Donepezil Markedly Improves Long-Term Survival in Rats With Chronic Heart Failure After Extensive Myocardial Infarction

Li, Meihua; Zheng, Can; Kawada, Toru; Inagaki, Masumi; Uemura, Kazunori; Shishido, Toshiaki; Sugimachi, Masaru

doi:10.1253/circj.cj-13-0476

Cited by 41 publications

(59 citation statements)

References 40 publications

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“…2,3 A similar result was also obtained by Handa et al in mice with CHF. 4 Chronic administration of donepezil for 2 weeks could not only induce vagal nerve activation, but could also reduce sympathetic nerve activation, as demonstrated by Umegaki and Khookhor in a recent study.…”

Section: Donepezil a Potential Therapeutic Agent For Heart Failuresupporting

confidence: 72%

Donepezil, a potential therapeutic agent for heart failure

Chen

2015

European J of Heart Fail

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Section: Donepezil a Potential Therapeutic Agent For Heart Failuresupporting

confidence: 72%

Donepezil, a potential therapeutic agent for heart failure

Chen

2015

European J of Heart Fail

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“…b-Blockers prevent such adverse outcomes and ameliorate cardiac remodeling by inhibiting sympathetic activity [12]. Interestingly, direct vagal nerve stimulation or using cholinesterase inhibitor can also be beneficial for HF [14,15]. This illustrates that reducing sympathetic drive or increasing vagal drive can both improve HF.…”

Section: Discussionmentioning

confidence: 99%

Effects of the Galanin Receptor Antagonist M40 on Cardiac Function and Remodeling in Rats with Heart Failure

Chen

Song

et al. 2015

Cardiovascular Therapeutics

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SUMMARYBackground: Sympathetic activation and parasympathetic withdrawal are important characteristics of heart failure. Recent studies demonstrate that galanin reduces the discharge of acetylcholine and inhibits vagal bradycardia by acting on galanin receptor type 1 (GalR1). We speculated that blocking GalR1 is beneficial for heart failure. Methods: Rats with heart failure were induced by myocardial infarction. The rats were injected intraperitoneally with galanin receptor antagonist M40 solution (30 nmol/kg) or saline for 4 weeks. Cardiac function was assessed by echocardiography and brain natriuretic peptide (BNP) in plasma. The ratio of heart weight to body weight (HW/BW), hematoxylin-eosin (HE), and Masson trichrome stain was used to evaluate cardiac remodeling. Tumor necrosis factor-a (TNF-a), interleukin 6 (IL-6) in plasma, and sarco(endo)plasmic reticulum Ca 2+ -ATPase

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“…This finding suggests that dialysate ACh concentration monitored by microdialysis mainly a candidate for pharmacological vagal activation therapy. 19 Because ACh esterase degrades ACh immediately after its release, an ACh esterase inhibitor will block ACh degradation and increase ACh in the synaptic cleft. Kubo et al have reported that donepezil, an ACh esterase inhibitor against Alzheimer's disease, significantly decreased plasma brain natriuretic peptide levels in patients with subclinical CHF.…”

Section: Discussionmentioning

confidence: 99%

Medetomidine Suppresses Cardiac and Gastric Sympathetic Nerve Activities but Selectively Activates Cardiac Vagus Nerve

Shimizu

Akiyama

Kawada

et al. 2014

Circ J

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Background: To identify a pharmacological agent that can selectively activate cardiac vagus nerve for potential use in vagal activation therapy against heart failure, the effects of medetomidine on autonomic nerve activities in both the heart and stomach were examined. Methods and Results:In anesthetized rabbits, microdialysis probes were implanted into both the right atrial and gastric walls. Dialysate acetylcholine (ACh) and norepinephrine (NE) concentrations were measured by high-performance liquid chromatography. First, the effects of 100 μg/kg of intravenous medetomidine on vagal ACh and sympathetic NE releases were examined. Medetomidine significantly increased cardiac ACh release (4.7±1.1 to 7.8±0.9 nmol/L, P<0.05), but suppressed gastric ACh release (8.0±2.6 to 3.5±1.5 nmol/L, P<0.01). In contrast, medetomidine suppressed both cardiac and gastric NE releases. Second, the effects of medetomidine on ACh releases induced by electrical vagus nerve stimulation (VNS; 10 Hz) were examined. Electrical VNS significantly increased both cardiac (6.7±1.2 to 14.8±1.8 nmol/L, P<0.01) and gastric (3.8±0.8 to 181.3±65.6 nmol/L, P<0.01) ACh releases. Medetomidine did not alter the VNS-induced increases in ACh release. Conclusions:Medetomidine suppresses both cardiac and gastric sympathetic nerve activities. In contrast, medetomidine activates cardiac vagus nerve but inhibits gastric vagal activity. Medetomidine might be one of the potential pharmacological agents for vagal activation therapy against heart failure without the risk of gastric adverse effects. (Circ J 2014; 78: 1405 -1413

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Donepezil Markedly Improves Long-Term Survival in Rats With Chronic Heart Failure After Extensive Myocardial Infarction

Cited by 41 publications

References 40 publications

Donepezil, a potential therapeutic agent for heart failure

Donepezil, a potential therapeutic agent for heart failure

Effects of the Galanin Receptor Antagonist M40 on Cardiac Function and Remodeling in Rats with Heart Failure

Medetomidine Suppresses Cardiac and Gastric Sympathetic Nerve Activities but Selectively Activates Cardiac Vagus Nerve

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