Literature DB >> 7762027

Cortical blood flow and cerebral perfusion pressure in a new noncraniotomy model of subarachnoid hemorrhage in the rat.

J B Bederson1, I M Germano, L Guarino.   

Abstract

BACKGROUND AND
PURPOSE: Acute cerebral ischemia after subarachnoid hemorrhage (SAH) is a major cause of morbidity whose precise etiology is unclear. The purpose of this study was to examine the relationships between cerebral perfusion pressure (CPP) and cortical blood flow during SAH using a new experimental model in the rat.
METHODS: CPP (mean arterial pressure minus intracranial pressure), cortical laser-Doppler flowmetry (LDF), and electroencephalogram were continuously recorded during and after SAH in 16 ventilated rats. SAH was produced by advancing an intraluminal suture from the external carotid artery through the internal carotid artery to perforate the vessel near its intracranial bifurcation.
RESULTS: Eight rats (50%) died within 24 hours of SAH. In all rats, blood was widely distributed throughout the basal, convexity, and interhemispheric subarachnoid spaces and throughout the ventricular system. CPP decreased after SAH at an initial rate of 1.1 +/- 0.2 mm Hg/s, reaching its nadir 59 +/- 9 seconds after the onset of SAH. During the same period, LDF fell at a rate of 1.4 +/- 0.3%/s (P = NS vs CPP). After reaching its nadir, CPP rose at a rate of 0.4 +/- 0.01 mm Hg/s, but LDF continued to fall at 0.2 +/- 0.03%/s (P < .05 vs CPP) reaching a nadir of 21.7 +/- 2.5% significantly later than CPP (189.5 +/- 39 s after SAH, P < .05). No correlation was found between peak changes in CPP and LDF. Electroencephalogram activity followed the changes in LDF, reaching nadir values 289 +/- 55 seconds after SAH.
CONCLUSIONS: These findings demonstrate that although reduced CPP causes the initial decrease in cortical blood flow after SAH, secondary reductions occurring after CPP has reached its nadir are caused by other factors such as acute vasoconstriction. This noncraniotomy model of SAH in the rat has several advantages over existing models.

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Year:  1995        PMID: 7762027     DOI: 10.1161/01.str.26.6.1086

Source DB:  PubMed          Journal:  Stroke        ISSN: 0039-2499            Impact factor:   7.914


  116 in total

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4.  Expression and cell distribution of neuroglobin in the brain tissue after experimental subarachnoid hemorrhage in rats: a pilot study.

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8.  Role of gap junctions in early brain injury following subarachnoid hemorrhage.

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9.  CT perfusion evidence of early global cerebral hypoperfusion after aneurysmal subarachnoid hemorrhage with cardiac arrest.

Authors:  Joseph D Burns; Jeffrey T Jacob; Patrick H Luetmer; Eelco F M Wijdicks
Journal:  Neurocrit Care       Date:  2010-04       Impact factor: 3.210

10.  Role of SCH79797 in maintaining vascular integrity in rat model of subarachnoid hemorrhage.

Authors:  Junhao Yan; Anatol Manaenko; Sheng Chen; Damon Klebe; Qingyi Ma; Basak Caner; Mutsumi Fujii; Changman Zhou; John H Zhang
Journal:  Stroke       Date:  2013-03-28       Impact factor: 7.914

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