scholarly journals Cardioprotection stimulated by resveratrol and grape products prevents lethal cardiac arrhythmias in an animal model of ischemia and reperfusion

2021 ◽  
Vol 36 (3) ◽  
Author(s):  
Francisco Sandro Menezes-Rodrigues ◽  
Paolo Ruggero Errante ◽  
Erisvaldo Amarante Araújo ◽  
Mariana Pontes Pacheco Fernandes ◽  
Michele Mendes da Silva ◽  
...  
2012 ◽  
Vol 2012 ◽  
pp. 1-15 ◽  
Author(s):  
Hannah J. Whittington ◽  
Girish G. Babu ◽  
Mihaela M. Mocanu ◽  
Derek M. Yellon ◽  
Derek J. Hausenloy

Diabetes mellitus is a major risk factor for ischemic heart disease (IHD). Patients with diabetes and IHD experience worse clinical outcomes, suggesting that the diabetic heart may be more susceptible to ischemia-reperfusion injury (IRI). In contrast, the animal data suggests that the diabetic heart may be either more, equally, or even less susceptible to IRI. The conflicting animal data may be due to the choice of diabetic and/or IRI animal model. Ischemic conditioning, a phenomenon in which the heart is protected against IRI by one or more brief nonlethal periods of ischemia and reperfusion, may provide a novel cardioprotective strategy for the diabetic heart. Whether the diabetic heart is amenable to ischemic conditioning remains to be determined using relevant animal models of IRI and/or diabetes. In this paper, we review the limitations of the current experimental models used to investigate IRI and cardioprotection in the diabetic heart.


2012 ◽  
Vol 26 (1) ◽  
pp. 21-25 ◽  
Author(s):  
Zijun Wang ◽  
Janet L. Colli ◽  
Christopher Keel ◽  
Kayleen Bailey ◽  
Leah Grossman ◽  
...  

1989 ◽  
Vol 67 (7) ◽  
pp. 772-779 ◽  
Author(s):  
Margaret P. Moffat ◽  
Gregory R. Ferrier ◽  
Morris Karmazyn

The possible role of prostaglandins (PG) in arrhythmias associated with ischemia and reperfusion was studied in isolated, superfused canine Purkinje tissues. Ischemic conditions caused partial depolarization and decrease of excitability. Neither inhibition of PG synthesis (ibuprofen, 30 μg/mL) nor addition of exogenous PGF2α (1 ng/mL) modified responses to "ischemia." Reperfusion with normal Tyrode's solution stimulated PG production (measured as 6-keto-PGF1α) and induced a series of electrophysiological events. Under control conditions, Purkinje fibres rapidly repolarized. Subsequently, these tissues began to depolarize and oscillatory afterpotentials appeared. Purkinje tissues depolarized further and became temporarily inexcitable. Return of activity was associated with depolarization-induced automaticity. Ibuprofen prevented reperfusion-stimulated PG release. Ibuprofen also increased the magnitude of early repolarization and greatly attenuated subsequent depolarization. Depolarization-induced automaticity was not observed under these conditions; however, oscillatory afterpotentials were not abolished by ibuprofen. Addition of PGF2α to "ischemic" and reperfusion solutions in the presence of ibuprofen restored the arrhythmogenic responses. We conclude that release of endogenous prostaglandins contributes to electrophysiological changes elicited by reperfusion in canine Purkinje fibres.Key words: arrhythmias, ischemia, reperfusion, ibuprofen, prostaglandins.


2015 ◽  
Vol 29 (S1) ◽  
Author(s):  
Giuseppe Bruschetta ◽  
Daniela Impellizzeri ◽  
Rosalba Siracusa ◽  
Rosanna Di Paola ◽  
Irene Paterniti ◽  
...  

2010 ◽  
Vol 49 ◽  
pp. S158-S159
Author(s):  
Sidhartha Tan ◽  
Lei Yu ◽  
Alexander Drobyshevsky ◽  
Matthew Derrick ◽  
Kehuan Luo ◽  
...  

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