Hypothermia and neuroprotection by sulfide after cardiac arrest and cardiopulmonary resuscitation

• Verfasst von: Knapp, Jürgen [VerfasserIn]
• Verfasst von: Heinzmann, Anna Constanze [VerfasserIn]
• Verfasst von: Schneider, Andreas [VerfasserIn]
• Verfasst von: Padosch, Stephan A. [VerfasserIn]
• Verfasst von: Böttiger, Bernd W. [VerfasserIn]
• Verfasst von: Teschendorf, Peter [VerfasserIn]
• Verfasst von: Popp, Erik [VerfasserIn]
• Titel: Hypothermia and neuroprotection by sulfide after cardiac arrest and cardiopulmonary resuscitation
• Verf.angabe: Jürgen Knapp, Anna Heinzmann, Andreas Schneider, Stephan A. Padosch, Bernd W. Böttiger, Peter Teschendorf, Erik Popp
• E-Jahr: 2011
• Jahr: 20 April 2011
• Umfang: 5 S.
• Fussnoten: Gesehen am 26.09.2022
• Titel Quelle: Enthalten in: Resuscitation
• Ort Quelle: Amsterdam [u.a.] : Elsevier Science, 1972
• Jahr Quelle: 2011
• Band/Heft Quelle: 82(2011), 8, Seite 1076-1080
• ISSN Quelle: 1873-1570
• DOI: doi:10.1016/j.resuscitation.2011.03.038
• Datenträger: Online-Ressource
• Sprache: eng
• Sach-SW: Cardiac arrest
• Sach-SW: Global cerebral ischaemia
• Sach-SW: Hydrogen sulfide
• Sach-SW: Hypothermia
• Sach-SW: Resuscitation
• K10plus-PPN: 1817391437

Abstract

Background - Poor neurological outcome remains a major problem in patients suffering cardiac arrest. Recent data have demonstrated potent neuroprotective effects of the administration of sulfide donor compounds after ischaemia/reperfusion injury following cardiac arrest and resuscitation. Therefore, we sought to evaluate the impact of sodium sulfide (Na2S), a liquid hydrogen sulfide donor on core body temperature and neurological outcome after cardiac arrest in rats. - Methods - Fifty male Wistar rats were randomized into two groups (sulfide vs. placebo, n=25 per group). Cardiac arrest was induced by transoesophageal ventricular fibrillation during general anaesthesia. After 6min of global cerebral ischaemia, animals were resuscitated by external chest compressions combined with defibrillation. An investigator blinded bolus of either Na2S (0.5mg/kgbody weight) or placebo 1min before the beginning of CPR, followed by a continuous infusion of Na2S (1mg/kgbody weight/h) or placebo for 6h, was administered intravenously. 1 day, 3 days, and 7 days after restoration of spontaneous circulation, neurological outcome was evaluated by a tape removal test. After 7 days of reperfusion, coronal brain sections were analyzed by TUNEL- and Nissl-staining. A caspase activity assay was used to determine antiapoptotic properties of Na2S. - Results - Temperature course was similar in both groups (mean minimal temperature in the sulfide group 31.3±1.2°C vs. 30.8±1.9°C in the placebo group; p=0.29). Despite significant neuroprotection demonstrated by the tape removal test after 3 days of reperfusion in the sulfide treated group, there was no significant difference in neuronal survival at day 7. Likewise results from TUNEL-staining revealed no differences in the amount of apoptotic cell death between the groups after 7 days of reperfusion. - Conclusion - In our rat model of cardiac arrest, sulfide therapy was associated with only a short term beneficial effect on neurological outcome.