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Diltiazem and verapamil reduce the loss of adenine nucleotide metabolites from hypoxic hearts.
TLDR
Both diltiazem and verapamil are capable of preventing Hypoxia-induced increase in the transmembrane flux of cellular components, which may be beneficial for the preservation of substances necessary for the ATP regeneration after hypoxia and for the inhibition of calcium overload in cardiac cells. Expand
Role of endogenous endothelin-1 in post-ischemic cardiac dysfunction and norepinephrine overflow in rat hearts.
TLDR
Cardiac endothelin-1 production is enhanced by ischemia/reperfusion, and this endogenously increased endotheli-1 is involved in post-ischemic norepinephrine overflow and cardiac dysfunction via the activation of endothelins ET(A) receptors. Expand
Role of ATP metabolites in induction of incomplete recovery of cardiac contractile force after hypoxia.
TLDR
The results suggest that loss of ATP metabolites is a vital step in the induction of incomplete recovery of cardiac contractile force after hypoxia, from the view of energy metabolism in the myocardium. Expand
Effects of exogenous big endothelin-1 on postischemic cardiac dysfunction and norepinephrine overflow in rat hearts
TLDR
It is suggested that exogenous big ET-1 has beneficial effects on ischemia/reperfusion-induced cardiac injury and it seems likely that bigET-1 is converted to Et-1, locally in the heart, and this ET- 1 preferentially binds to ETB receptors to exert its related beneficial actions. Expand
Sex Differences in Postischemic Cardiac Dysfunction and Norepinephrine Overflow in Rat Heart: The Role of Estrogen Against Myocardial Ischemia–reperfusion Damage Via an NO-mediated Mechanism
TLDR
It is suggested that estrogen plays a key role in the cardioprotective effect against I/R injury in female rats, by suppressing NE release via the enhancement of NO production. Expand
Postconditioning Improves Postischemic Cardiac Dysfunction Independently of Norepinephrine Overflow After Reperfusion in Rat Hearts: Comparison With Preconditioning
TLDR
Findings indicate that the beneficial effect of postC on I/R-induced cardiac dysfunction depends on nitric oxide and is irrelevant to NE overflow after reperfusion in contrast to the preC effect. Expand
Protective effects of 17beta-estradiol on post-ischemic cardiac dysfunction and norepinephrine overflow through the non-genomic estrogen receptor/nitric oxide-mediated pathway in the rat heart.
TLDR
The findings suggest that 17β-estradiol exerts cardioprotective effects against ischemia/reperfusion-induced cardiac dysfunction, at least in part, by suppressing norepinephrine overflow, and that nitric oxide production via estrogen receptor activation plays a key role in this process. Expand
Contribution of Nitric Oxide in Big Endothelin-1–induced Cardioprotective Effects on Ischemia/Reperfusion Injury in Rat Hearts
TLDR
The findings suggest that NO produced by ETB receptor activation plays an important role in exogenous big ET-1-induced actions. Expand
Different Effects of AT1 Receptor Antagonist and ETA Receptor Antagonist on Ischemia-Induced Norepinephrine Release in Rat Hearts
TLDR
It is suggested that ETAR antagonist may be more useful than AT1R antagonist in the clinical settings of ischemic heart disease because of its ability to inhibit the exocytotic NE release, but the carrier-mediated NE release induced by prolonged ischemia cannot be avoided by AT2R antagonist. Expand