Effects of S-nitrosoglutathione on acute vasoconstriction and glutamate release after subarachnoid hemorrhage
Subarachnoid hemorrhage (SAH) causes acute vasoconstriction that contributes to ischemic brain injury shortly after the initial bleed. It has been theorized that decreased availability of nitric oxide (NO) may contribute to acute vasoconstriction. Therefore we examined the effect of the NO donor N-n...
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| Veröffentlicht in: | Stroke (1970) 1999-09, Vol.30 (9), p.1955-1961 |
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| container_issue | 9 |
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| container_title | Stroke (1970) |
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| creator | Sehba, F A Ding, W H Chereshnev, I Bederson, J B |
| description | Subarachnoid hemorrhage (SAH) causes acute vasoconstriction that contributes to ischemic brain injury shortly after the initial bleed. It has been theorized that decreased availability of nitric oxide (NO) may contribute to acute vasoconstriction. Therefore we examined the effect of the NO donor N-nitroso glutathione (GSNO) on acute vasoconstriction and early ischemic glutamate release after experimental SAH.
SAH was induced by the endovascular suture method in anesthetized rats. GSNO (1 micromol/L/kg, n=31) or saline (n=21) was injected 5 minutes after SAH. Sham-operated rats received GSNO (1 micromol/L/kg, n=5) 5 minutes after sham surgery. Arterial and intracranial pressures, cerebral blood flow (CBF), and extracellular glutamate release were measured serially for 60 minutes after SAH. SAH size was determined, and vascular measurements were made histologically.
GSNO had no effect on resting blood pressure, intracranial pressure, cerebral perfusion pressure, or CBF in sham-operated animals. However, administration of GSNO after SAH was associated with significantly increased CBF (161.6+/-26.6% versus saline 37.1+/-5.5%, 60 minutes after SAH, P |
| doi_str_mv | 10.1161/01.STR.30.9.1955 |
| format | Article |
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SAH was induced by the endovascular suture method in anesthetized rats. GSNO (1 micromol/L/kg, n=31) or saline (n=21) was injected 5 minutes after SAH. Sham-operated rats received GSNO (1 micromol/L/kg, n=5) 5 minutes after sham surgery. Arterial and intracranial pressures, cerebral blood flow (CBF), and extracellular glutamate release were measured serially for 60 minutes after SAH. SAH size was determined, and vascular measurements were made histologically.
GSNO had no effect on resting blood pressure, intracranial pressure, cerebral perfusion pressure, or CBF in sham-operated animals. However, administration of GSNO after SAH was associated with significantly increased CBF (161.6+/-26.6% versus saline 37.1+/-5.5%, 60 minutes after SAH, P<0.05), increased blood vessel diameter (internal carotid artery [ICA] 285.0+/-16.5 microm versus saline 149.2+/-14.1 microm, P<0.01), decreased vessel wall thickness (ICA12.9+/-0.7 microm versus saline 25.1+/-1.6 microm, P<0.01), and decreased extracellular glutamate levels (3315.6+/-1048.3% versus saline469. 7+/-134.3%, P<0.05). Blood pressure decreased transiently, whereas intracranial pressure, cerebral perfusion pressure, and SAH size were not affected.
These results suggest that GSNO can reverse acute vasoconstriction and prevent ischemic brain injury after SAH. This further implies that acute vasoconstriction contributes significantly to ischemic brain injury after SAH and is mediated in part by decreased availability of NO.</description><identifier>ISSN: 0039-2499</identifier><identifier>EISSN: 1524-4628</identifier><identifier>DOI: 10.1161/01.STR.30.9.1955</identifier><identifier>PMID: 10471450</identifier><identifier>CODEN: SJCCA7</identifier><language>eng</language><publisher>United States: American Heart Association, Inc</publisher><subject>Animals ; Blood Vessels - drug effects ; Blood Vessels - pathology ; Cerebrovascular Circulation - drug effects ; Extracellular Space - metabolism ; Glutamic Acid - metabolism ; Glutathione - analogs & derivatives ; Glutathione - pharmacology ; Male ; Nitric Oxide Donors - pharmacology ; Nitroso Compounds - pharmacology ; Rats ; Rats, Sprague-Dawley ; S-Nitrosoglutathione ; Subarachnoid Hemorrhage - metabolism ; Subarachnoid Hemorrhage - pathology ; Subarachnoid Hemorrhage - physiopathology ; Vasoconstriction - drug effects ; Vasodilation</subject><ispartof>Stroke (1970), 1999-09, Vol.30 (9), p.1955-1961</ispartof><rights>Copyright American Heart Association, Inc. Sep 1999</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c364t-48432afdbcf1c8b6f6b061fe1f7ea5f590a878e89ae75305e46aa383470bbf813</citedby><cites>FETCH-LOGICAL-c364t-48432afdbcf1c8b6f6b061fe1f7ea5f590a878e89ae75305e46aa383470bbf813</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,776,780,3674,27901,27902</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/10471450$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Sehba, F A</creatorcontrib><creatorcontrib>Ding, W H</creatorcontrib><creatorcontrib>Chereshnev, I</creatorcontrib><creatorcontrib>Bederson, J B</creatorcontrib><title>Effects of S-nitrosoglutathione on acute vasoconstriction and glutamate release after subarachnoid hemorrhage</title><title>Stroke (1970)</title><addtitle>Stroke</addtitle><description>Subarachnoid hemorrhage (SAH) causes acute vasoconstriction that contributes to ischemic brain injury shortly after the initial bleed. It has been theorized that decreased availability of nitric oxide (NO) may contribute to acute vasoconstriction. Therefore we examined the effect of the NO donor N-nitroso glutathione (GSNO) on acute vasoconstriction and early ischemic glutamate release after experimental SAH.
