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Long-Term Cardioprotection With Phosphodiesterase-5 Inhibition Against Ischemia-Reperfusion Injury: Role Of Nitric Oxide., Vladimir Paul Daoud
Long-Term Cardioprotection With Phosphodiesterase-5 Inhibition Against Ischemia-Reperfusion Injury: Role Of Nitric Oxide., Vladimir Paul Daoud
Theses and Dissertations
Recent studies have shown that the potent phosphodiesterase-5 (PDE-5) inhibitor, sildenafil citrate, induces a powerful cardioprotective effect against ischemia-reperfusion (I/R) injury in rabbit and mouse hearts. However, the effect of this drug in inducing long-term protection against I/R injury remains unknown. The goal of this study was to identify the duration of the protective window of sildenafil citrate as well as vardenafil, a more potent PDE-5 inhibitor. Rabbits were treated with sildenafil (0.7 mg/kg, iv), vardenafil (0.143 mg/kg), or an equivalent volume of saline. After 24 hrs, 48 hrs, 96 hrs, or 7 days of sildenafil treatment, the hearts were …
Novel Strategies In Cardioprotection Against Ischemia/Reperfusion Injury, Fadi N. Salloum
Novel Strategies In Cardioprotection Against Ischemia/Reperfusion Injury, Fadi N. Salloum
Theses and Dissertations
Cell damage represents a major pathomechanism in many diseases of high clinical interest, such as myocardial infarction (MI), where it plays an important role in ischemia-reperfusion (I/R) injury. Considerable progress has been made towards identifying physiological and pharmacological agents that play a key role in myocardial preconditioning against I/R injury and also elucidating the molecular changes leading to such protection.Second messengers in cellular signaling pathways, such as cGMP have been well implicated as key players in ischemic and pharmacological preconditioning (PC) of the heart. Phosphodiesterase type 5 (PDE-5) is an enzyme that specifically hydrolyzes cGMP thereby decreasing its tissue concentration. …
Type-5 Phosphodiesterase Inhibition In The Prevention Of Doxorubicin Cardiomyopathy, Patrick William Fisher
Type-5 Phosphodiesterase Inhibition In The Prevention Of Doxorubicin Cardiomyopathy, Patrick William Fisher
Theses and Dissertations
Prior studies have demonstrated the effect of diazoxide in protecting against apoptosis via mitochondrial KATP channel opening in vitro. The current investigations are designed to determine if sildenafil, a phosphodiesterase-5 inhibitor and known mitochondrial KATP channel opener, would protect against chronic doxorubicin cardiomyopathy both in vivo and in vitro.Male ICR mice were randomized to 1 of 4 treatments: saline, sildenafil (0.7 mg/kg IP), doxorubicin (5 mg/kg IP), and sildenafil (0.7 mg/kg IP)+doxorubicin. Apoptosis was determined using the terminal deoxynucleotidyl transferase mediated dUTP nick-end labeling and in situ oligo ligation methods. Desmin distribution was determined via immunofluorescence. Bcl-2 was analyzed by …