Basal Forebrain Histaminergic Transmission Modulates Electroencephalographic Activity and Emergence from Isoflurane Anesthesia
The tuberomammillary histaminergic neurons are involved in the sedative component of anesthetic action. The nucleus basalis magnocellularis (NBM) in the basal forebrain receives dense excitatory innervation from the tuberomammillary nucleus and is recognized as an important site of sleep-wake regula...
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| Veröffentlicht in: | Anesthesiology (Philadelphia) 2009-10, Vol.111 (4), p.725-733 |
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| description | The tuberomammillary histaminergic neurons are involved in the sedative component of anesthetic action. The nucleus basalis magnocellularis (NBM) in the basal forebrain receives dense excitatory innervation from the tuberomammillary nucleus and is recognized as an important site of sleep-wake regulation. This study investigated whether NBM administration of histaminergic drugs may modulate arousal/emergence from isoflurane anesthesia.
Microinjections of histaminergic agonists and antagonists were made into the NBM of rats anesthetized with isoflurane. The changes in electroencephalographic activity, including electroencephalographic burst suppression ratio and power spectra, as well as respiratory rate, were recorded under basal conditions and after NBM injection. Time to resumption of righting reflex was recorded as a measure of emergence from anesthesia.
The rats displayed a burst suppression electroencephalographic pattern at inhaled isoflurane concentrations of 1.4-2.1%. Application of histamine (1 microg/0.5 microl) to the NBM reversed the electroencephalographic depressant effect of isoflurane; i.e., electroencephalographic activity shifted from the burst suppression pattern toward delta activity at 1.4% isoflurane, and the burst suppression ratio decreased at 2.1% isoflurane. Histamine-evoked activation of electroencephalography was blocked by NBM pretreatment with a H1 receptor antagonist, triprolidine (5 microg/1 microl), but not by a H2 receptor antagonist, cimetidine (25 microg/1 microl). The respiratory rate was significantly increased after histamine injection. NBM application of histamine facilitated, while triprolidine delayed, emergence from isoflurane anesthesia.
Histamine activation of H1 receptors in the NBM induces electroencephalographic arousal and facilitates emergence from isoflurane anesthesia. The basal forebrain histaminergic pathway appears to play a role in modulating arousal/emergence from anesthesia. |
| doi_str_mv | 10.1097/aln.0b013e3181b061a0 |
| format | Article |
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Microinjections of histaminergic agonists and antagonists were made into the NBM of rats anesthetized with isoflurane. The changes in electroencephalographic activity, including electroencephalographic burst suppression ratio and power spectra, as well as respiratory rate, were recorded under basal conditions and after NBM injection. Time to resumption of righting reflex was recorded as a measure of emergence from anesthesia.
The rats displayed a burst suppression electroencephalographic pattern at inhaled isoflurane concentrations of 1.4-2.1%. Application of histamine (1 microg/0.5 microl) to the NBM reversed the electroencephalographic depressant effect of isoflurane; i.e., electroencephalographic activity shifted from the burst suppression pattern toward delta activity at 1.4% isoflurane, and the burst suppression ratio decreased at 2.1% isoflurane. Histamine-evoked activation of electroencephalography was blocked by NBM pretreatment with a H1 receptor antagonist, triprolidine (5 microg/1 microl), but not by a H2 receptor antagonist, cimetidine (25 microg/1 microl). The respiratory rate was significantly increased after histamine injection. NBM application of histamine facilitated, while triprolidine delayed, emergence from isoflurane anesthesia.
Histamine activation of H1 receptors in the NBM induces electroencephalographic arousal and facilitates emergence from isoflurane anesthesia. The basal forebrain histaminergic pathway appears to play a role in modulating arousal/emergence from anesthesia.</description><identifier>ISSN: 0003-3022</identifier><identifier>EISSN: 1528-1175</identifier><identifier>DOI: 10.1097/aln.0b013e3181b061a0</identifier><identifier>PMID: 19741500</identifier><identifier>CODEN: ANESAV</identifier><language>eng</language><publisher>Hagerstown, MD: Lippincott Williams & Wilkins</publisher><subject>Anesthesia ; Anesthesia Recovery Period ; Anesthesia, Inhalation ; Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy ; Anesthetics, Inhalation ; Animals ; Arousal - drug effects ; Basal Nucleus of Meynert - drug effects ; Basal Nucleus of Meynert - physiology ; Behavior, Animal - drug effects ; Biological and medical sciences ; Electroencephalography ; Histamine - pharmacology ; Histamine - physiology ; Histamine H1 Antagonists - administration & dosage ; Histamine H1 Antagonists - pharmacology ; Histamine H2 Antagonists - administration & dosage ; Histamine H2 Antagonists - pharmacology ; Injections ; Isoflurane ; Male ; Medical sciences ; Motor Activity - drug effects ; Rats ; Rats, Long-Evans ; Respiratory Mechanics - drug effects ; Synaptic Transmission - physiology</subject><ispartof>Anesthesiology (Philadelphia), 2009-10, Vol.111 (4), p.725-733</ispartof><rights>2009 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c499t-4b1d0430a7e78eed2a8ae0ffd743cba031477a03c5fde6f1772db9c522651f7f3</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=21975930$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/19741500$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>TAO LUO</creatorcontrib><creatorcontrib>LEUNG, L. Stan</creatorcontrib><title>Basal Forebrain Histaminergic Transmission Modulates Electroencephalographic Activity and Emergence from Isoflurane Anesthesia</title><title>Anesthesiology (Philadelphia)</title><addtitle>Anesthesiology</addtitle><description>The tuberomammillary histaminergic neurons are involved in the sedative component of anesthetic action. The nucleus basalis magnocellularis (NBM) in the basal forebrain receives dense excitatory innervation from the tuberomammillary nucleus and is recognized as an important site of sleep-wake regulation. This study investigated whether NBM administration of histaminergic drugs may modulate arousal/emergence from isoflurane anesthesia.
