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

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/repe...

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Bibliographic Details
Published inPhysiological research Vol. 64; no. 5; pp. 783 - 787
Main Authors Alánová, P, Kolář, F, Oštádal, B, Neckář, J
Format Journal Article
LanguageEnglish
Published Czech Republic Institute of Physiology 01.01.2015
Subjects
Adaptation
Animals
Cardiology
Chronic Disease
Coronary vessels
Cyclic GMP - physiology
Drugs
Heart attacks
Hypoxia - metabolism
Ischemia
Laboratory animals
Male
Myocardial Ischemia - metabolism
Nitric oxide
Nitric Oxide - physiology
Ostomy
Rats
Rats, Wistar
Rodents
Signal Transduction - physiology
Studies
Veins & arteries
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Summary: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 % O(2), 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.
ISSN:0862-8408
1802-9973
DOI:10.33549/physiolres.932939