Please use this identifier to cite or link to this item: http://hdl.handle.net/11452/29017
Title: Experimental subarachnoid haemorrhage models in rats
Authors: Kanpolat, Y.
Uludağ Üniversitesi/Tıp Fakültesi/Nöroloji Anabilim Dalı.
0000-0003-0841-8201
Alkan, Tülin
Korfalı, Ender
Kahveci, Nevzat
AAG-7070-2021
6601953747
7004641343
6602597846
Keywords: Acute vasoconstriction
Neurosciences & neurology
Cerebral blood flow
Animal models
Intracranial pressure
Subarachnoid haemorrhage
Cerebral blood-flow
Canine carotid arteries
In-vivo angioplasty
Basılar Artery
Primate model
Acute vasoconstriction
Morphological analyses
Animal-Model
Nitric-oxide
Hemorrhage
Issue Date: 2002
Publisher: Springer-Verlag Wien
Citation: Alkan, T. vd. (2002). "Experimental subarachnoid haemorrhage models in rats". Ed. Kanpolat, Y. Acta Neurochirurgica Supplement, Research and Publishing in Neurosurgery, 83, 61-69.
Abstract: There 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.
Description: Bu çalışma, 2001 yılında Antalya'da düzenlenen Conference on Research and Publishing Neurosurgery'da bildiri olarak sunulmuştur.
URI: https://doi.org/10.1007/978-3-7091-6743-4_11
https://link.springer.com/chapter/10.1007/978-3-7091-6743-4_11
http://hdl.handle.net/11452/29017
ISSN: 0065-1419
Appears in Collections:PubMed
Scopus
Web of Science

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