Role of NO/cGMP signaling pathway in cardiac ischemic tolerance of chronically hypoxic rats

0454181 - FGÚ 2016 RIV CZ eng J - Článek v odborném periodiku
Alánová, Petra - Kolář, František - Ošťádal, Bohuslav - Neckář, Jan
Role of NO/cGMP signaling pathway in cardiac ischemic tolerance of chronically hypoxic rats.
Physiological Research. Roč. 64, č. 5 (2015), s. 783-787. ISSN 0862-8408. E-ISSN 1802-9973
Grant CEP: GA ČR(CZ) GA13-10267S; GA ČR(CZ) GAP303/12/1162
Institucionální podpora: RVO:67985823
Klíčová slova: hypoxia * cardioprotection * nitric oxide * molsidomine * sildenafil
Kód oboru RIV: FA - Kardiovaskulární nemoci vč. kardiochirurgie
Impakt faktor: 1.643, rok: 2015

It has been suggested that increase in acute nitric oxide (NO) or cyclic guanosine monophosphate production may be involved in cardioprotection induced by chronic hypoxia (CH). We studied the effect of NO donor molsidomine and phosphodiesterase type 5 inhibitor sildenafil on myocardial ischemia/reperfusion (I/R) injury in rats adapted to CH. Male Wistar rats were exposed to continuous hypoxia in a normobaric chamber (10 % O2, 4 weeks). Rats received either saline, molsidomine (10 mg/kg body weight, i.v.) or sildenafil (0.7 mg/kg body weight, i.v.) 30 min before ischemia. Control rats were kept under normoxia and treated in a corresponding manner. Adaptation to CH increased the myocardial ischemic tolerance. Acute treatment with either molsidomine or sildenafil significantly reduced infarct size in normoxic rats and further enhanced cardioprotection induced by CH. However, the cardioprotective effect of CH on I/R injury was not additive to the cardioprotection provided by the drugs
Trvalý link: http://hdl.handle.net/11104/0254878