Upregulation of Connexin 40 Mediated by Nitric Oxide Attenuates Cerebral Vasospasm After Subarachnoid Hemorrhage via the Nitric Oxide-Cyclic Guanosine Monophosphate-Protein Kinase G Pathway
The present study was performed to elucidate the role of nitric oxide (NO) and connexin 40 (Cx40) in the induction of cerebral vasospasm after subarachnoid hemorrhage (SAH) in vivo. A SAH rat model was established using the double-bleed method. A total of 108 Sprague-Dawley rats weighing 250–300 g w...
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| creator | Lan, Shi Hai Lai, Wen Tao Zheng, Su Yue Yang, Le Fang, Lin Chun Zhou, Lin Tang, Bin Duan, Jian Hong, Tao |
| description | The present study was performed to elucidate the role of nitric oxide (NO) and connexin 40 (Cx40) in the induction of cerebral vasospasm after subarachnoid hemorrhage (SAH) in vivo.
A SAH rat model was established using the double-bleed method. A total of 108 Sprague-Dawley rats weighing 250–300 g were randomly divided into 6 groups: SAH; SAH plus diethylenetriamine (DETA)/NO (exogenous NO donor); SAH plus 8-bromoadenosine (8-Br)-cyclic guanosine monophosphate (cGMP; protein kinase G [PKG] activator); SAH plus DETA/NO plus KT5823 (PKG inhibitor); SAH plus DETA/NO plus 40Gap27 (Cx40 inhibitor); and sham. The changes in the diameter of the branch microvessels in the middle cerebral artery were recorded. The neurological score was evaluated using the Garcia scoring system. Basilar artery (BA) tension was measured using the Danish Myo Technology myograph system. Cx40 protein expression was analyzed using immunofluorescence and Western blotting. Endothelial NO synthase, soluble guanylate cyclase, and PKG protein expression were measured by Western blotting.
A considerable narrowing of the cerebral vessels was detected in the SAH group compared with that in the sham group. Moreover, compared with the sham group, the SAH group showed a marked decrease in Cx40, endothelial NO synthase, soluble guanylate cyclase, and PKG expression. The expression of Cx40 and PKG were obviously higher in the SAH plus DETA/NO and SAH plus 8-Br-cGMP groups than in the SAH group. However, Cx40 was lower in the SAH plus DETA/NO plus KT5823 and SAH plus DETA/NO plus 40Gap27 groups than in the SAH plus ETA/NO group. The BAs showed significant vasodilation in the SAH plus DETA/NO and SAH plus 8-Br-cGMP groups. However, the vasodilation response of BAs was inhibited in the SAH plus DETA/NO plus KT5823 and SAH plus DETA-NO plus 40Gap27 groups.
The NO-cGMP-PKG pathway alleviated cerebral vasospasm via Cx40 upregulation. |
| doi_str_mv | 10.1016/j.wneu.2020.01.026 |
| format | Article |
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A SAH rat model was established using the double-bleed method. A total of 108 Sprague-Dawley rats weighing 250–300 g were randomly divided into 6 groups: SAH; SAH plus diethylenetriamine (DETA)/NO (exogenous NO donor); SAH plus 8-bromoadenosine (8-Br)-cyclic guanosine monophosphate (cGMP; protein kinase G [PKG] activator); SAH plus DETA/NO plus KT5823 (PKG inhibitor); SAH plus DETA/NO plus 40Gap27 (Cx40 inhibitor); and sham. The changes in the diameter of the branch microvessels in the middle cerebral artery were recorded. The neurological score was evaluated using the Garcia scoring system. Basilar artery (BA) tension was measured using the Danish Myo Technology myograph system. Cx40 protein expression was analyzed using immunofluorescence and Western blotting. Endothelial NO synthase, soluble guanylate cyclase, and PKG protein expression were measured by Western blotting.