SAH was induced by the endovascular suture method in anesthetized rats. GSNO (1 micromol/L/kg, n=31) or saline (n=21) was injected 5 minutes after SAH. Sham-operated rats received GSNO (1 micromol/L/kg, n=5) 5 minutes after sham surgery. Arterial and intracranial pressures, cerebral blood flow (CBF), and extracellular glutamate release were measured serially for 60 minutes after SAH. SAH size was determined, and vascular measurements were made histologically.
GSNO had no effect on resting blood pressure, intracranial pressure, cerebral perfusion pressure, or CBF in sham-operated animals. However, administration of GSNO after SAH was associated with significantly increased CBF (161.6+/-26.6% versus saline 37.1+/-5.5%, 60 minutes after SAH, P<0.05), increased blood vessel diameter (internal carotid artery [ICA] 285.0+/-16.5 microm versus saline 149.2+/-14.1 microm, P<0.01), decreased vessel wall thickness (ICA12.9+/-0.7 microm versus saline 25.1+/-1.6 microm, P<0.01), and decreased extracellular glutamate levels (3315.6+/-1048.3% versus saline469. 7+/-134.3%, P<0.05). Blood pressure decreased transiently, whereas intracranial pressure, cerebral perfusion pressure, and SAH size were not affected.
These results suggest that GSNO can reverse acute vasoconstriction and prevent ischemic brain injury after SAH. This further implies that acute vasoconstriction contributes significantly to ischemic brain injury after SAH and is mediated in part by decreased availability of NO.</description><subject>Animals</subject><subject>Blood Vessels - drug effects</subject><subject>Blood Vessels - pathology</subject><subject>Cerebrovascular Circulation - drug effects</subject><subject>Extracellular Space - metabolism</subject><subject>Glutamic Acid - metabolism</subject><subject>Glutathione - analogs & derivatives</subject><subject>Glutathione - pharmacology</subject><subject>Male</subject><subject>Nitric Oxide Donors - pharmacology</subject><subject>Nitroso Compounds - pharmacology</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>S-Nitrosoglutathione</subject><subject>Subarachnoid Hemorrhage - metabolism</subject><subject>Subarachnoid Hemorrhage - pathology</subject><subject>Subarachnoid Hemorrhage - physiopathology</subject><subject>Vasoconstriction - drug effects</subject><subject>Vasodilation</subject><issn>0039-2499</issn><issn>1524-4628</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1999</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkUFr3DAQhUVJaTZp7z0FkUNvdkeWZEvHEtI2EAgk6VmMtaOsg20lkhzIv6-3m0PJaWDme4_hPca-CqiFaMV3EPXd_W0toba1sFp_YBuhG1WptjFHbAMgbdUoa4_ZSc6PANBIoz-xYwGqE0rDhk2XIZAvmcfA76p5KCnm-DAuBctuiDPxOHP0SyH-gjn6OOeSBl-G_Xre8n_khOs50UiYiWMolHheekzod3MctnxHU0xphw_0mX0MOGb68jZP2Z-fl_cXv6vrm19XFz-uKy9bVSpllGwwbHsfhDd9G9oeWhFIhI5QB20BTWfIWKROS9CkWkRppOqg74MR8pR9O_g-pfi8UC5uGrKnccSZ4pJdt49CmGYFz9-Bj3FJ8_qbE7YzEmTTrhAcIL-GkxMF95SGCdOrE-D2PTgQbu3BSXDW7XtYJWdvvks_0fY_wSF4-RdnNYWm</recordid><startdate>19990901</startdate><enddate>19990901</enddate><creator>Sehba, F A</creator><creator>Ding, W H</creator><creator>Chereshnev, I</creator><creator>Bederson, J B</creator><general>American Heart Association, Inc</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>K9.</scope><scope>NAPCQ</scope><scope>7X8</scope></search><sort><creationdate>19990901</creationdate><title>Effects of S-nitrosoglutathione on acute vasoconstriction and glutamate release after subarachnoid hemorrhage</title><author>Sehba, F A ; Ding, W H ; Chereshnev, I ; Bederson, J B</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c364t-48432afdbcf1c8b6f6b061fe1f7ea5f590a878e89ae75305e46aa383470bbf813</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1999</creationdate><topic>Animals</topic><topic>Blood Vessels - drug effects</topic><topic>Blood Vessels - pathology</topic><topic>Cerebrovascular Circulation - drug effects</topic><topic>Extracellular Space - metabolism</topic><topic>Glutamic Acid - metabolism</topic><topic>Glutathione - analogs & derivatives</topic><topic>Glutathione - pharmacology</topic><topic>Male</topic><topic>Nitric Oxide Donors - pharmacology</topic><topic>Nitroso Compounds - pharmacology</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>S-Nitrosoglutathione</topic><topic>Subarachnoid Hemorrhage - metabolism</topic><topic>Subarachnoid Hemorrhage - pathology</topic><topic>Subarachnoid Hemorrhage - physiopathology</topic><topic>Vasoconstriction - drug effects</topic><topic>Vasodilation</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Sehba, F A</creatorcontrib><creatorcontrib>Ding, W H</creatorcontrib><creatorcontrib>Chereshnev, I</creatorcontrib><creatorcontrib>Bederson, J B</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>MEDLINE - Academic</collection><jtitle>Stroke (1970)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Sehba, F A</au><au>Ding, W H</au><au>Chereshnev, I</au><au>Bederson, J B</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effects of S-nitrosoglutathione on acute vasoconstriction and glutamate release after subarachnoid hemorrhage</atitle><jtitle>Stroke (1970)</jtitle><addtitle>Stroke</addtitle><date>1999-09-01</date><risdate>1999</risdate><volume>30</volume><issue>9</issue><spage>1955</spage><epage>1961</epage><pages>1955-1961</pages><issn>0039-2499</issn><eissn>1524-4628</eissn><coden>SJCCA7</coden><abstract>Subarachnoid hemorrhage (SAH) causes acute vasoconstriction that contributes to ischemic brain injury shortly after the initial bleed. It has been theorized that decreased availability of nitric oxide (NO) may contribute to acute vasoconstriction. Therefore we examined the effect of the NO donor N-nitroso glutathione (GSNO) on acute vasoconstriction and early ischemic glutamate release after experimental SAH.
SAH was induced by the endovascular suture method in anesthetized rats. GSNO (1 micromol/L/kg, n=31) or saline (n=21) was injected 5 minutes after SAH. Sham-operated rats received GSNO (1 micromol/L/kg, n=5) 5 minutes after sham surgery. Arterial and intracranial pressures, cerebral blood flow (CBF), and extracellular glutamate release were measured serially for 60 minutes after SAH. SAH size was determined, and vascular measurements were made histologically.
GSNO had no effect on resting blood pressure, intracranial pressure, cerebral perfusion pressure, or CBF in sham-operated animals. However, administration of GSNO after SAH was associated with significantly increased CBF (161.6+/-26.6% versus saline 37.1+/-5.5%, 60 minutes after SAH, P<0.05), increased blood vessel diameter (internal carotid artery [ICA] 285.0+/-16.5 microm versus saline 149.2+/-14.1 microm, P<0.01), decreased vessel wall thickness (ICA12.9+/-0.7 microm versus saline 25.1+/-1.6 microm, P<0.01), and decreased extracellular glutamate levels (3315.6+/-1048.3% versus saline469. 7+/-134.3%, P<0.05). Blood pressure decreased transiently, whereas intracranial pressure, cerebral perfusion pressure, and SAH size were not affected.
These results suggest that GSNO can reverse acute vasoconstriction and prevent ischemic brain injury after SAH. This further implies that acute vasoconstriction contributes significantly to ischemic brain injury after SAH and is mediated in part by decreased availability of NO.</abstract><cop>United States</cop><pub>American Heart Association, Inc</pub><pmid>10471450</pmid><doi>10.1161/01.STR.30.9.1955</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; American Heart Association Journals; Elektronische Zeitschriftenbibliothek - Frei zugängliche E-Journals; Alma/SFX Local Collection; Journals@Ovid Complete |
| subjects | Animals Blood Vessels - drug effects Blood Vessels - pathology Cerebrovascular Circulation - drug effects Extracellular Space - metabolism Glutamic Acid - metabolism Glutathione - analogs & derivatives Glutathione - pharmacology Male Nitric Oxide Donors - pharmacology Nitroso Compounds - pharmacology Rats Rats, Sprague-Dawley S-Nitrosoglutathione Subarachnoid Hemorrhage - metabolism Subarachnoid Hemorrhage - pathology Subarachnoid Hemorrhage - physiopathology Vasoconstriction - drug effects Vasodilation |
| title | Effects of S-nitrosoglutathione on acute vasoconstriction and glutamate release after subarachnoid hemorrhage |
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