Extra-intracranial blood shunt mimicking aneurysm rupture: Intracranial-pressure-controlled rabbit subarachnoid hemorrhage model

被引:20
作者
Marbacher, Serge [1 ,2 ,3 ,4 ]
Sherif, Camillo [1 ,2 ,3 ]
Neuschmelting, Volker [1 ,2 ,3 ]
Schlaeppi, Janine-Ai [3 ,4 ]
Takala, Jukka [2 ,3 ]
Jakob, Stephan M. [2 ,3 ]
Fandino, Javier [1 ,2 ,3 ]
机构
[1] Kantonsspital Aarau, Dept Neurosurg, CH-5000 Aarau, Switzerland
[2] Univ Hosp Bern, Dept Intens Care Med, CH-3010 Bern, Switzerland
[3] Univ Bern, CH-3010 Bern, Switzerland
[4] Univ Hosp Bern, Dept Neurosurg, CH-3010 Bern, Switzerland
关键词
Rabbit; Model; Subarachnoid hemorrhage; Delayed cerebral vasospasm; CEREBRAL VASOSPASM; BASILAR ARTERY; BRAIN-INJURY; TIME;
D O I
10.1016/j.jneumeth.2010.07.004
中图分类号
Q5 [生物化学];
学科分类号
070307 [化学生物学];
摘要
Introduction: The achieved degree of delayed cerebral vasospasm (DCVS) in the rabbits most frequently applied cistern magna blood injection model is often mild. The aim of this study was to characterize and evaluate the feasibility of an experimental SAH technique that mimics pathophysiological mechanisms and triggers higher degrees of DCVS. Materials and methods: SAH was induced by extracranial-intracranial (EC/IC) shunting of blood from the subclavian artery into the great cerebral cistern. Intracranial pressure (ICP), arterial blood pressure, heart rate, arterial blood gas analysis, and neurological status were monitored throughout the experiments. The magnitude of spasm was determined by comparison of pre-SAH (day 0) and post-SAH (day 3) angiograms and postmortem morphometric analysis of the basilar artery. Results: A total of 13 experiments (SAH, n = 11; controls, n = 2) were performed. Two animals died after initiation of the EC/IC blood shunt in respiratory arrest. In SAH animals, ICP (baseline: 12 +/- 1 [mean +/- SD]; peak: 51 +/- 4: steady-state level: 15 +/- 2 mm Hg) rose to diastolic blood pressure levels (56 +/- 3 mm Hg) within 98 +/- 20 s, and fell to a steady state within 186 +/- 41 s. SAH-induced vasoconstriction of the basilar artery was 53.1 +/- 2.8% on day 3 compared to baseline (P < 0.05) and histology confirmed marked vasoconstriction. Conclusions: This novel technique of SAH induction closely mimics the pathophysiological sequelae of aneurysm rupture and triggers constant higher degrees of delayed cerebral vasospasm than previously described rabbit models. The severity of vasospasm attained offers a unique opportunity to evaluate future therapeutic treatment options. (C) 2010 Elsevier B.V. All rights reserved.
引用
收藏
页码:227 / 233
页数:7
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