"2017-12-31+01:00"^^ . . . "Ischemick\u00E1 tolerance srdc\u00ED spont\u00E1nn\u011B hypertenzn\u00EDch potkan\u016F: v\u00FDznam mitochondri\u00E1ln\u00EDho genomu" . . "0"^^ . "2014-04-18+02:00"^^ . . . "3"^^ . . "Spont\u00E1nn\u011B hypertenzn\u00ED potkani (SHR) jsou experiment\u00E1ln\u00EDm modelem esenci\u00E1ln\u00ED hypertenze s vysokou citlivost\u00ED srdce k akutn\u00EDmu ischemicko-reperfuzn\u00EDmu (I/R) po\u0161kozen\u00ED. Je zn\u00E1mo, \u017Ee v patogenezi I/R po\u0161kozen\u00ED hraj\u00ED z\u00E1sadn\u00ED roli mitochondrie. C\u00EDlem tohoto projektu je charakterizovat ischemickou toleranci srdc\u00ED SHR a konplastick\u00FDch kmen\u016F SHR-mitoBN, SHR-mitoF344 a SHR-mitoLEW s mitochondri\u00E1ln\u00EDm genomem poch\u00E1zej\u00EDc\u00ED z kmen\u016F Brown Norway, Fischer 344 a Lewis, kter\u00E9 jsou odoln\u011Bj\u0161\u00ED k akutn\u00ED I/R ne\u017E SHR. Zam\u011B\u0159\u00EDme se p\u0159edev\u0161\u00EDm na \u00FAlohu mitochondri\u00E1ln\u00EDch membr\u00E1nov\u00FDch struktur zodpov\u011Bdn\u00FDch za toleranci srdce k I/R (drasl\u00EDkov\u00E9 kan\u00E1ly z\u00E1visl\u00E9 na ATP, v\u00E1pn\u00EDkem aktivovan\u00E9 drasl\u00EDkov\u00E9 kan\u00E1ly s vysokou vodivost\u00ED, tzv. permeability transition pore a komplexy d\u00FDchac\u00EDho \u0159et\u011Bzce) za klidov\u00FDch podm\u00EDnek a po adaptaci na chronickou hypoxii a zv\u00FD\u0161enou fyzickou z\u00E1t\u011B\u017E, je\u017E zvy\u0161uj\u00ED odolnost srdce k I/R. Bli\u017E\u0161\u00ED objasn\u011Bn\u00ED vlivu mitochondri\u00E1ln\u00EDho genomu na citlivost myokardu k akutn\u00ED ischemii m\u016F\u017Ee pomoci odhalit molekul\u00E1rn\u00ED mechanismy zodpov\u011Bdn\u00E9 za zhor\u0161enou ischemickou toleranci srdc\u00ED hypertenzn\u00EDch potkan\u016F." . . " hypertension" . . "3"^^ . " ischemia" . "1"^^ . "2015-04-23+02:00"^^ . "heart, ischemia, hypertension, mitochondria"@en . . "1"^^ . "Cardiac ischemic tolerance of spontaneously hypertensive rats: involvement of mitochondrial genome"@en . . "heart" . . . . "Spontaneously hypertesive rats (SHR) is a pathophysiological animal model for human essential hypertension with increased sensitivity of the heart to ischemia/reperfusion (I/R) injury. It has been shown that mitochondria are one of the main targets and sources of cellular damage during I/R. The aim of project is to characterize cardiac ischemic tolerance of SHR and conplastic strains SHR-mitoBN, -mitoF344 and -mitoLEW with replaced mitochondrial genome from more I/R resistant strains Brown Norway, Fischer 344 and Lewis. An attention will be devote to the role of mitochondrial membrane structures responsible for cardiac ischemic tolerance (ATP-sensitive & large-conductance Ca2+-activated K+ channels, permeability transition pore and respiratory chain complexes) under basal conditions and after cardioprotective adaptation to chronic hypoxia and regular exercise training. Delineation of the relationship between the myocardial susceptibility to I/R injury and mitochondrial genes may help to identify molecular targets responsible for the impaired ischemic tolerance of hypertensive rats."@en . . "http://www.isvav.cz/projectDetail.do?rowId=GA13-10267S"^^ . . . "GA13-10267S" . "2013-02-01+01:00"^^ . .