Cigarette smoke-induced bronchoconstriction: causative agents and role of thromboxane receptors
Ju-Lun Hong and Lu-Yuan Lee Department of Physiology, University of Kentucky, Lexington, Kentucky 40536-0084 Received 14 December 1995; accepted in final form 12 July 1996. Hong, Ju-Lun, and Lu-Yuan Lee. Cigarette smoke-induced bronchoconstriction: causative agents and role of thromboxane receptors....
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| creator | Hong, Ju-Lun Lee, Lu-Yuan |
| description | Ju-Lun
Hong and
Lu-Yuan
Lee
Department of Physiology, University of Kentucky, Lexington,
Kentucky 40536-0084
Received 14 December 1995; accepted in final form 12 July 1996.
Hong, Ju-Lun, and Lu-Yuan Lee. Cigarette smoke-induced
bronchoconstriction: causative agents and role of thromboxane receptors. J. Appl. Physiol. 81(5):
2053-2059, 1996. Inhalation of cigarette smoke induces a biphasic
bronchoconstriction in guinea pigs: the first phase is induced by a
combination of cholinergic reflex and tachykinins, whereas the second
phase involves cyclooxygenase metabolites (J.-L. Hong, I. W. Rodger,
and L.-Y. Lee. J. Appl. Physiol. 78:
2260-2266, 1995). This study was carried out to further determine
the causative agents in the smoke and the types of prostanoid receptors
and endogenous prostanoids mediating the bronchoconstriction. Inhalation of 10 ml of high-nicotine cigarette smoke consistently elicited the biphasic bronchoconstriction in anesthetized and artificially ventilated guinea pigs. Pretreatment with hexamethonium (10 mg/kg iv) significantly reduced the first-phase bronchoconstriction but did not have any measurable effect on the second-phase response. In
sharp contrast, gas-phase smoke did not elicit any bronchoconstrictive effect. Furthermore, when the animals were challenged with low-nicotine cigarette smoke, only a single second-phase response was evoked, accompanied by increases in thromboxane (Tx)
B 2 (a stable metabolite of
TxA 2 ), prostaglandin (PG)
D 2 ,
PGF 2 in the bronchoalveolar lavage fluid. The bronchoconstrictive response induced by low-nicotine smoke was completely prevented by pretreatment with SQ-29548 (0.3 mg/kg
iv), a TxA 2 -receptor antagonist.
These results indicate that 1 )
nicotine is the primary causative agent responsible for the first-phase
bronchoconstriction and 2 )
nonnicotine smoke particulates evoke the release of
TxA 2 ,
PGD 2 , and
PGF 2 , which act on
TxA 2 receptors on airway smooth
muscles and induce the second-phase response to cigarette smoke.
hexamethonium; SQ-29548; tachykinins; guinea pigs; prostaglandins
0161-7567/96 $5.00
Copyright © 1996 the American Physiological Society |
| doi_str_mv | 10.1152/jappl.1996.81.5.2053 |
| format | Article |
| fullrecord | <record><control><sourceid>pubmed_cross</sourceid><recordid>TN_cdi_pubmed_primary_8941529</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>8941529</sourcerecordid><originalsourceid>FETCH-LOGICAL-c409t-57756c9e856143b568b2ea8e03cef14f68bd3230fa46b2f9bd79dedf0df2309c3</originalsourceid><addsrcrecordid>eNp1kEFPHCEYhompsVv1H9iEQw9eZoQZmIHezKa2JiZe9EwY-NhBZ4cJsNb9987qZtuLJwLv-_B9eRC6oKSklFdXT3qahpJK2ZSClrysCK-P0GKOqoI2hH5BC9FyUrRctF_Rt5SeCKGMcXqCToRkc08ukFr6lY6QM-C0Ds9Q-NFuDFjcxTCaPpgwphy9yT6MP7HRm6SzfwGsVzDmhPVocQwD4OBw7mNYd-FVj4AjGJhyiOkMHTs9JDjfn6fo8ebXw_JPcXf_-3Z5fVcYRmQueNvyxkgQvKGs7ngjugq0AFIbcJS5-W7rqiZOs6arnOxsKy1YR6ybX6WpTxH7-NfEkFIEp6bo1zpuFSVqp0u961I7XUpQxdVO14x9_8CmTbcGe4D2fub8xz7XyejBRT0anw61ikkmWPtveu9X_V8fQU39NvkwhNVW3WyG4QFe826Dw2Q1WTdjl59jc_u_Rd8AdTGYKA</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype></control><display><type>article</type><title>Cigarette smoke-induced bronchoconstriction: causative agents and role of thromboxane receptors</title><source>MEDLINE</source><source>American Physiological Society</source><source>EZB-FREE-00999 freely available EZB journals</source><creator>Hong, Ju-Lun ; Lee, Lu-Yuan</creator><creatorcontrib>Hong, Ju-Lun ; Lee, Lu-Yuan</creatorcontrib><description>Ju-Lun
Hong and
Lu-Yuan
Lee
Department of Physiology, University of Kentucky, Lexington,
Kentucky 40536-0084
Received 14 December 1995; accepted in final form 12 July 1996.
