On the genesis of myocardial ischemia

Sroka, Knut

doi:10.1007/s00392-004-0137-6

Cited by 25 publications

(24 citation statements)

References 138 publications

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“…It is now widely accepted that imbalanced autonomic nervous system especially reduced vagal activity is an independent risk factor of cardiovascular diseases including heart failure, hypertension and myocardial infarction [13,14]. Vagal nerve stimulation has been implicated in chronic heart failure patients [15].…”

Section: Introductionmentioning

confidence: 99%

Acetylcholine Mediates AMPK-Dependent Autophagic Cytoprotection in H9c2 Cells During Hypoxia/Reoxygenation Injury

Zhao

Sun

et al. 2013

Cell Physiol Biochem

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Background: Acetylcholine (ACh), a neurotransmitter of vagal nerve, offers tolerance to ischemia/reperfusion injury. Given the regulation of autophagy in cardioprotection, this study was to examine the role of autophagy in ACh-elicited protection against hypoxia/reoxygenation (HR) injury. Methods: H9c2 cells were subjected to HR injury. Autophagy was determined by transmission electron microscopy, MDC staining and western blot. MTT kit, LDH and CK release, ATP content and TUNEL assay were used to evaluate cardiomyocytes injury. Atg7 and AMPK knockdown was performed with siRNA transfection. Results: Following 4, 8, 12 and 16 h reoxygenation, autophagosomes were decreased along with reduced cell viability. ACh during 4 h reoxygenation facilitated autophagy as evidence by increased autophagosomes and MDC labeling autophagic vacuoles. H9c2 cells treated with ACh also underwent a biochemical changes by increased ratio of LC3-II/LC3-I and autophagy flux (decreased p62), while muscarinic receptor antagonist atropine suppressed these effects. Induction of autophagy was correlated with enhanced cell survival and decreased apoptosis. Autophagy inhibition with chloroquine and Atg7 siRNA significantly attenuated ACh-induced cytoprotection. ACh-elicited autophagy activation could be related to increased AMPK phosphorylation and decreased mTOR phosphorylation. AMPK siRNA exhibited an elevation in mTOR phosphorylation and reduced the ratio of LC3-II/LC3-I. Importantly, AMPK knockdown desensitized H9c2 cells to ACh-mediated protection. Conclusions: These data provided first evidence that ACh-induced autophagy elicited cytoprotective effects through muscarinic receptor activated-AMPK-mTOR pathway, and suggested a novel mechanism of ACh-induced tolerance against HR injury.

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Section: Introductionmentioning

confidence: 99%

Acetylcholine Mediates AMPK-Dependent Autophagic Cytoprotection in H9c2 Cells During Hypoxia/Reoxygenation Injury

Zhao

Sun

et al. 2013

Cell Physiol Biochem

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“…Electrochemical redox reaction of Cu(II) in different supporting electrolytes media in the acidic pH range [5][6][7][8][9][10] and basic medium 11,12 has been investigated because of its application in electrolysis, microelectronics, electroplating, sensors, batteries and biochemical catalytic systems 13 . The mechanism and kinetic behavior of the reduction of aquoCu(II) have been investigated using a number of electrochemical techniques, such as dc polarography 6,10,14 , ac polarography [6][7][8][9][10][11][12][13][14][15][16][17] , hydrodynamic voltammetry [18][19][20] , chronoamperometry at constant potential 8,21 , and coulometry 22,23 .…”

Section: Introductionmentioning

confidence: 99%

A Cyclic Voltammetric Study of the Redox Reaction of Cu(II) in Presence of Ascorbic Acid in Different pH Media

Haque

Rahman

Ahmed

et al. 2013

Dhaka Univ. J. Sci.

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The electrochemical redox behavior of Cu(II), and Cu(II) in presence of ascorbic acid has been investigated at glassy carbon electrode (GCE) in aqueous phosphate buffer solution (PBS) at various pH. In the studied pH range the voltammogram consists of a cathodic and an anodic peak. Cu(II) follows one step two-electron transfer electrochemical redox reaction. The intensities of both cathodic and anodic peak current increase with increasing scan rate that are consistent with Randles-Sevcik equation. The linear behavior of peak current with the square root of scan rate indicates that the electrochemical processes are diffusion controlled. In presence of ascorbic acid both of the cathodic and anodic peak current of Cu(II) is reduced and peak positions are shifted compared to those of Cu(II) alone. These observation suggest that Cu(II) undergoes a strong interaction with ascorbic acid in the studied medium.

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“…Similarly, expression of catecholaminergic traits such as DBH and TH are concurrently upregulated in these parasympathetic neurons after sympathectomy (Mione et al, 1991; Warn et al, 1997). If similar mechanisms are operative in the heart, then this could have major implications regarding cardiac function under conditions such as congestive heart failure and Parkinson’s disease, both of which are characterized by sympathetic nerve abnormalities and possible disturbances in vagal control of heart rate (Azevedo et al, 1999; Goldstein et al, 2002; Goldstein, 2004; Sroka, 2004). …”

Section: Discussionmentioning

confidence: 99%

Modulation of rat parasympathetic cardiac ganglion phenotype and NGF synthesis by adrenergic nerves

Hasan

Smith

2009

Autonomic Neuroscience

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Cardiac function is regulated by interactions among intrinsic and extrinsic autonomic neurons, and the mechanisms responsible for organizing these circuits are poorly understood. Parasympathetic neurons elsewhere synthesize the neurotrophin NGF, which may promote postganglionic axonal associations where parasympathetic axons inhibit sympathetic transmitter release. Previous studies have shown that parasympathetic NGF content and neurochemical phenotype are regulated by sympathetic innervation. In this study we assessed contributions of sympathetic input on cardiac ganglion neuronal phenotype and NGF expression. Because cardiac ganglia are reported to contain putative noradrenergic neurons, we eliminated sympathetic input both surgically (extrinsic) and chemically (extrinsic plus intrinsic). In controls, most cardiac ganglion neurons expressed vesicular acetylcholine transporter, frequently colocalized with vesicular monoamine transporter, but lacked catecholamine histofluorescence. Most cardiac ganglion neurons expressed NGF transcripts, and 40% contained mature and 47% proNGF immunoreactivity. Guanethidine treatment for 7 days decreased numbers of neurons expressing vesicular acetylcholine transporter, NGF transcripts and NGF immunoreactivity, but did not affect proNGF or vesicular monoamine transporter immunoreactivity. Stellate ganglionectomy had comparable effects on neurochemical phenotype and mature NGF immunoreactivity, but proNGF expression was additionally reduced.These findings show that individual cardiac ganglion neurons display markers of both cholinergic and noradrenergic transmission. Sympathetic noradrenergic innervation maintains levels of cholinergic but not noradrenergic marker protein. Sympathetic innervation also promotes cardiac ganglion neuronal NGF synthesis. Because chemical blockade of all noradrenergic transmission is no more effective than extrinsic sympathectomy, local intrinsic noradrenergic transmission is not a factor in regulating ganglion neuron phenotype.

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On the genesis of myocardial ischemia

Cited by 25 publications

References 138 publications

Acetylcholine Mediates AMPK-Dependent Autophagic Cytoprotection in H9c2 Cells During Hypoxia/Reoxygenation Injury

Acetylcholine Mediates AMPK-Dependent Autophagic Cytoprotection in H9c2 Cells During Hypoxia/Reoxygenation Injury

A Cyclic Voltammetric Study of the Redox Reaction of Cu(II) in Presence of Ascorbic Acid in Different pH Media

Modulation of rat parasympathetic cardiac ganglion phenotype and NGF synthesis by adrenergic nerves

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