Role of nitric oxide in post-ischemic gingival hyperemia in anesthetized dogs
The possible involvement of nitric oxide ( * NO) in the preservation of blood flow to the canine gingiva after compression of gingival tissue was studied. Gingival blood flow, gingival tissue oxygen partial pressure (PO 2 ), external carotid arterial blood pressure and external carotid arterial bloo...
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| Veröffentlicht in: | Redox report : communications in free radical research 2002-01, Vol.7 (5), p.300-303 |
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| creator | Omori, Yoichi Takahashi, Shun-Suke Todoki, Kazuo |
| description | The possible involvement of nitric oxide (
*
NO) in the preservation of blood flow to the canine gingiva after compression of gingival tissue was studied. Gingival blood flow, gingival tissue oxygen partial pressure (PO
2
), external carotid arterial blood pressure and external carotid arterial blood flow were monitored before, during, and after compression of gingival tissue in the presence and absence of the nitric oxide synthase inhibitor, N
ω
-nitro-L-arginine-methyl-ester (L-NAME). Compression of gingival tissue resulted in an immediate decrease in gingival blood flow and tissue PO
2
. After the compression of gingival tissue, hyperemia was observed in the gingiva, which depended on the duration of ischemia. Gingival tissue PO
2
slowly recovered during hyperemia. Pretreatment with L-NAME (60 mg/kg, i.a.) significantly suppressed reactive hyperemia in gingival tissue. The L-NAME-suppressed reactive hyperemia was partially reversed by treatment with L-arginine (60 mg/kg, i.a.). In addition,
*
NO was detected using an
*
NO selective electrode during interruption of blood flow and during reactive hyperemia in the gingiva. These results suggest that
*
NO contributes to the vasodilation during reactive hyperemia in gingival tissue, and aids in the maintenance of homeostasis in gingival circulation. |
| doi_str_mv | 10.1179/135100002125000839 |
| format | Article |
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*
NO) in the preservation of blood flow to the canine gingiva after compression of gingival tissue was studied. Gingival blood flow, gingival tissue oxygen partial pressure (PO
2
), external carotid arterial blood pressure and external carotid arterial blood flow were monitored before, during, and after compression of gingival tissue in the presence and absence of the nitric oxide synthase inhibitor, N
ω
-nitro-L-arginine-methyl-ester (L-NAME). Compression of gingival tissue resulted in an immediate decrease in gingival blood flow and tissue PO
2
. After the compression of gingival tissue, hyperemia was observed in the gingiva, which depended on the duration of ischemia. Gingival tissue PO
2
slowly recovered during hyperemia. Pretreatment with L-NAME (60 mg/kg, i.a.) significantly suppressed reactive hyperemia in gingival tissue. The L-NAME-suppressed reactive hyperemia was partially reversed by treatment with L-arginine (60 mg/kg, i.a.). In addition,
*
NO was detected using an
*
NO selective electrode during interruption of blood flow and during reactive hyperemia in the gingiva. These results suggest that
*