A considerable narrowing of the cerebral vessels was detected in the SAH group compared with that in the sham group. Moreover, compared with the sham group, the SAH group showed a marked decrease in Cx40, endothelial NO synthase, soluble guanylate cyclase, and PKG expression. The expression of Cx40 and PKG were obviously higher in the SAH plus DETA/NO and SAH plus 8-Br-cGMP groups than in the SAH group. However, Cx40 was lower in the SAH plus DETA/NO plus KT5823 and SAH plus DETA/NO plus 40Gap27 groups than in the SAH plus ETA/NO group. The BAs showed significant vasodilation in the SAH plus DETA/NO and SAH plus 8-Br-cGMP groups. However, the vasodilation response of BAs was inhibited in the SAH plus DETA/NO plus KT5823 and SAH plus DETA-NO plus 40Gap27 groups.
The NO-cGMP-PKG pathway alleviated cerebral vasospasm via Cx40 upregulation.</description><identifier>ISSN: 1878-8750</identifier><identifier>EISSN: 1878-8769</identifier><identifier>DOI: 10.1016/j.wneu.2020.01.026</identifier><identifier>PMID: 31953101</identifier><language>eng</language><publisher>NEW YORK: Elsevier Inc</publisher><subject>Animals ; Cerebral vasospasm ; Clinical Neurology ; Connexin 40 ; Connexins - metabolism ; Connexins - physiology ; Cyclic GMP-Dependent Protein Kinases - metabolism ; Disease Models, Animal ; Gap Junction alpha-5 Protein ; Guanosine Monophosphate - metabolism ; Life Sciences & Biomedicine ; Neurosciences & Neurology ; Nitric oxide ; Nitric Oxide - metabolism ; Nitric Oxide - physiology ; Nitric Oxide Synthase - metabolism ; Rats, Sprague-Dawley ; Science & Technology ; Signal Transduction - physiology ; Soluble Guanylyl Cyclase - metabolism ; Subarachnoid hemorrhage ; Subarachnoid Hemorrhage - physiopathology ; Surgery ; Up-Regulation - physiology ; Vasospasm, Intracranial - physiopathology</subject><ispartof>World neurosurgery, 2020-04, Vol.136, p.e476-e486</ispartof><rights>2020 Elsevier Inc.</rights><rights>Copyright © 2020 Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>true</woscitedreferencessubscribed><woscitedreferencescount>5</woscitedreferencescount><woscitedreferencesoriginalsourcerecordid>wos000520838600051</woscitedreferencesoriginalsourcerecordid><citedby>FETCH-LOGICAL-c356t-fb1ada36c9981c0d0dea003e66c5769c0fec3a2d0fc2f4f817fb79eb89172ef3</citedby><cites>FETCH-LOGICAL-c356t-fb1ada36c9981c0d0dea003e66c5769c0fec3a2d0fc2f4f817fb79eb89172ef3</cites><orcidid>0000-0002-2693-8991 ; 0000-0002-6110-9179</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.wneu.2020.01.026$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>315,781,785,3551,27928,27929,45999</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31953101$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Lan, Shi Hai</creatorcontrib><creatorcontrib>Lai, Wen Tao</creatorcontrib><creatorcontrib>Zheng, Su Yue</creatorcontrib><creatorcontrib>Yang, Le</creatorcontrib><creatorcontrib>Fang, Lin Chun</creatorcontrib><creatorcontrib>Zhou, Lin</creatorcontrib><creatorcontrib>Tang, Bin</creatorcontrib><creatorcontrib>Duan, Jian</creatorcontrib><creatorcontrib>Hong, Tao</creatorcontrib><title>Upregulation of Connexin 40 Mediated by Nitric Oxide Attenuates Cerebral Vasospasm After Subarachnoid Hemorrhage via the Nitric Oxide-Cyclic Guanosine Monophosphate-Protein Kinase G Pathway</title><title>World neurosurgery</title><addtitle>WORLD NEUROSURG</addtitle><addtitle>World Neurosurg</addtitle><description>The present study was performed to elucidate the role of nitric oxide (NO) and connexin 40 (Cx40) in the induction of cerebral vasospasm after subarachnoid hemorrhage (SAH) in vivo.
