NECA and bradykinin at reperfusion reduce infarction in rabbit hearts by signaling through PI3K, ERK, and NO

Yang, Xi‐Ming; Krieg, Thomas; Cui, Lin; Downey, James M.; Cohen, Michael V.

doi:10.1016/j.yjmcc.2003.12.008

Cited by 137 publications

(114 citation statements)

References 44 publications

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“…*Significantly (P < 0.05) different from baseline. isoforms observed in this study 10 were abolished by PD 098059 pretreatment. Another adenosine A 1 /A 2 receptor agonist (AMP579) also exerted protective effects during reperfusion in rabbits 15 via an Erk1/2-dependent mechanism.…”

Section: Discussionsupporting

confidence: 57%

“…16 The adenosine A 1 /A 2 subtype receptor agonist 5'-(N-ethylcardoxamido) adenosine (NECA) and bradykinin administered during early reperfusion reduced infarct size by activation of Erk1/2 in isolated rabbit hearts. 10 N-ethylcardoxamido adenosine and bradykinin-induced phosphorylation of Erk1/2 FIGURE 3 Schematic illustration of potential sites of action of isoflurane on cardioprotective signaling during early reperfusion. G protein-coupled receptor ligands, insulin, statins, growth factors, and volatile anesthetics activate parallel phosphoinositol-3-kinase (PI3K) or extracellular signal regulated kinase (Erk1/2) cascades to produce protection.…”

Section: Discussionmentioning

confidence: 99%

“…We recently demonstrated that isoflurane-induced postconditioning is mediated by activation of the prosurvival phosphatidylinositol-3-kinase (PI3K)-Akt signaling cascade. 5,6 This pathway has also been implicated in myocardial protection during early reperfusion produced by brief, repetitive ischemic stimuli 5,[7][8][9] (termed "ischemic postconditioning") 8 and other drugs including bradykinin, 10 adenosine receptor agonists, 10 statins, 11 and opioids. 12 The extracellular signal-related kinases (Erk1/2) are mitogen-activated protein kinases that play important roles in cell differentiation, proliferation, and survival.…”

Section: Résultats : L'exposition Brève à Une Concentration Alvéolairmentioning

confidence: 99%

“…13 Activation of Erk1/2 has been proposed as a redundant mechanism by which downstream elements of the PI3K-Akt cascade may be stimulated to favourably modulate reperfusion injury. 13 The extracellular signal-related kinases mediate ischemic 14 and pharmacological postconditioning, 10,15 and also play important roles in preconditioning produced by the volatile anesthetic desflurane. 16 Thus, the current investigation tested the hypothesis isoflurane-induced postconditioning is dependent on activation of Erk1/2.…”

Section: Résultats : L'exposition Brève à Une Concentration Alvéolairmentioning

confidence: 99%

“…13 A selective inhibitor of this enzyme (rapamycin) abolished cardioprotection during ischemic 9 and pharmacological postconditioning. 10,12 The phosphatidylinositol-3-kinase-Akt also activates endothelial nitric oxide (NO) synthase (eNOS), and a central role for NO has also been implicated in postconditioning by ischemia, 9 an adenosine agonist, 10 and bradykinin. 10 Thus, we also tested the hypothesis that p70s6K and eNOS mediate the protective effects of isoflurane during early reperfusion after prolonged coronary artery occlusion in vivo.…”

Section: Résultats : L'exposition Brève à Une Concentration Alvéolairmentioning

confidence: 99%

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Role of Erk1/2, p70s6K, and eNOS in isofluraneinduced cardioprotection during early reperfusionin vivo

Krolikowski

Weihrauch

Bienengraeber

et al. 2006

Can J Anesth/J Can Anesth

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Purpose: Administration of isoflurane during early reperfusion after prolonged coronary artery occlusion decreases myocardial infarct size by activating phosphatidylinositol-3-kinase (PI3K) signal transduction. The extracellular signal-related kinases (Erk1/2) represent a redundant mechanism by which signaling elements downstream from PI3K, including 70-kDA ribosomal protein s6 kinase (p70s6K) and endothelial nitric oxide synthase (eNOS), may be activated to reduce reperfusion injury. We tested the hypothesis Erk1/2, p70s6K, and eNOS mediate isoflurane-induced postconditioning in rabbit myocardium in vivo. Methods: Barbiturate-anesthetized rabbits (n = 78) instrumented for measurement of systemic hemodynamics were subjected to a 30-min coronary occlusion followed by three hours reperfusion. Rabbits were randomly assigned to receive 0.9% saline (control), the Erk1/2 inhibitor PD 098059 (2 mg·kg -1 ), the p70s6K inhibitor rapamycin (0.25 mg·kg -1 ), the nonselective nitric oxide synthase (NOS) inhibitor N-nitro-L-arginine methyl ester (L-NAME; 10 mg·kg -1 ), the selective inducible NOS antagonist aminoguanidine hydrochloride (AG, 300 mg·kg -1 ), or the selective neuronal NOS inhibitor 7-nitroindazole (7-NI, 50 mg·kg -1 ) in the presence or absence of 1.0 minimum alveolar concentration isoflurane administered for three minutes before and two minutes after reperfusion. Results: Brief exposure to 1.0 minimum alveolar concentration isoflurane reduced (P < 0.05) infarct size (21 ± 4% [mean ± SD] of left ventricle area at risk, respectively; triphenyltetrazolium staining) as compared to control (41 ± 5%). PD 098059, rapamycin, and L-NAME, but not AG nor 7-NI, abolished the protection produced by isoflurane. Conclusion:The results suggest that the protective effects of isoflurane against infarction during early reperfusion are mediated by Erk1/2, p70s6K, and eNOS in vivo. Objectif : L'administration d'isoflurane pendant la reperfusion pré-coce qui suit une occlusion prolongée de l'artère coronaire diminue la taille de l'infarctus myocardique en activant la transduction du signal de la phosphatidylinositol-3-kinase (PI3K). Les kinases extracellulaires reliées au signal (Erk1/2) représentent un mécanisme redondant par lequel le signalement des éléments en aval à partir de PI3K, incluant la s6 kinase de protéines ribosomales

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Section: Discussionsupporting

confidence: 57%

Section: Discussionmentioning

confidence: 99%

Section: Résultats : L'exposition Brève à Une Concentration Alvéolairmentioning

confidence: 99%

Section: Résultats : L'exposition Brève à Une Concentration Alvéolairmentioning

confidence: 99%

Section: Résultats : L'exposition Brève à Une Concentration Alvéolairmentioning

confidence: 99%

See 3 more Smart Citations

Role of Erk1/2, p70s6K, and eNOS in isofluraneinduced cardioprotection during early reperfusionin vivo

Krolikowski

Weihrauch

Bienengraeber

et al. 2006

Can J Anesth/J Can Anesth

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show abstract

Ischemic Preconditioning

Downey

Cohen

2006

Myocardial Ischemia

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Thioredoxin Attenuates Post-ischemic Damage in Ventricular and Mitochondrial Function

D'Annunzio

Pérez

Mazo

et al. 2016

Biochemistry of Oxidative Stress

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NECA and bradykinin at reperfusion reduce infarction in rabbit hearts by signaling through PI3K, ERK, and NO

Cited by 137 publications

References 44 publications

Role of Erk1/2, p70s6K, and eNOS in isofluraneinduced cardioprotection during early reperfusionin vivo

Role of Erk1/2, p70s6K, and eNOS in isofluraneinduced cardioprotection during early reperfusionin vivo

Ischemic Preconditioning

Thioredoxin Attenuates Post-ischemic Damage in Ventricular and Mitochondrial Function

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