Xenon (Xe) is neuroprotective when given 1h after cardiopulmonary resuscitation (CPR). Here, we investigated if an earlier administration of Xe or isoflurane (Iso) would also reduce neurological dysfunction.
10 min after CPR from 8 min of cardiac arrest 21 pigs were randomized to three groups (n=7/group) and then ventilated for 1h 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.
Prior to CPR there were no differences in hemodynamics and neurological status between groups. CO and MAP were significantly reduced after starting Iso 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.
In this study early administration of Xe and Iso did not significantly reduce neurological dysfunction and histopathological alterations induced by cardiac arrest and CPR.
Department of Anaesthesiology, University Hospital RWTH Aachen, Pauwelsstr. 30, 52074 Aachen, Germany. mfries [at] ukaachen.de
Resuscitation. 2009 May;80(5):584-90
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