A SAH rat model was established using the double-bleed method. A total of 108 Sprague-Dawley rats weighing 250–300 g were randomly divided into 6 groups: SAH; SAH plus diethylenetriamine (DETA)/NO (exogenous NO donor); SAH plus 8-bromoadenosine (8-Br)-cyclic guanosine monophosphate (cGMP; protein kinase G [PKG] activator); SAH plus DETA/NO plus KT5823 (PKG inhibitor); SAH plus DETA/NO plus 40Gap27 (Cx40 inhibitor); and sham. The changes in the diameter of the branch microvessels in the middle cerebral artery were recorded. The neurological score was evaluated using the Garcia scoring system. Basilar artery (BA) tension was measured using the Danish Myo Technology myograph system. Cx40 protein expression was analyzed using immunofluorescence and Western blotting. Endothelial NO synthase, soluble guanylate cyclase, and PKG protein expression were measured by Western blotting.
A considerable narrowing of the cerebral vessels was detected in the SAH group compared with that in the sham group. Moreover, compared with the sham group, the SAH group showed a marked decrease in Cx40, endothelial NO synthase, soluble guanylate cyclase, and PKG expression. The expression of Cx40 and PKG were obviously higher in the SAH plus DETA/NO and SAH plus 8-Br-cGMP groups than in the SAH group. However, Cx40 was lower in the SAH plus DETA/NO plus KT5823 and SAH plus DETA/NO plus 40Gap27 groups than in the SAH plus ETA/NO group. The BAs showed significant vasodilation in the SAH plus DETA/NO and SAH plus 8-Br-cGMP groups. However, the vasodilation response of BAs was inhibited in the SAH plus DETA/NO plus KT5823 and SAH plus DETA-NO plus 40Gap27 groups.
The NO-cGMP-PKG pathway alleviated cerebral vasospasm via Cx40 upregulation.</description><subject>Animals</subject><subject>Cerebral vasospasm</subject><subject>Clinical Neurology</subject><subject>Connexin 40</subject><subject>Connexins - metabolism</subject><subject>Connexins - physiology</subject><subject>Cyclic GMP-Dependent Protein Kinases - metabolism</subject><subject>Disease Models, Animal</subject><subject>Gap Junction alpha-5 Protein</subject><subject>Guanosine Monophosphate - metabolism</subject><subject>Life Sciences & Biomedicine</subject><subject>Neurosciences & Neurology</subject><subject>Nitric oxide</subject><subject>Nitric Oxide - metabolism</subject><subject>Nitric Oxide - physiology</subject><subject>Nitric Oxide Synthase - metabolism</subject><subject>Rats, Sprague-Dawley</subject><subject>Science & Technology</subject><subject>Signal Transduction - physiology</subject><subject>Soluble Guanylyl Cyclase - metabolism</subject><subject>Subarachnoid hemorrhage</subject><subject>Subarachnoid Hemorrhage - physiopathology</subject><subject>Surgery</subject><subject>Up-Regulation - physiology</subject><subject>Vasospasm, Intracranial - physiopathology</subject><issn>1878-8750</issn><issn>1878-8769</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>AOWDO</sourceid><sourceid>EIF</sourceid><recordid>eNqNkcFu1DAURSMEolXpD7BAXiKhBDuZJI7EZhSVaUVLK1HYWo793HiU2IPtdDofx7_VYYaR2CC88bN87332O0nyluCMYFJ9XGdbA1OW4xxnmGQ4r14kp4TWNKV11bw81iU-Sc69X-O4CrKgdfE6OSlIUxYx5jT59X3j4GEaeNDWIKtQa42BJ23QAqMbkJoHkKjboa86OC3Q7ZOWgJYhgJnilUctOOgcH9AP7q3fcD-ipQrg0Lep446L3lgt0SWM1rmePwB61ByFHv4KTNudGOJhNXFjvTaAbqyxmz4G9rFLeudsgPimL9pwD2iF7njot3z3Jnml-ODh_LCfJfefL-7by_T6dnXVLq9TUZRVSFVHuORFJZqGEoEllsDjNKCqRBmHJbACUfBcYiVytVCU1KqrG-hoQ-ocVHGWvN_Hbpz9OYEPbNRewDBwA3byLC8WpMI0RkZpvpcKZ713oNjG6ZG7HSOYzeDYms3g2AyOYcIiuGh6d8ifuhHk0fIHUxR82Au20FnlhQYj4CiLZMsc04JWczWr6f-rWx1-s2_tZEK0ftpbIU7zUYNjB7vUDkRg0up_feQZkTzOmA</recordid><startdate>202004</startdate><enddate>202004</enddate><creator>Lan, Shi Hai</creator><creator>Lai, Wen