Microinjections of histaminergic agonists and antagonists were made into the NBM of rats anesthetized with isoflurane. The changes in electroencephalographic activity, including electroencephalographic burst suppression ratio and power spectra, as well as respiratory rate, were recorded under basal conditions and after NBM injection. Time to resumption of righting reflex was recorded as a measure of emergence from anesthesia.
The rats displayed a burst suppression electroencephalographic pattern at inhaled isoflurane concentrations of 1.4-2.1%. Application of histamine (1 microg/0.5 microl) to the NBM reversed the electroencephalographic depressant effect of isoflurane; i.e., electroencephalographic activity shifted from the burst suppression pattern toward delta activity at 1.4% isoflurane, and the burst suppression ratio decreased at 2.1% isoflurane. Histamine-evoked activation of electroencephalography was blocked by NBM pretreatment with a H1 receptor antagonist, triprolidine (5 microg/1 microl), but not by a H2 receptor antagonist, cimetidine (25 microg/1 microl). The respiratory rate was significantly increased after histamine injection. NBM application of histamine facilitated, while triprolidine delayed, emergence from isoflurane anesthesia.
Histamine activation of H1 receptors in the NBM induces electroencephalographic arousal and facilitates emergence from isoflurane anesthesia. The basal forebrain histaminergic pathway appears to play a role in modulating arousal/emergence from anesthesia.</description><subject>Anesthesia</subject><subject>Anesthesia Recovery Period</subject><subject>Anesthesia, Inhalation</subject><subject>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy</subject><subject>Anesthetics, Inhalation</subject><subject>Animals</subject><subject>Arousal - drug effects</subject><subject>Basal Nucleus of Meynert - drug effects</subject><subject>Basal Nucleus of Meynert - physiology</subject><subject>Behavior, Animal - drug effects</subject><subject>Biological and medical sciences</subject><subject>Electroencephalography</subject><subject>Histamine - pharmacology</subject><subject>Histamine - physiology</subject><subject>Histamine H1 Antagonists - administration & dosage</subject><subject>Histamine H1 Antagonists - pharmacology</subject><subject>Histamine H2 Antagonists - administration & dosage</subject><subject>Histamine H2 Antagonists - pharmacology</subject><subject>Injections</subject><subject>Isoflurane</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Motor Activity - drug effects</subject><subject>Rats</subject><subject>Rats, Long-Evans</subject><subject>Respiratory Mechanics - drug effects</subject><subject>Synaptic Transmission - physiology</subject><issn>0003-3022</issn><issn>1528-1175</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2009</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkE1r3DAQhkVpSTZp_kEpupScnI4ka2Uft2HzAdv2kp7NWB5lVWRrK9mFXPrbo5ClhZ6GgWfemXkY-yDgSkBrPmOYrqAHoUiJRvSwFghv2Epo2VRCGP2WrQBAVQqkPGVnOf8srdGqOWGnojW10AAr9ucLZgz8JibqE_qJ3_k84-gnSo_e8oeEUx59zj5O_GscloAzZb4NZOcUabJ02GOIjwkP-4Jv7Ox_-_mJ4zTw7VgyXhDuUhz5fY4uLCWP-GaiPO8pe3zP3jkMmS6O9Zz9uNk-XN9Vu--399ebXWXrtp2ruhcD1ArQkGmIBokNEjg3mFrZHkGJ2phSrHYDrZ0wRg59a7WUay2cceqcXb7mHlL8tZTtXXnKUgjlnLjkzqhagi5GClm_kjbFnBO57pD8iOmpE9C9iO82u2_d_-LL2MfjgqUfafg3dDRdgE9HALPF4IoI6_NfThZQtwrUMzvgkBo</recordid><startdate>20091001</startdate><enddate>20091001</enddate><creator>TAO LUO</creator><creator>LEUNG, L. Stan</creator><general>Lippincott Williams & Wilkins</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>20091001</creationdate><title>Basal Forebrain Histaminergic Transmission Modulates Electroencephalographic Activity and Emergence from Isoflurane Anesthesia</title><author>TAO LUO ; LEUNG, L. Stan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c499t-4b1d0430a7e78eed2a8ae0ffd743cba031477a03c5fde6f1772db9c522651f7f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2009</creationdate><topic>Anesthesia</topic><topic>Anesthesia Recovery Period</topic><topic>Anesthesia, Inhalation</topic><topic>Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy</topic><topic>Anesthetics, Inhalation</topic><topic>Animals</topic><topic>Arousal - drug effects</topic><topic>Basal Nucleus of Meynert - drug effects</topic><topic>Basal Nucleus of Meynert - physiology</topic><topic>Behavior, Animal - drug effects</topic><topic>Biological and medical