Xenon reduces neurohistopathological damage and improves the early neurological deficit after cardiac arrest in pigs
| Autor: | Katharina Siepmann, Joachim Weis, Mark Coburn, Martin Häusler, Steffen Rex, Kay Nolte, Michael Fries, Rolf Rossaint, Anne Timper, Kai Kottmann |
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| Rok vydání: | 2008 |
| Předmět: |
Male
Resuscitation Brain Diseases Xenon business.industry Swine medicine.medical_treatment Putamen S100 Proteins Caudate nucleus Hemodynamics Brain damage Critical Care and Intensive Care Medicine Neuroprotection Cardiopulmonary Resuscitation Heart Arrest Neuroprotective Agents Intensive care Anesthesia medicine Animals Cardiopulmonary resuscitation medicine.symptom business Psychomotor Performance |
| Zdroj: | Critical care medicine. 36(8) |
| ISSN: | 1530-0293 |
| Popis: | OBJECTIVE Treatment options to ameliorate brain damage following cardiopulmonary resuscitation from cardiac arrest are limited. DESIGN In a porcine model, we evaluated the effects of xenon treatment on neuropathologic and functional outcomes after cardiopulmonary resuscitation. SETTING Prospective, randomized laboratory animal study. SUBJECTS Male pigs. INTERVENTIONS Following successful resuscitation from 8 mins of cardiac arrest and 5 mins of cardiopulmonary resuscitation, 24 pigs were randomized to one of three groups receiving either 70% xenon for 1 or 5 hrs or untreated controls receiving 70% nitrogen. MEASUREMENTS AND MAIN RESULTS Gas exchange, hemodynamics, and lactate and glucose levels were measured at baseline and in the postresuscitation period. On four postoperative days, neurocognitive and overall neurologic deficits were assessed before day 5, when the brains were harvested for histologic analysis of predefined regions using a semiquantitative score (0-10% = 1, 10-20% = 2, 20-50% = 3, 50-80% = 4, 80-100% = 5). No differences in gas exchange, hemodynamics, or lactate and glucose levels were observed among the groups. Animals exposed to 1 and 5 hrs of xenon showed significantly reduced scores for necrotic neurons in the putamen (1.25 +/- 0.5 and 1.25 +/- 0.5 vs. 2.5 +/- 1.2; p < 0.05), accompanied by significantly lesser scores for perivascular inflammation in putamen (0.8 +/- 0.5 and 1.1 +/- 0.8 vs. 2.1 +/- 1.1; p < 0.05) and caudate nucleus (1.0 +/- 0.8 and 0.6 +/- 0.7 vs. 2.0 +/- 1.1; p < 0.05). This resulted in improved neurocognitive and neurologic function on day 1 to 3 after cardiopulmonary resuscitation in xenon-treated animals. CONCLUSIONS In this experimental study of cardiac arrest-induced neurologic damage, xenon conferred neurohistopathologic protection, translating in transiently improved functional outcome. |
| Databáze: | OpenAIRE |
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