National Repository of Grey Literature 2 records found  Search took 0.00 seconds. 
Possibilities of organ protection after global ischemia during cardiac arrest.
Mudrochová, Hana ; Ošťádal, Petr (advisor) ; Rokyta, Richard (referee) ; Malý, Jiří (referee)
Successful cardiopulmonary resuscitation is the first step to rescue life during cardiac arrest. High mortality even after successful restoration of spontaneous circulation is substantially caused by patophysiological process associated with ischemia-reperfusion injury and it is widely called post-cardiac arrest syndrome (PCAS). There are many patophysiological mechanisms involved in the development and progress of this syndrom; the key role seems to play oxidative stress, triggering the activation cascade of systemic inflammatory reaction. In our study we have tested different possibilities of influencing the post-cardiac arrest syndrom. In the first experimental study we have compared the effect of mild therapeutic hypothermia with controlled normothermia on PCAS in a porcine model of cardiac arrest. In the second study we have compared in the same model the protective effects of mild therapeutic hypothermia, administration of nitric oxide and ischemic postconditioning. Results of the first experiment have revealed that mild therapeutic hypotermia is superior in the resuscitability, maintenance of blood pressure, oxidative stress suppression and organ damage protection than controlled normothermia. In the second experiment we have shown that neither nitric oxide administration, nor ischemic...
The role of sphingosin kinase in cardioprotection
Pospíšilová, Barbora ; Nováková, Olga (advisor) ; Kolář, David (referee)
Sphingosine-1-phosphate (S1P) is bioactive mediator with cardioprotective effect. Sphingosine kinase (SK) is a key enzyme in the synthesis of S1P. It exists in the two isoforms sphingosine kinase 1 and sphingosine kinase 2. Although SK1 has antiapoptotic feature and SK2 has proapoptotic feature both are crucial for the effect of S1P. S1P can act and affect the cellular faith by intracellular or extracellular functioning. Extracellular S1P binds and activates specific cell surface receptors on the plasma membrane. These receptors are members of the group of G protein-coupled receptors. There are tree subtypes of S1P receptors in the heart tissue (S1P1, S1P2, S1P3). Exogenous S1P increases viability of cardiomyocytes after myocardiacal ischemia/reperfusion injury (I/R). It also reduces the infarct size in isolated rat heart. During conditions of ischemic preconditioning (IPC) or postconditioning (IPOST) which consist of the short periods of ischemia before or after major ischemia insult generate S1P. Released S1P increased viability of the cell and faster recovery of hemodynamic functions in the heart tissue. Effects of S1P and its role in cardioprotection are explored in the genetically modified organisms mainly in the mouses. The evidence of the cardioprotective effect of S1P were experiments using...

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