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PubMed:20624427 JSONTXT

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Allie

Id Subject Object Predicate Lexical cue
SS1_20624427_2_0 167-193 expanded denotes delayed cerebral vasospasm
SS2_20624427_2_0 195-199 abbr denotes DCVS
SS1_20624427_5_0 516-541 expanded denotes extracranial-intracranial
SS2_20624427_5_0 543-548 abbr denotes EC/IC
SS1_20624427_6_0 628-649 expanded denotes Intracranial pressure
SS2_20624427_6_0 651-654 abbr denotes ICP
AE1_20624427_2_0 SS1_20624427_2_0 SS2_20624427_2_0 abbreviatedTo delayed cerebral vasospasm,DCVS
AE1_20624427_5_0 SS1_20624427_5_0 SS2_20624427_5_0 abbreviatedTo extracranial-intracranial,EC/IC
AE1_20624427_6_0 SS1_20624427_6_0 SS2_20624427_6_0 abbreviatedTo Intracranial pressure,ICP

PubMed_Structured_Abstracts

Id Subject Object Predicate Lexical cue
T1 144-473 BACKGROUND denotes 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.
T2 497-952 METHODS denotes 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.
T3 962-1484 RESULTS denotes 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+/-20s, 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.
T4 1498-1823 CONCLUSIONS denotes 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.