Hong, Ju-Lun, and Lu-Yuan Lee. Cigarette smoke-induced
bronchoconstriction: causative agents and role of thromboxane receptors. J. Appl. Physiol. 81(5):
2053-2059, 1996. Inhalation of cigarette smoke induces a biphasic
bronchoconstriction in guinea pigs: the first phase is induced by a
combination of cholinergic reflex and tachykinins, whereas the second
phase involves cyclooxygenase metabolites (J.-L. Hong, I. W. Rodger,
and L.-Y. Lee. J. Appl. Physiol. 78:
2260-2266, 1995). This study was carried out to further determine
the causative agents in the smoke and the types of prostanoid receptors
and endogenous prostanoids mediating the bronchoconstriction. Inhalation of 10 ml of high-nicotine cigarette smoke consistently elicited the biphasic bronchoconstriction in anesthetized and artificially ventilated guinea pigs. Pretreatment with hexamethonium (10 mg/kg iv) significantly reduced the first-phase bronchoconstriction but did not have any measurable effect on the second-phase response. In
sharp contrast, gas-phase smoke did not elicit any bronchoconstrictive effect. Furthermore, when the animals were challenged with low-nicotine cigarette smoke, only a single second-phase response was evoked, accompanied by increases in thromboxane (Tx)
B 2 (a stable metabolite of
TxA 2 ), prostaglandin (PG)
D 2 ,
PGF 2 in the bronchoalveolar lavage fluid. The bronchoconstrictive response induced by low-nicotine smoke was completely prevented by pretreatment with SQ-29548 (0.3 mg/kg
iv), a TxA 2 -receptor antagonist.
These results indicate that 1 )
nicotine is the primary causative agent responsible for the first-phase
bronchoconstriction and 2 )
nonnicotine smoke particulates evoke the release of
TxA 2 ,
PGD 2 , and
PGF 2 , which act on
TxA 2 receptors on airway smooth
muscles and induce the second-phase response to cigarette smoke.
