4.5 Article

Early administration of xenon or isoflurane may not improve functional outcome and cerebral alterations in a porcine model of cardiac arrest

Journal

RESUSCITATION
Volume 80, Issue 5, Pages 584-590

Publisher

ELSEVIER IRELAND LTD
DOI: 10.1016/j.resuscitation.2009.02.019

Keywords

Heart; Cardiac massage; Brain; Ischaemia; Anaesthetics volatile; Isoflurane; Xenon

Funding

  1. GEMI Fund, Lichngo, Sweden

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Background: Xenon (Xe) is neuroprotective when given 1 h after cardiopulmonary resuscitation (CPR). Here, we investigated if an earlier ad ministration of Xe or isoflurane (Iso) Would a Iso reduce neurological dysfunction. Methods: 10 min after CPR from 8 min of cardiac arrest 21 pigs were randomized to three groups (n = 7/group) and then ventilated for 1 h with gas mixtures as follows: (1) control: 30% O-2 + 70% N-2; (2) Iso: 30% O-2 + 69% N-2 + 1% Iso: (3) Xe: 30% O-2 + 70% Xe. Physiological variables were obtained before cardiac arrest and 10, 60 and 240 min post-CPR including cardiac output (CO) and mean arterial pressure (MAP). Four days after CPR we assessed functional performance using an established neurocognitive test and overall neurological Status using a neurologic deficit score (NDS). On day 5, brains of the re-anaesthetized pigs were harvested for neurohistopathological analyses. Results: Prior to CPR there were no differences in hemodynamics and neurological status between groups. CO and MAP were significantly reduced after starting so administration. Both variables were also significantly lower in comparison to Xe and control animals. Control animals presented severe neurological dysfunction as measured by the NDS and the neurocognitive tests. Although Xe and Iso animals showed slightly better functional Outcome this trend was not significant. Histopathological evaluation revealed ischaemic damage of neurons predominantly in the CA1 sector of the hippocampus with no differences between groups. Conclusions: In this study early administration of Xe and Iso did not significantly reduce neurological dysfunction and histopathological alterations induced by cardiac arrest and CPR. (C) 2009 Elsevier Ireland Ltd. All rights reserved.

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