Please use this identifier to cite or link to this item: http://hdl.handle.net/11452/29017
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dc.contributor.authorKanpolat, Y.-
dc.date.accessioned2022-10-07T06:57:58Z-
dc.date.available2022-10-07T06:57:58Z-
dc.date.issued2002-
dc.identifier.citationAlkan, T. vd. (2002). "Experimental subarachnoid haemorrhage models in rats". Ed. Kanpolat, Y. Acta Neurochirurgica Supplement, Research and Publishing in Neurosurgery, 83, 61-69.en_US
dc.identifier.issn0065-1419-
dc.identifier.urihttps://doi.org/10.1007/978-3-7091-6743-4_11-
dc.identifier.urihttps://link.springer.com/chapter/10.1007/978-3-7091-6743-4_11-
dc.identifier.urihttp://hdl.handle.net/11452/29017-
dc.descriptionBu çalışma, 2001 yılında Antalya'da düzenlenen Conference on Research and Publishing Neurosurgery'da bildiri olarak sunulmuştur.tr_TR
dc.description.abstractThere is no comprehensive and reliable model available in small animals that are suitable for the study of subarachnoid haemorrhage (SAH). In the study we reviewed the advantages and disadvantages of available SAH models in rats and presented our model. Experimental SAH was induced in a group of 350-450 g SpragueDawley rats. A 2 mm-diameter burr hole was drilled and, working under a microscope, haemorrhage was produced by transclival puncture of the basilar artery with a 20 mum thick piece of glass. The rats were assigned to either the experimental group (n: 7) or the control group (n: 7). Local cerebral blood flow (LCBF), intracranial pressure (ICP), and cerebral perfusion pressure (CPP) were measured for 60 min after SAH, after which the rats were decapitated. Microscopic examinations were done on three different segments of the basilar artery. There was a significant and sharp drop in LCBF just after SAH was induced (56.17 +/- 12.80 mILD/min/100 g and 13.57 +/- 5.85 mILD/min/100 g for baseline and post-SAH, respectively; p < 0.001), the flow slowly increased by the end of the experiment but never recovered to pre-SAH values (43,63 +/- 7.6 mILD/min/ 100 g, p < 0.05). ICP (baseline 7.33 +/- 0.8 mmHg) increased acutely to 70.6 +/- 9.2 mmHg, and also returned to normal levels by 60 min after SAH. CPP (baseline 75.1 +/- 4.9 mmHg) dropped accordingly (to 21.0 +/- 6.3 mmHg) and then increased, reaching 70.1 +/- 4.9 mmHg at 60 min after SAH. Examinations of the arteries revealed decreased inner luminal diameter and distortion of the elastica layer. We present an inexpensive and reliable model of SAH in the rat that allows single and multiple haemorrhages and to study the early and late course of pathological changes.en_US
dc.description.sponsorshipEuropean Association of Neurosurgical Societiesen_US
dc.language.isoenen_US
dc.publisherSpringer-Verlag Wienen_US
dc.rightsinfo:eu-repo/semantics/closedAccessen_US
dc.subjectAcute vasoconstrictionen_US
dc.subjectNeurosciences & neurologyen_US
dc.subjectCerebral blood flowen_US
dc.subjectAnimal modelsen_US
dc.subjectIntracranial pressureen_US
dc.subjectSubarachnoid haemorrhageen_US
dc.subjectCerebral blood-flowen_US
dc.subjectCanine carotid arteriesen_US
dc.subjectIn-vivo angioplastyen_US
dc.subjectBasılar Arteryen_US
dc.subjectPrimate modelen_US
dc.subjectAcute vasoconstrictionen_US
dc.subjectMorphological analysesen_US
dc.subjectAnimal-Modelen_US
dc.subjectNitric-oxideen_US
dc.subjectHemorrhageen_US
dc.subject.meshPuncturesen_US
dc.subject.meshAnimalsen_US
dc.subject.meshBasilar arteryen_US
dc.subject.meshBlood pressureen_US
dc.subject.meshBrain ischemiaen_US
dc.subject.meshDisease models, animalen_US
dc.subject.meshHumansen_US
dc.subject.meshIntracranial pressureen_US
dc.subject.meshMaleen_US
dc.subject.meshRatsen_US
dc.subject.meshVasospasm, intracranialen_US
dc.subject.meshVertebrobasilar insufficiencyen_US
dc.subject.meshReproducibility of resultsen_US
dc.subject.meshRats, sprague-Dawleyen_US
dc.subject.meshRegional blood flowen_US
dc.subject.meshSubarachnoid hemorrhageen_US
dc.titleExperimental subarachnoid haemorrhage models in ratsen_US
dc.typeProceedings Paperen_US
dc.identifier.wos000180585100011tr_TR
dc.identifier.scopus2-s2.0-0036436266tr_TR
dc.relation.publicationcategoryKonferans Öğesi - Uluslararasıtr_TR
dc.contributor.departmentUludağ Üniversitesi/Tıp Fakültesi/Nöroloji Anabilim Dalı.tr_TR
dc.contributor.orcid0000-0003-0841-8201tr_TR
dc.identifier.startpage61tr_TR
dc.identifier.endpage69tr_TR
dc.identifier.volume83tr_TR
dc.relation.journalResearch and Publishing in Neurosurgeryen_US
dc.contributor.buuauthorAlkan, Tülin-
dc.contributor.buuauthorKorfalı, Ender-
dc.contributor.buuauthorKahveci, Nevzat-
dc.contributor.researcheridAAG-7070-2021tr_TR
dc.identifier.pubmed12442623tr_TR
dc.subject.wosClinical neurologyen_US
dc.indexed.wosCPCISen_US
dc.indexed.scopusScopusen_US
dc.indexed.pubmedPubMeden_US
dc.contributor.scopusid6601953747tr_TR
dc.contributor.scopusid7004641343tr_TR
dc.contributor.scopusid6602597846tr_TR
dc.subject.scopusIntracranial Vasospasm; Subarachnoid Hemorrhage; Ictusen_US
dc.subject.emtreeMaleen_US
dc.subject.emtreeAnimalen_US
dc.subject.emtreeArticleen_US
dc.subject.emtreeBasilar arteryen_US
dc.subject.emtreeBlood flowen_US
dc.subject.emtreeBlood pressureen_US
dc.subject.emtreeBrain ischemiaen_US
dc.subject.emtreeBrain vasospasmen_US
dc.subject.emtreeDisease modelen_US
dc.subject.emtreeHumanen_US
dc.subject.emtreeIntracranial pressureen_US
dc.subject.emtreePathologyen_US
dc.subject.emtreeSprague Dawley raten_US
dc.subject.emtreePathophysiologyen_US
dc.subject.emtreeSubarachnoid hemorrhageen_US
dc.subject.emtreeReproducibilityen_US
dc.subject.emtreePunctureen_US
dc.subject.emtreePhysiologyen_US
dc.subject.emtreeVertebrobasilar insufficiencyen_US
dc.subject.emtreeRaten_US
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