Pharmacological postconditioning with sevoflurane after cardiopulmonary resuscitation reduces myocardial dysfunction

Critical Care

Berthold Bein³  Jens Scholz³  Jürgen Schrezenmeir¹  Sabine Tacke²  Moritz Maracke³  Nikola Foesel³  Karina Zitta³  Christina Müller³  Martin Albrecht³  Matthias Gruenewald³  Patrick Meybohm³ 

[1] Department of Physiology and Biochemistry of Nutrition, Max Rubner-Institut Kiel, Federal Research Institute of Nutrition and Food, Hermann-Weigmann-Straße 1, D-24103 Kiel, Germany;Department of Veterinary Clinical Sciences, Clinic for Small Animals-Surgery, Justus-Liebig University Giessen, Frankfurter Straße 108, D-35392 Giessen, Germany;Department of Anaesthesiology and Intensive Care Medicine, Schleswig-Holstein University Hospital, Campus Kiel, Schwanenweg 21, D-24105 Kiel, Germany

关键词: neurological deficits;    inhalation anesthetics;    echocardiography;    cardiopulmonary resuscitation;   

Others  :  1093661
DOI  :  10.1186/cc10496

 received in 2011-07-29, accepted in 2011-10-19,  发布年份 2011

【 摘 要 】

Introduction

In this study, we sought to examine whether pharmacological postconditioning with sevoflurane (SEVO) is neuro- and cardioprotective in a pig model of cardiopulmonary resuscitation.

Methods

Twenty-two pigs were subjected to cardiac arrest. After 8 minutes of ventricular fibrillation and 2 minutes of basic life support, advanced cardiac life support was started. After successful return of spontaneous circulation (N = 16), animals were randomized to either (1) propofol (CONTROL) anesthesia or (2) SEVO anesthesia for 4 hours. Neurological function was assessed 24 hours after return of spontaneous circulation. The effects on myocardial and cerebral damage, especially on inflammation, apoptosis and tissue remodeling, were studied using cellular and molecular approaches.

Results

Animals treated with SEVO had lower peak troponin T levels (median [IQR]) (CONTROL vs SEVO = 0.31 pg/mL [0.2 to 0.65] vs 0.14 pg/mL [0.09 to 0.25]; P < 0.05) and improved left ventricular systolic and diastolic function compared to the CONTROL group (P < 0.05). SEVO was associated with a reduction in myocardial IL-1β protein concentrations (0.16 pg/μg total protein [0.14 to 0.17] vs 0.12 pg/μg total protein [0.11 to 0.14]; P < 0.01), a reduction in apoptosis (increased procaspase-3 protein levels (0.94 arbitrary units [0.86 to 1.04] vs 1.18 arbitrary units [1.03 to 1.28]; P < 0.05), increased hypoxia-inducible factor (HIF)-1α protein expression (P < 0.05) and increased activity of matrix metalloproteinase 9 (P < 0.05). SEVO did not, however, affect neurological deficit score or cerebral cellular and molecular pathways.

Conclusions

SEVO reduced myocardial damage and dysfunction after cardiopulmonary resuscitation in the early postresuscitation period. The reduction was associated with a reduced rate of myocardial proinflammatory cytokine expression, apoptosis, increased HIF-1α expression and increased activity of matrix metalloproteinase 9. Early administration of SEVO may not, however, improve neurological recovery.

【 授权许可】

   
2011 Meybohm et al.; licensee BioMed Central Ltd.

【 图 表 】

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