Published in Experimental and clinical cardiology
During cardiac ischemia or hypoxia, increased levels of extracellular Mg show cardioprotective effects. The mechanisms of high level Mg-induced cardioprotection were examined in Langendorff perfused rat hearts. In the control group (1.2 mM Mg during hypoxia), the recovery of the left ventricular developed pressure (LVDP) after 30 min of reoxygenati...
Published in Naunyn-Schmiedeberg's Archives of Pharmacology
The anti-anginal drug nicorandil has been demonstrated to protect the myocardium against ischemic injury in both experimental and clinical studies. Although nicorandil seems to protect the myocardium via activation of mitochondrial ATP-sensitive K+ (mitoKATP) channels, the mechanisms underlying its cardioprotection have remained elusive. We therefo...
Published in Cardiovascular Toxicology
The corticotrophin-releasing hormone-related factor, urocortin (Ucn) and the interleukin (IL)-6 family cytokine cardiotrophin-1 (CT-1) are both cardioprotective agents able to protect the heart from ischemic damage. In both cases the protective effect involves activation of the p42/p44 MAPK and PI-3 kinase/Akt pathways, but the protective effect of...
Published in Biochemical and Biophysical Research Communications
The p38 mitogen-activated protein kinase (p38) is activated in the heart during ischemia–reperfusion. However, it is not clear whether the activation of p38 is the protective response or the kinase mediates the cellular damage by ischemia–reperfusion. We examined the role of p38α in ischemia–reperfusion injury by studying p38α +/− mice. The p38α pr...
Published in Biochemical and Biophysical Research Communications
We investigated which PKC isoforms are involved in high glucose-induced protection against hypoxic injury. Treatment for 48 h with high glucose (22 mM) markedly increased the expression of PKC-ε in the particulate fraction (213 ± 22.1% of the control) but had no effect on other types of PKC isoforms, suggesting that the high glucose-induced increas...
Published in Biochemical and Biophysical Research Communications
We had previously reported that activation of histamine H 3-receptors (H 3R) on cardiac adrenergic nerve terminals decreases norepinephrine (NE) overflow from ischemic hearts and alleviates reperfusion arrhythmias. Thus, we used transgenic mice lacking H 3R (H 3R −/−) to investigate whether ischemic arrhythmias might be more severe in H 3R −/− hear...
Published in Biochemical Pharmacology
Cardioprotective effect of a free radical-scavenging compound (HO-3073) was examined during ischaemia-reperfusion (IR) in isolated heart perfusion system and its influence on the pro-survival Akt signalling pathway was addressed. Rat hearts were perfused according to the Langendorff method and subjected to a global 25-min ischaemia and 15, 45 and 9...
Published in Experimental and clinical cardiology
The anthracycline doxorubicin is an antineoplastic agent, eliciting chronic cardiac toxicity. It occurs in patients after prolonged administration of doxorubicin, leading to congestive heart failure. The pathogenesis of the doxorubicin-induced car-diomyopathy is not well understood. The present article summarizes the unique effect of doxorubicin on...
Le manque crucial d'organes est un problème majeur rencontré en transplantation cardiaque. L'objectif de ce travail est de tenter d'améliorer la protection du greffon cardiaque durant la conservation froide et lors de la reperfusion. Les résultats majeurs que nous avons obtenus sont les suivants : Parmi les solutions de conservation cardiaque les p...
Published in Experimental and clinical cardiology
Activation of both the ADO receptors (A(1)R and A(3)R) leads to positive beneficial effects in cultured cardiomyocytes in 90 min hypoxia, but only A(3)R activation renders positive response against slowly developed DOX toxicity. Hence, the cascade of events involved in cardioprotection appears to be distinct for A(1) and A(3) receptor signalling.
