Successfull cardiopulmonary resuscitation is an essential life-saving tool; nevertheless, general ischemia during cardiac arrest may trigger different pathways that could turn even into a fatal damage; this condition is called post-cardiac arrest syndrome. It has been repeatedly shown that oxidative stress (OS) plays one of the key roles in the development of ischemia-reperfusion injury. However, current evidence on the possible participation of OS in the pathogenesis of post-cardiac arrest syndrome is insufficient. We tested following hypotheses: (i) ischaemia-reperfusion injury after cardiac arrest is accompanied by OS and (ii) mild therapeutical hypothermia decreases OS cardiac arrest. In the experimental part of our work we studied the effects of hypothermia and normothermia on hemodynamic parameters, markers of organ damage and on the OS burden in porcine model of cardiac arrest. Furthermore, we compared the effects of hypothermia with ischaemic postconditioning and nitric oxide administration in the porcine model of extracorporeal cardiopulmonary resuscitation. We found protective effects of hypothermia on all major endpoints including OS in comparison with normothermia; moreover, hypothermia improved also selected variables compared to ischemic postconditioning and nitric oxide. In the...
| Identifer | oai:union.ndltd.org:nusl.cz/oai:invenio.nusl.cz:353392 |
| Date | January 2016 |
| Creators | Krüger, Andreas |
| Contributors | Ošťádal, Petr, Vízek, Martin, Rokyta, Richard |
| Source Sets | Czech ETDs |
| Language | Czech |
| Detected Language | English |
| Type | info:eu-repo/semantics/doctoralThesis |
| Rights | info:eu-repo/semantics/restrictedAccess |
Page generated in 0.002 seconds