Tao</creator><creator>Zheng, Su Yue</creator><creator>Yang, Le</creator><creator>Fang, Lin Chun</creator><creator>Zhou, Lin</creator><creator>Tang, Bin</creator><creator>Duan, Jian</creator><creator>Hong, Tao</creator><general>Elsevier Inc</general><general>Elsevier</general><scope>AOWDO</scope><scope>BLEPL</scope><scope>DTL</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><orcidid>https://orcid.org/0000-0002-2693-8991</orcidid><orcidid>https://orcid.org/0000-0002-6110-9179</orcidid></search><sort><creationdate>202004</creationdate><title>Upregulation of Connexin 40 Mediated by Nitric Oxide Attenuates Cerebral Vasospasm After Subarachnoid Hemorrhage via the Nitric Oxide-Cyclic Guanosine Monophosphate-Protein Kinase G Pathway</title><author>Lan, Shi Hai ; Lai, Wen Tao ; Zheng, Su Yue ; Yang, Le ; Fang, Lin Chun ; Zhou, Lin ; Tang, Bin ; Duan, Jian ; Hong, Tao</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c356t-fb1ada36c9981c0d0dea003e66c5769c0fec3a2d0fc2f4f817fb79eb89172ef3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Animals</topic><topic>Cerebral vasospasm</topic><topic>Clinical Neurology</topic><topic>Connexin 40</topic><topic>Connexins - metabolism</topic><topic>Connexins - physiology</topic><topic>Cyclic GMP-Dependent Protein Kinases - metabolism</topic><topic>Disease Models, Animal</topic><topic>Gap Junction alpha-5 Protein</topic><topic>Guanosine Monophosphate - metabolism</topic><topic>Life Sciences & Biomedicine</topic><topic>Neurosciences & Neurology</topic><topic>Nitric oxide</topic><topic>Nitric Oxide - metabolism</topic><topic>Nitric Oxide - physiology</topic><topic>Nitric Oxide Synthase - metabolism</topic><topic>Rats, Sprague-Dawley</topic><topic>Science & Technology</topic><topic>Signal Transduction - physiology</topic><topic>Soluble Guanylyl Cyclase - metabolism</topic><topic>Subarachnoid hemorrhage</topic><topic>Subarachnoid Hemorrhage - physiopathology</topic><topic>Surgery</topic><topic>Up-Regulation - physiology</topic><topic>Vasospasm, Intracranial - physiopathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Lan, Shi Hai</creatorcontrib><creatorcontrib>Lai, Wen Tao</creatorcontrib><creatorcontrib>Zheng, Su Yue</creatorcontrib><creatorcontrib>Yang, Le</creatorcontrib><creatorcontrib>Fang, Lin Chun</creatorcontrib><creatorcontrib>Zhou, Lin</creatorcontrib><creatorcontrib>Tang, Bin</creatorcontrib><creatorcontrib>Duan, Jian</creatorcontrib><creatorcontrib>Hong, Tao</creatorcontrib><collection>Web of Science - Science Citation Index Expanded - 2020</collection><collection>Web of Science Core Collection</collection><collection>Science Citation Index Expanded</collection><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>World neurosurgery</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Lan, Shi Hai</au><au>Lai, Wen Tao</au><au>Zheng, Su Yue</au><au>Yang, Le</au><au>Fang, Lin Chun</au><au>Zhou, Lin</au><au>Tang, Bin</au><au>Duan, Jian</au><au>Hong, Tao</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Upregulation of Connexin 40 Mediated by Nitric Oxide Attenuates Cerebral Vasospasm After Subarachnoid Hemorrhage via the Nitric Oxide-Cyclic Guanosine Monophosphate-Protein Kinase G Pathway</atitle><jtitle>World neurosurgery</jtitle><stitle>WORLD NEUROSURG</stitle><addtitle>World Neurosurg</addtitle><date>2020-04</date><risdate>2020</risdate><volume>136</volume><spage>e476</spage><epage>e486</epage><pages>e476-e486</pages><issn>1878-8750</issn><eissn>1878-8769</eissn><abstract>The present study was performed to elucidate the role of nitric oxide (NO) and connexin 40 (Cx40) in the induction of cerebral vasospasm after subarachnoid hemorrhage (SAH) in vivo.
