Vagal Nerve Stimulation

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Harald M. Stauss - One of the best experts on this subject based on the ideXlab platform.

Masaru Sugimachi - One of the best experts on this subject based on the ideXlab platform.

  • Chronic Vagal Nerve Stimulation exerts additional beneficial effects on the beta-blocker-treated failing heart
    The Journal of Physiological Sciences, 2019
    Co-Authors: Meihua Li, Can Zheng, Toru Kawada, Masashi Inagaki, Kazunori Uemura, Masaru Sugimachi
    Abstract:

    Vagal Nerve Stimulation (VNS) induces bradycardia in chronic heart failure (CHF). We hypothesized that beta-blocker would cover the beneficial effects of VNS on CHF if the anti-beta-adrenergic effect was the main VNS effect. This study investigated the effects of VNS on cardiac remodeling in rats with CHF treated with metoprolol. Two weeks after myocardial infarction, surviving rats were randomly assigned to groups of sham Stimulation (SS), sham Stimulation with metoprolol (SSM), or VNS with metoprolol (VSM). Compared to the SS group, heart rate was significantly reduced in the SSM and VSM groups. Hemodynamic assessments showed that VSM rats maintained better cardiac pump function and presented higher cardiac index and lower heart weight than SSM rats. VSM was also associated with lower plasma brain natriuretic peptide and norepinephrine levels than SSM. VSM but not SSM improved the 50-day survival rate compared with the SS group. The results suggest that VNS may exert its beneficial effects on the failing heart independently of its anti-beta-adrenergic mechanism.

  • early short term Vagal Nerve Stimulation attenuates cardiac remodeling after reperfused myocardial infarction
    Journal of Cardiac Failure, 2010
    Co-Authors: Kazunori Uemura, Meihua Li, Can Zheng, Toru Kawada, Masaru Sugimachi
    Abstract:

    Background: Vagal Nerve Stimulation (VS) has been suggested to be an effective adjunct to reperfusion therapy in myocardial infarction (MI). However, the effect of VS on left ventricular (LV) remodeling after reperfused MI has not been examined. Methods and Results: We investigated the effects of early, brief VS on acute inflammatory reactions (study 1) and chronic LV remodeling (study 2) in a rabbit model of reperfused MI. In study 1, rabbits were subjected to 60-minute coronary artery occlusion followed by reperfusion alone (MI, n 5 8) or treated with 24-hour VS (MI-VS, n 5 8). At 24 hours after ischemia-reperfusion, MI-VS rabbits showed significantly decreased myocardial infiltration of neutrophils and reduced myocardial expressions of tumor necrosis factor-a and matrix metalloproteinase-8 and -9, compared with MI rabbits. Myocardial expression of interleukin-6 was not affected by VS. In study 2, rabbits were subjected to coronary occlusion and reperfusion alone (n 5 16) or treated with VS for 3 days (n 5 14). At 8 weeks after ischemiareperfusion, MI-VS rabbits showed significantly improved LV dysfunction and dilatation, and significantly reduced infarct size, infarct wall thinning, and LV weight compared with MI rabbits. Conclusion: Early, short-term VS attenuates LV remodeling after reperfused MI, which may be associated with suppression of acute inflammatory reactions. (J Cardiac Fail 2010;16:689e699)

  • efferent Vagal Nerve Stimulation induces tissue inhibitor of metalloproteinase 1 in myocardial ischemia reperfusion injury in rabbit
    American Journal of Physiology-heart and Circulatory Physiology, 2007
    Co-Authors: Kazunori Uemura, Meihua Li, Toru Kawada, Masashi Inagaki, Takaki Tsutsumi, Toji Yamazaki, Atsunori Kamiya, Kenji Sunagawa, Masaru Sugimachi
    Abstract:

    Vagal Nerve Stimulation has been suggested to ameliorate left ventricular (LV) remodeling in heart failure. However, it is not known whether and to what degree Vagal Nerve Stimulation affects matrix metalloproteinase (MMP) and tissue inhibitor of MMP (TIMP) in myocardium, which are known to play crucial roles in LV remodeling. We therefore investigated the effects of electrical Stimulation of efferent Vagal Nerve on myocardial expression and activation of MMPs and TIMPs in a rabbit model of myocardial ischemia-reperfusion (I/R) injury. Anesthetized rabbits were subjected to 60 min of left coronary artery occlusion and 180 min of reperfusion with (I/R-VS, n = 8) or without Vagal Nerve Stimulation (I/R, n = 7). Rabbits not subjected to coronary occlusion with (VS, n = 7) or without Vagal Stimulation (sham, n = 7) were used as controls. Total MMP-9 protein increased significantly after left coronary artery occlusion in I/R-VS and I/R to a similar degree compared with VS and sham values. Endogenous active MMP-9 protein level was significantly lower in I/R-VS compared with I/R. TIMP-1 mRNA expression was significantly increased in I/R-VS compared with the I/R, VS, and sham groups. TIMP-1 protein was significantly increased in I/R-VS and VS compared with the I/R and sham groups. Cardiac microdialysis technique demonstrated that topical perfusion of acetylcholine increased dialysate TIMP-1 protein level, which was suppressed by coperfusion of atropine. Immunohistochemistry demonstrated a strong expression of TIMP-1 protein in cardiomyocytes around the dialysis probe used to perfuse acetylcholine. In conclusion, in a rabbit model of myocardial I/R injury, Vagal Nerve Stimulation induced TIMP-1 expression in cardiomyocytes and reduced active MMP-9.

Mark W. Chapleau - One of the best experts on this subject based on the ideXlab platform.

Kenji Sunagawa - One of the best experts on this subject based on the ideXlab platform.

  • optimal titration is important to maximize the beneficial effects of Vagal Nerve Stimulation in chronic heart failure
    Journal of Cardiac Failure, 2016
    Co-Authors: Akiko Nishizaki, Kazuo Sakamoto, Keita Saku, Kazuya Hosokawa, Takafumi Sakamoto, Takuya Akashi, Yoshinori Murayama, Takuya Kishi, Kenji Sunagawa
    Abstract:

    Abstract Background Although Vagal Nerve Stimulation (VNS) benefits patients with chronic heart failure (CHF), the optimal dose of VNS remains unknown. In clinical trials, adverse symptoms limited up-titration. In this study, we evaluated the impact of various voltages of VNS which were titrated below symptom threshold on cardiac function and CHF parameters in rat myocardial infarction (MI) models. Methods and Results We randomly allocated MI rats to Vagal (VNS; n = 41) and sham (Sham; n = 16) Stimulation groups. We stimulated the right Vagal Nerve with 20 Hz at 3 different voltages for 4 weeks. We defined Max as the highest voltage that did not evoke any symptom, Half as one-half of Max, and Quarter as one-fourth of Max. All 3 VNS groups significantly reduced biventricular weight compared with Sham (P  Conclusion The optimal titration of VNS would maximize benefits for CHF and minimize adverse effects.

  • afferent Vagal Nerve Stimulation resets baroreflex neural arc and inhibits sympathetic Nerve activity
    Physiological Reports, 2014
    Co-Authors: Keita Saku, Kazuo Sakamoto, Kazuya Hosokawa, Takafumi Sakamoto, Yoshinori Murayama, Takuya Kishi, Takamori Kakino, Masataka Ikeda, Kenji Sunagawa
    Abstract:

    It has been established that Vagal Nerve Stimulation (VNS) benefits patients and/or animals with heart failure. However, the impact of VNS on sympathetic Nerve activity (SNA) remains unknown. In this study, we investigated how Vagal afferent Stimulation (AVNS) impacts baroreflex control of SNA. In 12 anesthetized Sprague–Dawley rats, we controlled the pressure in isolated bilateral carotid sinuses (CSP), and measured splanchnic SNA and arterial pressure (AP). Under a constant CSP, increasing the voltage of AVNS dose dependently decreased SNA and AP. The averaged maximal inhibition of SNA was ‐28.0 ± 10.3%. To evaluate the dynamic impacts of AVNS on SNA, we performed random AVNS using binary white noise sequences, and identified the transfer function from AVNS to SNA and that from SNA to AP. We also identified transfer functions of the native baroreflex from CSP to SNA (neural arc) and from SNA to AP (peripheral arc). The transfer function from AVNS to SNA strikingly resembled the baroreflex neural arc and the transfer functions of SNA to AP were indistinguishable whether we perturbed ANVS or CSP, indicating that they likely share common central and peripheral neural mechanisms. To examine the impact of AVNS on baroreflex, we changed CSP stepwise and measured SNA and AP responses with or without AVNS. AVNS resets the sigmoidal neural arc downward, but did not affect the linear peripheral arc. In conclusion, AVNS resets the baroreflex neural arc and induces sympathoinhibition in the same manner as the control of SNA and AP by the native baroreflex.

  • modulation of the myocardial redox state by Vagal Nerve Stimulation after experimental myocardial infarction
    Cardiovascular Research, 2008
    Co-Authors: Takaki Tsutsumi, Mayumi Yamato, Wataru Kudou, Makoto Andou, Yoshitaka Hirooka, Hideo Utsumi, Hiroyuki Tsutsui, Kenji Sunagawa
    Abstract:

    Aims Redox alteration plays a major role in the pathogenesis of heart failure (HF). Since Vagal Nerve Stimulation (VNS) is known to improve survival and attenuate cardiac remodelling, we hypothesized that VNS may modulate the myocardial redox state. Methods and results Using a chronic HF mouse model, we applied VNS for 15 min and measured myocardial redox status using in vivo electron spin resonance spectroscopy. Signal decay rate of the nitroxyl probe, an index of redox status, was enhanced in HF compared with sham (0.16 ± 0.01 vs. 0.13 ± 0.01 min−1, P < 0.05; n = 6), and VNS normalized this enhancement (0.13 ± 0.01 min−1, P < 0.05). Atropine sulphate abolished the VNS effects, indicating that the VNS modulates myocardial redox state via muscarinic receptors. N ω-Nitro-L-arginine methyl ester treatment and fixed-rate atrial pacing showed a trend to suppress the VNS effects, suggesting the involvement of nitric oxide-based signalling and myocardial oxygen consumption. Moreover, VNS decreased the myocardial norepinephrine (NE) level (0.25 ± 0.07 vs. 0.60 ± 0.12 ng/mL, P < 0.05; n = 6). Reactive oxygen species production from cultured cardiomyocytes was enhanced by β-adrenergic activation, which was partially antagonized by 10 µmol/L acetylcholine (ACh) (relative value compared with control: NE 3.7 ± 0.5, NE + ACh 2.5 ± 0.3, P < 0.05; n = 12). Conclusion The present study suggests that VNS modulates the cardiac redox status and adrenergic drive, and thereby suppresses free radical generation in the failing heart.

  • efferent Vagal Nerve Stimulation induces tissue inhibitor of metalloproteinase 1 in myocardial ischemia reperfusion injury in rabbit
    American Journal of Physiology-heart and Circulatory Physiology, 2007
    Co-Authors: Kazunori Uemura, Meihua Li, Toru Kawada, Masashi Inagaki, Takaki Tsutsumi, Toji Yamazaki, Atsunori Kamiya, Kenji Sunagawa, Masaru Sugimachi
    Abstract:

    Vagal Nerve Stimulation has been suggested to ameliorate left ventricular (LV) remodeling in heart failure. However, it is not known whether and to what degree Vagal Nerve Stimulation affects matrix metalloproteinase (MMP) and tissue inhibitor of MMP (TIMP) in myocardium, which are known to play crucial roles in LV remodeling. We therefore investigated the effects of electrical Stimulation of efferent Vagal Nerve on myocardial expression and activation of MMPs and TIMPs in a rabbit model of myocardial ischemia-reperfusion (I/R) injury. Anesthetized rabbits were subjected to 60 min of left coronary artery occlusion and 180 min of reperfusion with (I/R-VS, n = 8) or without Vagal Nerve Stimulation (I/R, n = 7). Rabbits not subjected to coronary occlusion with (VS, n = 7) or without Vagal Stimulation (sham, n = 7) were used as controls. Total MMP-9 protein increased significantly after left coronary artery occlusion in I/R-VS and I/R to a similar degree compared with VS and sham values. Endogenous active MMP-9 protein level was significantly lower in I/R-VS compared with I/R. TIMP-1 mRNA expression was significantly increased in I/R-VS compared with the I/R, VS, and sham groups. TIMP-1 protein was significantly increased in I/R-VS and VS compared with the I/R and sham groups. Cardiac microdialysis technique demonstrated that topical perfusion of acetylcholine increased dialysate TIMP-1 protein level, which was suppressed by coperfusion of atropine. Immunohistochemistry demonstrated a strong expression of TIMP-1 protein in cardiomyocytes around the dialysis probe used to perfuse acetylcholine. In conclusion, in a rabbit model of myocardial I/R injury, Vagal Nerve Stimulation induced TIMP-1 expression in cardiomyocytes and reduced active MMP-9.

Jerome V Murphy - One of the best experts on this subject based on the ideXlab platform.

  • Vagal Nerve Stimulation in refractory epilepsy the first 100 patients receiving Vagal Nerve Stimulation at a pediatric epilepsy center
    JAMA Pediatrics, 2003
    Co-Authors: Jerome V Murphy, Richard D Torkelson, Irene Dowler, Stephen D Simon, Sara Hudson
    Abstract:

    Objective To determine the outcome of intermittent left Vagal Nerve Stimulation on the first 100 consecutive patients treated at our pediatric epilepsy center. Methods Patients were identified by means of operating room records. Data collected described the patient's epilepsy, previous and subsequent therapies, adverse events, nonepileptic changes, and outcomes. Results Average age was 10.4 years; years of epilepsy, 8.5; total number of antiepileptic therapies, 8.4; and median monthly seizure frequency, 120. Data on seizure frequency at follow-up were available for 96 of the 100 patients. Forty-five percent of patients achieved greater than 50% reduction; and 18% had had no seizures for the last 6 months. Response was similar in patients with more than 7 years of refractory epilepsy as compared with patients with a shorter history. Magnet-generated, on-demand current reduced seizure intensity in almost half of the patients with available data. Generator infections occurred in 3 patients. Twenty-four patients had their generators removed. Subsequently, 2 of these patients died. Conclusions Seizure reduction was the same in patients younger than 12 years and 12 years or older and in patients with shorter and longer histories of refractory epilepsy. Adverse effects were few in this population, particularly in those younger than 12 years. Vagal Nerve Stimulation appears to be a relatively safe and potentially effective treatment for children with severely intractable epilepsy.

  • Vagal Nerve Stimulation in tuberous sclerosis complex patients
    Pediatric Neurology, 2001
    Co-Authors: Dominique Parain, Marie J Penniello, Patrick Berquen, Thierry Delangre, Catherine Billard, Jerome V Murphy
    Abstract:

    This is an open-label, retrospective, multicenter study to determine the outcome of intermittent Stimulation of the left Vagal Nerve in children with tuberous sclerosis complex and medically refractory epilepsy. The records of all children treated with Vagal Nerve Stimulation were reviewed in five pediatric epilepsy centers to locate those with tuberous sclerosis complex who had been treated with Vagal Nerve Stimulation for at least 6 months. These patients were compared with (1) a series of patients obtained from the literature, (2) 10 similar control patients with epilepsy obtained from a registry of patients receiving Vagal Nerve Stimulation, and (3) four published series of tuberous sclerosis complex patients whose epilepsy was surgically managed. Ten tuberous sclerosis complex patients with medically refractory epilepsy treated with Vagal Nerve Stimulation were found. Nine experienced at least a 50% reduction in seizure frequency, and half had a 90% or greater reduction in seizure frequency. No adverse events were encountered. Comparison with published and registry patients revealed improved seizure control in the tuberous sclerosis complex patients. Comparison with the group undergoing seizure surgery demonstrated improved outcomes after surgery. Vagal Nerve Stimulation appears to be an effective and well-tolerated adjunctive therapy in patients with tuberous sclerosis complex and seizures refractory to medical therapy. Resective surgery has a better prospect for improved seizure control.

  • left Vagal Nerve Stimulation in six patients with hypothalamic hamartomas
    Pediatric Neurology, 2000
    Co-Authors: Jerome V Murphy, James W Wheless, Candy Schmoll
    Abstract:

    Six patients with medically refractory epilepsy secondary to hypothalamic hamartomas were treated with intermittent Stimulation of the left Vagal Nerve. Three of the patients had remarkable improvements in seizure control. Four of these six patients had severe autistic behaviors. Striking improvements in these behaviors were observed in all four during treatment with intermittent Stimulation. This finding suggests that Vagal Nerve Stimulation can control seizures and autistic behaviors in patients with hypothalamic hamartomas.

  • left Vagal Nerve Stimulation in children with medically refractory epilepsy
    The Journal of Pediatrics, 1999
    Co-Authors: Jerome V Murphy
    Abstract:

    Abstract Objective: To assess the use of intermittent left Vagal Nerve Stimulation in a large population of children with pharmacoresistant epilepsy. Study design: Sixty children who were entered into controlled or compassionate use protocols of left Vagal Nerve Stimulation all had been monitored for at least 3 months after their left Vagal Nerve stimulators were activated. Results: The age range was 3½ to 18 years (median 15 years). Sixteen of these 60 patients were younger than 12 years. Fifty-seven percent of the patients had partial complex seizures, and generalized tonic clonic seizures occurred in 27%. After 3 months of intermittent Stimulation of the left Vagal Nerve, a median reduction in seizure frequency of 23% occurred in 60 patients. At 6 months the median reduction was 31% in 55 patients, at 12 months 34% in 51 patients, and at 18 months 42% in 46 patients. Improvement was not associated with any seizure type or seizure cause. Adverse events during Stimulation included fever, coughing, colds, and voice alteration. None of these necessitated cessation of Stimulation. Complications included aspiration pneumonia and necrosis of skin overlying the generator. Conclusions: Intermittent Stimulation of the left Vagal Nerve appears to be a safe, adjunctive therapy for the treatment of children with epilepsy intractable to available antiepileptic drugs. The reduction in seizure frequency in children was similar to that reported in adults. (J Pediatr 1999;134:563-6)

  • adverse events in children receiving intermittent left Vagal Nerve Stimulation
    Pediatric Neurology, 1998
    Co-Authors: Jerome V Murphy, Gregory W Hornig, Gloria Schallert, Christie L Tilton
    Abstract:

    The purpose of this study was to determine the frequency of unexpected events during intermittent Vagal Nerve Stimulation in 24 patients stimulated for a total of 61 patient years. The charts of 24 children undergoing periodic Stimulation of the left Vagal Nerve on research protocols were reviewed to determine the nature and frequency of adverse events and the total length of time they were stimulated. Fifteen adverse events were discovered in 12 patients. Thirteen were likely related to the device, and four other events might have been related. Two of these resulted in voluntary termination of Vagal Nerve Stimulation, and the rest were treatable. Vagal Nerve Stimulation was tolerated in this series of patients. As opposed to the more standard drug therapies, adverse events during Vagal Nerve Stimulation do not necessitate termination of therapy, but these events frequently lead to unforeseen surgery under general anesthesia.

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