NO contributes to the vasodilation during reactive hyperemia in gingival tissue, and aids in the maintenance of homeostasis in gingival circulation.</description><identifier>ISSN: 1351-0002</identifier><identifier>EISSN: 1743-2928</identifier><identifier>DOI: 10.1179/135100002125000839</identifier><identifier>PMID: 12688514</identifier><language>eng</language><publisher>England: Taylor & Francis</publisher><subject>Anesthesia ; Animals ; Dogs ; Electrochemistry ; Enzyme Inhibitors - pharmacology ; Female ; Hemodynamics ; Ischemia ; Laser-Doppler Flowmetry ; NG-Nitroarginine Methyl Ester - pharmacology ; Nitric Oxide - antagonists & inhibitors ; Nitric Oxide - physiology ; Oxygen - metabolism ; Polyethylene - chemistry ; Pressure ; Time Factors</subject><ispartof>Redox report : communications in free radical research, 2002-01, Vol.7 (5), p.300-303</ispartof><rights>2002 Maney Publishing 2002</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c419t-5ae99bd197b37bec187597fbaef49310aa465e3b566ce293c4197ed547ad313e3</citedby><cites>FETCH-LOGICAL-c419t-5ae99bd197b37bec187597fbaef49310aa465e3b566ce293c4197ed547ad313e3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/12688514$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Omori, Yoichi</creatorcontrib><creatorcontrib>Takahashi, Shun-Suke</creatorcontrib><creatorcontrib>Todoki, Kazuo</creatorcontrib><title>Role of nitric oxide in post-ischemic gingival hyperemia in anesthetized dogs</title><title>Redox report : communications in free radical research</title><addtitle>Redox Rep</addtitle><description>The possible involvement of nitric oxide (
*
NO) in the preservation of blood flow to the canine gingiva after compression of gingival tissue was studied. Gingival blood flow, gingival tissue oxygen partial pressure (PO
2
), external carotid arterial blood pressure and external carotid arterial blood flow were monitored before, during, and after compression of gingival tissue in the presence and absence of the nitric oxide synthase inhibitor, N
ω
-nitro-L-arginine-methyl-ester (L-NAME). Compression of gingival tissue resulted in an immediate decrease in gingival blood flow and tissue PO
2
. After the compression of gingival tissue, hyperemia was observed in the gingiva, which depended on the duration of ischemia. Gingival tissue PO
2
slowly recovered during hyperemia. Pretreatment with L-NAME (60 mg/kg, i.a.) significantly suppressed reactive hyperemia in gingival tissue. The L-NAME-suppressed reactive hyperemia was partially reversed by treatment with L-arginine (60 mg/kg, i.a.). In addition,
*
NO was detected using an
*
NO selective electrode during interruption of blood flow and during reactive hyperemia in the gingiva. These results suggest that
*
NO contributes to the vasodilation during reactive hyperemia in gingival tissue, and aids in the maintenance of homeostasis in gingival circulation.</description><subject>Anesthesia</subject><subject>Animals</subject><subject>Dogs</subject><subject>Electrochemistry</subject><subject>Enzyme Inhibitors - pharmacology</subject><subject>Female</subject><subject>Hemodynamics</subject><subject>Ischemia</subject><subject>Laser-Doppler Flowmetry</subject><subject>NG-Nitroarginine Methyl Ester - pharmacology</subject><subject>Nitric Oxide - antagonists & inhibitors</subject><subject>Nitric Oxide - physiology</subject><subject>Oxygen - metabolism</subject><subject>Polyethylene - chemistry</subject><subject>Pressure</subject><subject>Time Factors</subject><issn>1351-0002</issn><issn>1743-2928</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kE9LxDAQxYMo7rr6BTxIT96qTdI0zcGDLP6DFUH0HNJkuhtpm5p01fXTm7ILHgTnMsPwezOPh9Apzi4w5uISU4azWAQTFltJxR6aYp7TlAhS7sc5AukITNBRCG9xooUoD9EEk6IsGc6n6PHZNZC4Ouns4K1O3Jc1kNgu6V0YUhv0Ctq4XtpuaT9Uk6w2Pfi4UiOjOgjDCgb7DSYxbhmO0UGtmgAnuz5Dr7c3L_P7dPF09zC_XqQ6x2JImQIhKoMFryivQOOSM8HrSkGdC4ozpfKCAa1YUWgggo4qDoblXBmKKdAZOt_e7b17X0cTso1WoWmiI7cOkpOS85wVESRbUHsXgoda9t62ym8kzuQYovwbYhSd7a6vqxbMr2SXWgSutoDtaudb9el8Y-SgNo3ztVedtkHSfx78ACE5f4Q</recordid><startdate>20020101</startdate><enddate>20020101</enddate><creator>Omori, Yoichi</creator><creator>Takahashi, Shun-Suke</creator><creator>Todoki, Kazuo</creator><general>Taylor & Francis</general><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>20020101</creationdate><title>Role