A SAH rat model was established using the double-bleed method. A total of 108 Sprague-Dawley rats weighing 250–300 g were randomly divided into 6 groups: SAH; SAH plus diethylenetriamine (DETA)/NO (exogenous NO donor); SAH plus 8-bromoadenosine (8-Br)-cyclic guanosine monophosphate (cGMP; protein kinase G [PKG] activator); SAH plus DETA/NO plus KT5823 (PKG inhibitor); SAH plus DETA/NO plus 40Gap27 (Cx40 inhibitor); and sham. The changes in the diameter of the branch microvessels in the middle cerebral artery were recorded. The neurological score was evaluated using the Garcia scoring system. Basilar artery (BA) tension was measured using the Danish Myo Technology myograph system. Cx40 protein expression was analyzed using immunofluorescence and Western blotting. Endothelial NO synthase, soluble guanylate cyclase, and PKG protein expression were measured by Western blotting.
A considerable narrowing of the cerebral vessels was detected in the SAH group compared with that in the sham group. Moreover, compared with the sham group, the SAH group showed a marked decrease in Cx40, endothelial NO synthase, soluble guanylate cyclase, and PKG expression. The expression of Cx40 and PKG were obviously higher in the SAH plus DETA/NO and SAH plus 8-Br-cGMP groups than in the SAH group. However, Cx40 was lower in the SAH plus DETA/NO plus KT5823 and SAH plus DETA/NO plus 40Gap27 groups than in the SAH plus ETA/NO group. The BAs showed significant vasodilation in the SAH plus DETA/NO and SAH plus 8-Br-cGMP groups. However, the vasodilation response of BAs was inhibited in the SAH plus DETA/NO plus KT5823 and SAH plus DETA-NO plus 40Gap27 groups.
The NO-cGMP-PKG pathway alleviated cerebral vasospasm via Cx40 upregulation.</abstract><cop>NEW YORK</cop><pub>Elsevier Inc</pub><pmid>31953101</pmid><doi>10.1016/j.wneu.2020.01.026</doi><tpages>11</tpages><orcidid>https://orcid.org/0000-0002-2693-8991</orcidid><orcidid>https://orcid.org/0000-0002-6110-9179</orcidid></addata></record> |
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| subjects | Animals Cerebral vasospasm Clinical Neurology Connexin 40 Connexins - metabolism Connexins - physiology Cyclic GMP-Dependent Protein Kinases - metabolism Disease Models, Animal Gap Junction alpha-5 Protein Guanosine Monophosphate - metabolism Life Sciences & Biomedicine Neurosciences & Neurology Nitric oxide Nitric Oxide - metabolism Nitric Oxide - physiology Nitric Oxide Synthase - metabolism Rats, Sprague-Dawley Science & Technology Signal Transduction - physiology Soluble Guanylyl Cyclase - metabolism Subarachnoid hemorrhage Subarachnoid Hemorrhage - physiopathology Surgery Up-Regulation - physiology Vasospasm, Intracranial - physiopathology |
| title | Upregulation of Connexin 40 Mediated by Nitric Oxide Attenuates Cerebral Vasospasm After Subarachnoid Hemorrhage via the Nitric Oxide-Cyclic Guanosine Monophosphate-Protein Kinase G Pathway |
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