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dc.contributor.authorYolaş, Coşkun
dc.contributor.authorKanat, Ayhan
dc.contributor.authorAydın, Mehmet Dumlu
dc.contributor.authorAltaş, Ender
dc.contributor.authorKanat, İlyas Ferit
dc.contributor.authorKazdal, Hızır
dc.contributor.authorDuman, Aslıhan
dc.contributor.authorGündoğdu, Betül
dc.contributor.authorGürsan, Nesrin
dc.date.accessioned2020-12-19T19:55:42Z
dc.date.available2020-12-19T19:55:42Z
dc.date.issued2016
dc.identifier.citationYolas, C., Kanat, A., Aydin, M. D., Altas, E., Kanat, I. F., Kazdal, H., Duman, A., Gundogdu, B., & Gursan, N. (2016). Unraveling of the Effect of Nodose Ganglion Degeneration on the Coronary Artery Vasospasm After Subarachnoid Hemorrhage: An Experimental Study. World neurosurgery, 86, 79–87. https://doi.org/10.1016/j.wneu.2015.09.004en_US
dc.identifier.issn1878-8750
dc.identifier.issn1878-8769
dc.identifier.urihttps://doi.org/10.1016/j.wneu.2015.09.004
dc.identifier.urihttps://hdl.handle.net/11436/2587
dc.descriptionaltas, enver/0000-0001-9351-6986; Kanat, Ayhan/0000-0002-8189-2877en_US
dc.descriptionWOS: 000369625300036en_US
dc.descriptionPubMed: 26365883en_US
dc.description.abstractBACKGROUND: Cardiac arrest is a major life-threatening complication of subarachnoid hemorrhage (SAH). Although medullary cardiocirculatuar center injury and central sympathetic overactivity have been suspected of initiating coronary artery spasm-induced cardiac arrest, we aimed to elucidate the effects of vagal ischemia at the brainstem on coronary vasospasm and sudden death in SAH. METHODS: Twenty-six rabbits were randomly divided into 3 groups. Control (n = 5); SHAM (n = 8), and SAH group (n = 13). Experimental SAH was applied by injecting homologous blood into the cisterna magna, and the SHAM group was injected with isotonic saline solution also in the cisterna magna., Twenty-one days after the injection, histopathologic changes of the neuron density of nodose ganglia, the vasospasm index values of the coronary arteries, and the electrocardiographic events were analyzed. RESULTS: Increased vasospasm index of the coronary arteries and degenerated neuron density of nodose ganglion were significantly different between animals with SAH, control, and SHAM groups (P < 0.005). If neurons of the nodose ganglia are lesioned due to ischemic insult during SAH, the heart rhythm regulation by vagus afferent reflexes is disturbed. CONCLUSIONS: We found that there is causal relationship between nodose ganglion degeneration and coronary vasospasm. Our finding could be the reason that many cardiac events occur in patients with SAH. Vagal pathway paralysis induced by indirect sympathetic overactivity may trigger coronary vasospasm and heart rhythm disturbances. Our findings will aid in the planning of future experimental studies and in determining the clinical relevance of such studies.en_US
dc.language.isoengen_US
dc.publisherElsevier Science Incen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectCoronary artery vasospasmen_US
dc.subjectNodose ganglionen_US
dc.subjectSubarachnoid hemorrhageen_US
dc.titleUnraveling of the effect of nodose ganglion degeneration on the coronary artery vasospasm after subarachnoid hemorrhage: an experimental studyen_US
dc.typearticleen_US
dc.contributor.departmentRTEÜ, Tıp Fakültesi, Cerrahi Tıp Bilimleri Bölümüen_US
dc.contributor.institutionauthorKanat, Ayhan
dc.contributor.institutionauthorKazdal, Hızır
dc.identifier.doi10.1016/j.wneu.2015.09.004
dc.identifier.volume86en_US
dc.identifier.startpage79en_US
dc.identifier.endpage87en_US
dc.relation.journalWorld Neurosurgeryen_US
dc.relation.publicationcategoryMakale - Uluslararası Hakemli Dergi - Kurum Öğretim Elemanıen_US


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