of nitric oxide in post-ischemic gingival hyperemia in anesthetized dogs</title><author>Omori, Yoichi ; Takahashi, Shun-Suke ; Todoki, Kazuo</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c419t-5ae99bd197b37bec187597fbaef49310aa465e3b566ce293c4197ed547ad313e3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Anesthesia</topic><topic>Animals</topic><topic>Dogs</topic><topic>Electrochemistry</topic><topic>Enzyme Inhibitors - pharmacology</topic><topic>Female</topic><topic>Hemodynamics</topic><topic>Ischemia</topic><topic>Laser-Doppler Flowmetry</topic><topic>NG-Nitroarginine Methyl Ester - pharmacology</topic><topic>Nitric Oxide - antagonists & inhibitors</topic><topic>Nitric Oxide - physiology</topic><topic>Oxygen - metabolism</topic><topic>Polyethylene - chemistry</topic><topic>Pressure</topic><topic>Time Factors</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Omori, Yoichi</creatorcontrib><creatorcontrib>Takahashi, Shun-Suke</creatorcontrib><creatorcontrib>Todoki, Kazuo</creatorcontrib><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>Redox report : communications in free radical research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Omori, Yoichi</au><au>Takahashi, Shun-Suke</au><au>Todoki, Kazuo</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Role of nitric oxide in post-ischemic gingival hyperemia in anesthetized dogs</atitle><jtitle>Redox report : communications in free radical research</jtitle><addtitle>Redox Rep</addtitle><date>2002-01-01</date><risdate>2002</risdate><volume>7</volume><issue>5</issue><spage>300</spage><epage>303</epage><pages>300-303</pages><issn>1351-0002</issn><eissn>1743-2928</eissn><abstract>The possible involvement of nitric oxide (
*
NO) in the preservation of blood flow to the canine gingiva after compression of gingival tissue was studied. Gingival blood flow, gingival tissue oxygen partial pressure (PO
2
), external carotid arterial blood pressure and external carotid arterial blood flow were monitored before, during, and after compression of gingival tissue in the presence and absence of the nitric oxide synthase inhibitor, N
ω
-nitro-L-arginine-methyl-ester (L-NAME). Compression of gingival tissue resulted in an immediate decrease in gingival blood flow and tissue PO
2
. After the compression of gingival tissue, hyperemia was observed in the gingiva, which depended on the duration of ischemia. Gingival tissue PO
2
slowly recovered during hyperemia. Pretreatment with L-NAME (60 mg/kg, i.a.) significantly suppressed reactive hyperemia in gingival tissue. The L-NAME-suppressed reactive hyperemia was partially reversed by treatment with L-arginine (60 mg/kg, i.a.). In addition,
*
NO was detected using an
*
NO selective electrode during interruption of blood flow and during reactive hyperemia in the gingiva. These results suggest that
*
NO contributes to the vasodilation during reactive hyperemia in gingival tissue, and aids in the maintenance of homeostasis in gingival circulation.</abstract><cop>England</cop><pub>Taylor & Francis</pub><pmid>12688514</pmid><doi>10.1179/135100002125000839</doi><tpages>4</tpages></addata></record> |
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| source | MEDLINE; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection |
| subjects | Anesthesia Animals Dogs Electrochemistry Enzyme Inhibitors - pharmacology Female Hemodynamics Ischemia Laser-Doppler Flowmetry NG-Nitroarginine Methyl Ester - pharmacology Nitric Oxide - antagonists & inhibitors Nitric Oxide - physiology Oxygen - metabolism Polyethylene - chemistry Pressure Time Factors |
| title | Role of nitric oxide in post-ischemic gingival hyperemia in anesthetized dogs |
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