hexamethonium; SQ-29548; tachykinins; guinea pigs; prostaglandins
0161-7567/96 $5.00
Copyright © 1996 the American Physiological Society</description><identifier>ISSN: 8750-7587</identifier><identifier>EISSN: 1522-1601</identifier><identifier>DOI: 10.1152/jappl.1996.81.5.2053</identifier><identifier>PMID: 8941529</identifier><identifier>CODEN: JAPHEV</identifier><language>eng</language><publisher>Bethesda, MD: Am Physiological Soc</publisher><subject>Air Pressure ; Animals ; Biological and medical sciences ; Bronchial Diseases - chemically induced ; Bronchial Diseases - physiopathology ; Bronchoalveolar Lavage Fluid ; Cholinergic Antagonists - pharmacology ; Constriction, Pathologic - physiopathology ; Dinoprost - pharmacology ; Guinea Pigs ; Hemodynamics - drug effects ; Hexamethonium - pharmacology ; Hydrazines - pharmacology ; Male ; Medical sciences ; Nicotine - administration & dosage ; Nicotine - pharmacology ; Nicotinic Agonists - administration & dosage ; Nicotinic Agonists - pharmacology ; Receptors, Thromboxane - drug effects ; Receptors, Thromboxane - physiology ; Smoke - analysis ; Smoking - physiopathology ; Tobacco, tobacco smoking ; Toxicology</subject><ispartof>Journal of applied physiology (1985), 1996-11, Vol.81 (5), p.2053-2059</ispartof><rights>1997 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c409t-57756c9e856143b568b2ea8e03cef14f68bd3230fa46b2f9bd79dedf0df2309c3</citedby><cites>FETCH-LOGICAL-c409t-57756c9e856143b568b2ea8e03cef14f68bd3230fa46b2f9bd79dedf0df2309c3</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&idt=2494847$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/8941529$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Hong, Ju-Lun</creatorcontrib><creatorcontrib>Lee, Lu-Yuan</creatorcontrib><title>Cigarette smoke-induced bronchoconstriction: causative agents and role of thromboxane receptors</title><title>Journal of applied physiology (1985)</title><addtitle>J Appl Physiol (1985)</addtitle><description>Ju-Lun
Hong and
Lu-Yuan
Lee
Department of Physiology, University of Kentucky, Lexington,
Kentucky 40536-0084
Received 14 December 1995; accepted in final form 12 July 1996.
Hong, Ju-Lun, and Lu-Yuan Lee. Cigarette smoke-induced
bronchoconstriction: causative agents and role of thromboxane receptors. J. Appl. Physiol. 81(5):
2053-2059, 1996. Inhalation of cigarette smoke induces a biphasic
bronchoconstriction in guinea pigs: the first phase is induced by a
combination of cholinergic reflex and tachykinins, whereas the second
phase involves cyclooxygenase metabolites (J.-L. Hong, I. W. Rodger,
and L.-Y. Lee. J. Appl. Physiol. 78:
2260-2266, 1995). This study was carried out to further determine
the causative agents in the smoke and the types of prostanoid receptors
and endogenous prostanoids mediating the bronchoconstriction. Inhalation of 10 ml of high-nicotine cigarette smoke consistently elicited the biphasic bronchoconstriction in anesthetized and artificially ventilated guinea pigs. Pretreatment with hexamethonium (10 mg/kg iv) significantly reduced the first-phase bronchoconstriction but did not have any measurable effect on the second-phase response. In
sharp contrast, gas-phase smoke did not elicit any bronchoconstrictive effect. Furthermore, when the animals were challenged with low-nicotine cigarette smoke, only a single second-phase response was evoked, accompanied by increases in thromboxane (Tx)
B 2 (a stable metabolite of
TxA 2 ), prostaglandin (PG)
D 2 ,
PGF 2 in the bronchoalveolar lavage fluid. The bronchoconstrictive response induced by low-nicotine smoke was completely prevented by pretreatment with SQ-29548 (0.3 mg/kg
iv), a TxA 2 -receptor antagonist.
These results indicate that 1 )
nicotine is the primary causative agent responsible for the first-phase
bronchoconstriction and 2 )
nonnicotine smoke particulates evoke the release of
TxA 2 ,
PGD 2 , and
PGF 2 , which act on
TxA 2 receptors on airway smooth
muscles and induce the second-phase response to cigarette smoke.
