulmonary arterial pressure, and vascular resistances, and an attenuation of the cold pressor response also were observed. This study determined the responses to increasing plasma concentrations of dexmedetomidine in humans.BACKGROUNDThis study determined the responses to increasing plasma concentrations of dexmedetomidine in humans.Ten healthy men (20-27 yr) provided informed consent and were monitored (underwent electrocardiography, measured arterial, central venous [CVP] and pulmonary artery [PAP] pressures, cardiac output, oxygen saturation, end-tidal carbon dioxide [ETCO2], respiration, blood gas, and catecholamines). Hemodynamic measurements, blood sampling, and psychometric, cold pressor, and baroreflex tests were performed at rest and during sequential 40-min intravenous target infusions of dexmedetomidine (0.5, 0.8, 1.2, 2.0, 3.2, 5.0, and 8.0 ng/ml; baroreflex testing only at 0.5 and 0.8 ng/ml).METHODSTen healthy men (20-27 yr) provided informed consent and were monitored (underwent electrocardiography, measured arterial, central venous [CVP] and pulmonary artery [PAP] pressures, cardiac output, oxygen saturation, end-tidal carbon dioxide [ETCO2], respiration, blood gas, and catecholamines). Hemodynamic measurements, blood sampling, and psychometric, cold pressor, and baroreflex tests were performed at rest and during sequential 40-min intravenous target infusions of dexmedetomidine (0.5, 0.8, 1.2, 2.0, 3.2, 5.0, and 8.0 ng/ml; baroreflex testing only at 0.5 and 0.8 ng/ml).The initial dose of dexmedetomidine decreased catecholamines 45-76% and eliminated the norepinephrine increase that was seen during the cold pressor test. Catecholamine suppression persisted in subsequent infusions. The first two doses of dexmedetomidine increased sedation 38 and 65%, and lowered mean arterial pressure by 13%, but did not change central venous pressure or pulmonary artery pressure. Subsequent higher doses increased sedation, all pressures, and calculated vascular resistance, and resulted in significant decreases in heart rate, cardiac output, and stroke volume. Recall and recognition decreased at a dose of more than 0.7 ng/ml. The pain rating and mean arterial pressure increase to cold pressor test progressively diminished as the dexmedetomidine dose increased. The baroreflex heart rate slowing as a result of phenylephrine challenge was potentiated at both doses of dexmedetomidine. Respiratory variables were minimally changed during infusions, whereas acid-base was unchanged.RESULTSThe initial dose of dexmedetomidine decreased catecholamines 45-76% and eliminated the norepinephrine increase that was seen during the cold pressor test. Catecholamine suppression persisted in subsequent infusions. The first two doses of dexmedetomidine increased sedation 38 and 65%, and lowered mean arterial pressure by 13%, but did not change central venous pressure or pulmonary artery pressure. Subsequent higher doses increased sedation, all pressures, and calculated vascular resistance, and resulted in significant decreases in heart rate, cardiac output, and stroke volume. Recall and recognition decreased at a dose of more than 0.7 ng/ml. The pain rating and mean arterial pressure increase to cold pressor test progressively diminished as the dexmedetomidine dose increased. The baroreflex heart rate slowing as a result of phenylephrine challenge was potentiated at both doses of dexmedetomidine. Respiratory variables were minimally changed during infusions, whereas acid-base was unchanged.Increasing concentrations of dexmedetomidine in humans resulted in progressive increases in sedation and analgesia, decreases in heart rate, cardiac output, and memory. A biphasic (low, then high) dose-response relation for mean arterial pressure, pulmonary arterial pressure, and vascular resistances, and an attenuation of the cold pressor response also were observed.CONCLUSIONSIncreasing concentrations of dexmedetomidine in humans resulted in progressive increases in sedation and analgesia, decreases in heart rate, cardiac output, and memory. A biphasic (low, then high) dose-response relation for mean arterial pressure, pulmonary arterial pressure, and vascular resistances, and an attenuation of the cold pressor response also were observed.
Author	Barney, Jill A. Colinco, Maelynn D. Ebert, Thomas J. Hall, Judith E. Uhrich, Toni D.
Author_xml	– sequence: 1 givenname: Thomas J. surname: Ebert fullname: Ebert, Thomas J. organization: Professor, Department of Anesthesiology – sequence: 2 givenname: Judith E. surname: Hall fullname: Hall, Judith E. organization: Consultant Anesthetist, Department of Anesthesiology. Current position: Professor, Department of Anaesthetics and Intensive Care Medicine, University of Wales College of Medicine, Heath Park, Cardiff, United Kingdom – sequence: 3 givenname: Jill A. surname: Barney fullname: Barney, Jill A. organization: Research Associate, Department of Anesthesiology – sequence: 4 givenname: Toni D. surname: Uhrich fullname: Uhrich, Toni D. organization: Research Associate, Department of Anesthesiology – sequence: 5 givenname: Maelynn D. surname: Colinco fullname: Colinco, Maelynn D. organization: Resident, Department of Anesthesiology
BackLink	http://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=1465466$$DView record in Pascal Francis https://www.ncbi.nlm.nih.gov/pubmed/10910487$$D View this record in MEDLINE/PubMed
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Snippet	This study determined the responses to increasing plasma concentrations of dexmedetomidine in humans. Ten healthy men (20-27 yr) provided informed consent and... This study determined the responses to increasing plasma concentrations of dexmedetomidine in humans.BACKGROUNDThis study determined the responses to...
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SubjectTerms	Adrenergic alpha-Agonists - administration & dosage Adrenergic alpha-Agonists - blood Adrenergic alpha-Agonists - pharmacology Adult Biological and medical sciences Conscious Sedation Dexmedetomidine - administration & dosage Dexmedetomidine - blood Dexmedetomidine - pharmacology Dose-Response Relationship, Drug Drug Synergism Epinephrine - blood Gas Chromatography-Mass Spectrometry Hemodynamics - drug effects Humans Hypnotics. Sedatives Infusions, Intravenous Male Medical sciences Mental Recall - drug effects Neuropharmacology Norepinephrine - blood Pharmacology. Drug treatments Phenylephrine - pharmacology Pressoreceptors - drug effects Psychology. Psychoanalysis. Psychiatry Psychometrics Psychopharmacology Regression Analysis
Title	The Effects of Increasing Plasma Concentrations of Dexmedetomidine in Humans
URI	https://www.ncbi.nlm.nih.gov/pubmed/10910487 https://www.proquest.com/docview/71256373
Volume	93
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