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dc.contributor.authorKepoglu, Umit
dc.contributor.authorKanat, Ayhan
dc.contributor.authorAydin, Mehmet Dumlu
dc.contributor.authorAkca, Nezih
dc.contributor.authorKazdal, Hizir
dc.contributor.authorZeynal, Mete
dc.contributor.authorSipal, Sare Altas
dc.date.accessioned2020-12-19T19:34:41Z
dc.date.available2020-12-19T19:34:41Z
dc.date.issued2020
dc.identifier.issn1049-2275
dc.identifier.issn1536-3732
dc.identifier.urihttps://doi.org/10.1097/SCS.0000000000006041
dc.identifier.urihttps://hdl.handle.net/11436/1146
dc.description18th International Congress of the International-Society-of-Craniofacial-Surgery (ISCFS) -- SEP 16-19, 2019 -- Paris, FRANCEen_US
dc.descriptionWOS: 000562524800106en_US
dc.descriptionPubMed: 31842081en_US
dc.description.abstractBackground: the Cushing response was first described in 1901. One of its components is elevated systemic blood pressure secondary to raised intracranial pressure. However, controversy still exists in its pathophysiologic mechanism. Hypertension is attributed to sympathetic overactivity and vagotomy increased renal-based hypertension. However, the role of the parasympathetic system in hypertension has not been investigated. This subject was investigated following subarachnoid hemorrhage (SAH). Methods: A total of 24 rabbits were used: control group (n = 5), SHAM group (n = 5), and an SAH group (n = 14; bolus injection of blood into the cisterna magna). Blood pressures were examined before, during, and after the experiment. After 3 weeks, animals were decapitated under general anesthesia. Vagal nodose ganglion, axonal degeneration, and renal artery vasospasm (RAV) indexes of all animals were determined histopathologically. Results: Significant degenerative changes were detected in the vagal axons and nodose ganglia following SAH in animals with severe hypertension. the mean degenerated neuron density of nodose ganglions, vasospasm index (VSI) values of renal arteries of control, SHAM, and study groups were estimated as 9.0 +/- 2.0 mm(3), 1.87 +/- 0.19; 65.0 +/- 12.0 mm(3), 1.91 +/- 0.34; and 986.0 +/- 112.0 mm(3), 2.32 +/- 0.89, consecutively. Blood pressure was measured as 94.0 +/- 10.0 mmHg in control group, 102.0 +/- 12.0 mmHg in SHAM; 112.0 +/- 14.0 mmHg in middle (n = 9); and >122.0 +/- 10.0 mmHg in severe RAV-developed animals (n = 5). Differences VSI values and blood pressure between groups were statistically significant (P < 0.05). Conclusion: the degeneration of vagal nodose ganglion has an important role in RAV and the development of RAV and hypertension following SAH.en_US
dc.description.sponsorshipInt Soc Craniofacial Surgen_US
dc.language.isoengen_US
dc.publisherLippincott Williams & Wilkinsen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectHypertensionen_US
dc.subjectrenal artery vasospasmen_US
dc.subjectsubarachnoid hemorrhageen_US
dc.titleNew Histopathologic Evidence for the Parasympathetic Innervation of the Kidney and the Mechanism of Hypertension Following Subarachnoid Hemorrhageen_US
dc.typeconferenceObjecten_US
dc.contributor.departmentRTEÜen_US
dc.identifier.doi10.1097/SCS.0000000000006041
dc.identifier.volume31en_US
dc.identifier.issue3en_US
dc.identifier.startpage865en_US
dc.identifier.endpage870en_US
dc.relation.journalJournal of Craniofacial Surgeryen_US
dc.relation.publicationcategoryKonferans Öğesi - Uluslararası - Kurum Öğretim Elemanıen_US


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