hexamethonium; SQ-29548; tachykinins; guinea pigs; prostaglandins
0161-7567/96 $5.00
Copyright © 1996 the American Physiological Society</description><subject>Air Pressure</subject><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Bronchial Diseases - chemically induced</subject><subject>Bronchial Diseases - physiopathology</subject><subject>Bronchoalveolar Lavage Fluid</subject><subject>Cholinergic Antagonists - pharmacology</subject><subject>Constriction, Pathologic - physiopathology</subject><subject>Dinoprost - pharmacology</subject><subject>Guinea Pigs</subject><subject>Hemodynamics - drug effects</subject><subject>Hexamethonium - pharmacology</subject><subject>Hydrazines - pharmacology</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Nicotine - administration & dosage</subject><subject>Nicotine - pharmacology</subject><subject>Nicotinic Agonists - administration & dosage</subject><subject>Nicotinic Agonists - pharmacology</subject><subject>Receptors, Thromboxane - drug effects</subject><subject>Receptors, Thromboxane - physiology</subject><subject>Smoke - analysis</subject><subject>Smoking - physiopathology</subject><subject>Tobacco, tobacco smoking</subject><subject>Toxicology</subject><issn>8750-7587</issn><issn>1522-1601</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1996</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp1kEFPHCEYhompsVv1H9iEQw9eZoQZmIHezKa2JiZe9EwY-NhBZ4cJsNb9987qZtuLJwLv-_B9eRC6oKSklFdXT3qahpJK2ZSClrysCK-P0GKOqoI2hH5BC9FyUrRctF_Rt5SeCKGMcXqCToRkc08ukFr6lY6QM-C0Ds9Q-NFuDFjcxTCaPpgwphy9yT6MP7HRm6SzfwGsVzDmhPVocQwD4OBw7mNYd-FVj4AjGJhyiOkMHTs9JDjfn6fo8ebXw_JPcXf_-3Z5fVcYRmQueNvyxkgQvKGs7ngjugq0AFIbcJS5-W7rqiZOs6arnOxsKy1YR6ybX6WpTxH7-NfEkFIEp6bo1zpuFSVqp0u961I7XUpQxdVO14x9_8CmTbcGe4D2fub8xz7XyejBRT0anw61ikkmWPtveu9X_V8fQU39NvkwhNVW3WyG4QFe826Dw2Q1WTdjl59jc_u_Rd8AdTGYKA</recordid><startdate>19961101</startdate><enddate>19961101</enddate><creator>Hong, Ju-Lun</creator><creator>Lee, Lu-Yuan</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></search><sort><creationdate>19961101</creationdate><title>Cigarette smoke-induced bronchoconstriction: causative agents and role of thromboxane receptors</title><author>Hong, Ju-Lun ; Lee, Lu-Yuan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c409t-57756c9e856143b568b2ea8e03cef14f68bd3230fa46b2f9bd79dedf0df2309c3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1996</creationdate><topic>Air Pressure</topic><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Bronchial Diseases - chemically induced</topic><topic>Bronchial Diseases - physiopathology</topic><topic>Bronchoalveolar Lavage Fluid</topic><topic>Cholinergic Antagonists - pharmacology</topic><topic>Constriction, Pathologic - physiopathology</topic><topic>Dinoprost - pharmacology</topic><topic>Guinea Pigs</topic><topic>Hemodynamics - drug effects</topic><topic>Hexamethonium - pharmacology</topic><topic>Hydrazines - pharmacology</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Nicotine - administration & dosage</topic><topic>Nicotine - pharmacology</topic><topic>Nicotinic Agonists - administration & dosage</topic><topic>Nicotinic Agonists - pharmacology</topic><topic>Receptors, Thromboxane - drug effects</topic><topic>Receptors, Thromboxane - physiology</topic><topic>Smoke - analysis</topic><topic>Smoking - physiopathology</topic><topic>Tobacco, tobacco smoking</topic><topic>Toxicology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Hong, Ju-Lun</creatorcontrib><creatorcontrib>Lee, Lu-Yuan</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><jtitle>Journal of applied physiology (1985)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Hong, Ju-Lun</au><au>Lee, Lu-Yuan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cigarette smoke-induced bronchoconstriction: causative agents and role of thromboxane receptors</atitle><jtitle>Journal of applied physiology (1985)</jtitle><addtitle>J Appl Physiol (1985)</addtitle><date>1996-11-01</date><risdate>1996</risdate><volume>81</volume><issue>5</issue><spage>2053</spage><epage>2059</epage><pages>2053-2059</pages><issn>8750-7587</issn><eissn>1522-1601</eissn><coden>JAPHEV</coden><abstract>Ju-Lun
Hong and
Lu-Yuan
Lee
Department of Physiology, University of Kentucky, Lexington,
Kentucky 40536-0084
Received 14 December 1995; accepted in final form 12 July 1996.