sciences</topic><topic>Electroencephalography</topic><topic>Histamine - pharmacology</topic><topic>Histamine - physiology</topic><topic>Histamine H1 Antagonists - administration & dosage</topic><topic>Histamine H1 Antagonists - pharmacology</topic><topic>Histamine H2 Antagonists - administration & dosage</topic><topic>Histamine H2 Antagonists - pharmacology</topic><topic>Injections</topic><topic>Isoflurane</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Motor Activity - drug effects</topic><topic>Rats</topic><topic>Rats, Long-Evans</topic><topic>Respiratory Mechanics - drug effects</topic><topic>Synaptic Transmission - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>TAO LUO</creatorcontrib><creatorcontrib>LEUNG, L. 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Stan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Basal Forebrain Histaminergic Transmission Modulates Electroencephalographic Activity and Emergence from Isoflurane Anesthesia</atitle><jtitle>Anesthesiology (Philadelphia)</jtitle><addtitle>Anesthesiology</addtitle><date>2009-10-01</date><risdate>2009</risdate><volume>111</volume><issue>4</issue><spage>725</spage><epage>733</epage><pages>725-733</pages><issn>0003-3022</issn><eissn>1528-1175</eissn><coden>ANESAV</coden><abstract>The tuberomammillary histaminergic neurons are involved in the sedative component of anesthetic action. The nucleus basalis magnocellularis (NBM) in the basal forebrain receives dense excitatory innervation from the tuberomammillary nucleus and is recognized as an important site of sleep-wake regulation. This study investigated whether NBM administration of histaminergic drugs may modulate arousal/emergence from isoflurane anesthesia.
Microinjections of histaminergic agonists and antagonists were made into the NBM of rats anesthetized with isoflurane. The changes in electroencephalographic activity, including electroencephalographic burst suppression ratio and power spectra, as well as respiratory rate, were recorded under basal conditions and after NBM injection. Time to resumption of righting reflex was recorded as a measure of emergence from anesthesia.
The rats displayed a burst suppression electroencephalographic pattern at inhaled isoflurane concentrations of 1.4-2.1%. Application of histamine (1 microg/0.5 microl) to the NBM reversed the electroencephalographic depressant effect of isoflurane; i.e., electroencephalographic activity shifted from the burst suppression pattern toward delta activity at 1.4% isoflurane, and the burst suppression ratio decreased at 2.1% isoflurane. Histamine-evoked activation of electroencephalography was blocked by NBM pretreatment with a H1 receptor antagonist, triprolidine (5 microg/1 microl), but not by a H2 receptor antagonist, cimetidine (25 microg/1 microl). The respiratory rate was significantly increased after histamine injection. NBM application of histamine facilitated, while triprolidine delayed, emergence from isoflurane anesthesia.
Histamine activation of H1 receptors in the NBM induces electroencephalographic arousal and facilitates emergence from isoflurane anesthesia. The basal forebrain histaminergic pathway appears to play a role in modulating arousal/emergence from anesthesia.</abstract><cop>Hagerstown, MD</cop><pub>Lippincott Williams & Wilkins</pub><pmid>19741500</pmid><doi>10.1097/aln.0b013e3181b061a0</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record> |
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| subjects | Anesthesia Anesthesia Recovery Period Anesthesia, Inhalation Anesthesia. Intensive care medicine. Transfusions. Cell therapy and gene therapy Anesthetics, Inhalation Animals Arousal - drug effects Basal Nucleus of Meynert - drug effects Basal Nucleus of Meynert - physiology Behavior, Animal - drug effects Biological and medical sciences Electroencephalography Histamine - pharmacology Histamine - physiology Histamine H1 Antagonists - administration & dosage Histamine H1 Antagonists - pharmacology Histamine H2 Antagonists - administration & dosage Histamine H2 Antagonists - pharmacology Injections Isoflurane Male Medical sciences Motor Activity - drug effects Rats Rats, Long-Evans Respiratory Mechanics - drug effects Synaptic Transmission - physiology |
| title | Basal Forebrain Histaminergic Transmission Modulates Electroencephalographic Activity and Emergence from Isoflurane Anesthesia |
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