Hong, Ju-Lun, and Lu-Yuan Lee. Cigarette smoke-induced
bronchoconstriction: causative agents and role of thromboxane receptors. J. Appl. Physiol. 81(5):
2053-2059, 1996. Inhalation of cigarette smoke induces a biphasic
bronchoconstriction in guinea pigs: the first phase is induced by a
combination of cholinergic reflex and tachykinins, whereas the second
phase involves cyclooxygenase metabolites (J.-L. Hong, I. W. Rodger,
and L.-Y. Lee. J. Appl. Physiol. 78:
2260-2266, 1995). This study was carried out to further determine
the causative agents in the smoke and the types of prostanoid receptors
and endogenous prostanoids mediating the bronchoconstriction. Inhalation of 10 ml of high-nicotine cigarette smoke consistently elicited the biphasic bronchoconstriction in anesthetized and artificially ventilated guinea pigs. Pretreatment with hexamethonium (10 mg/kg iv) significantly reduced the first-phase bronchoconstriction but did not have any measurable effect on the second-phase response. In
sharp contrast, gas-phase smoke did not elicit any bronchoconstrictive effect. Furthermore, when the animals were challenged with low-nicotine cigarette smoke, only a single second-phase response was evoked, accompanied by increases in thromboxane (Tx)
B 2 (a stable metabolite of
TxA 2 ), prostaglandin (PG)
D 2 ,
PGF 2 in the bronchoalveolar lavage fluid. The bronchoconstrictive response induced by low-nicotine smoke was completely prevented by pretreatment with SQ-29548 (0.3 mg/kg
iv), a TxA 2 -receptor antagonist.
These results indicate that 1 )
nicotine is the primary causative agent responsible for the first-phase
bronchoconstriction and 2 )
nonnicotine smoke particulates evoke the release of
TxA 2 ,
PGD 2 , and
PGF 2 , which act on
TxA 2 receptors on airway smooth
muscles and induce the second-phase response to cigarette smoke.
hexamethonium; SQ-29548; tachykinins; guinea pigs; prostaglandins
0161-7567/96 $5.00
Copyright © 1996 the American Physiological Society</abstract><cop>Bethesda, MD</cop><pub>Am Physiological Soc</pub><pmid>8941529</pmid><doi>10.1152/jappl.1996.81.5.2053</doi><tpages>7</tpages></addata></record> |
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| ispartof | Journal of applied physiology (1985), 1996-11, Vol.81 (5), p.2053-2059 |
| issn | 8750-7587 1522-1601 |
| language | eng |
| recordid | cdi_pubmed_primary_8941529 |
| source | MEDLINE; American Physiological Society; EZB-FREE-00999 freely available EZB journals |
| subjects | Air Pressure Animals Biological and medical sciences Bronchial Diseases - chemically induced Bronchial Diseases - physiopathology Bronchoalveolar Lavage Fluid Cholinergic Antagonists - pharmacology Constriction, Pathologic - physiopathology Dinoprost - pharmacology Guinea Pigs Hemodynamics - drug effects Hexamethonium - pharmacology Hydrazines - pharmacology Male Medical sciences Nicotine - administration & dosage Nicotine - pharmacology Nicotinic Agonists - administration & dosage Nicotinic Agonists - pharmacology Receptors, Thromboxane - drug effects Receptors, Thromboxane - physiology Smoke - analysis Smoking - physiopathology Tobacco, tobacco smoking Toxicology |
| title | Cigarette smoke-induced bronchoconstriction: causative agents and role of thromboxane receptors |
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