Vagus nerve stimulation-induced bradyarrhythmias in rats

Hotta, Harumi; Lazar, Jason; Orman, Rena; Koizumi, Kiyomi; Shiba, Kanako; Kamran, Haroon; Stewart, Mark

doi:10.1016/j.autneu.2009.07.008

Cited by 31 publications

(16 citation statements)

References 29 publications

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“…Lung volume changes (as observed by video recording) appeared not to be a controlling factor (data not shown). The rat heart can respond with rhythmic bradycardia to high intensity electrical stimulation of vagal efferents (6,25); thus it is likely that the lack of rhythmicity seen is due to either sporadic afferent activity or sporadic efferent activity.…”

Section: Discussionmentioning

confidence: 99%

Characterization of cardiovascular reflexes evoked by airway stimulation with allylisothiocyanate, capsaicin, and ATP in Sprague-Dawley rats

Hooper

Hadley

Morris

et al. 2016

Journal of Applied Physiology

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Acute inhalation of airborne pollutants alters cardiovascular function and evidence suggests that pollutant-induced activation of airway sensory nerves via the gating of ion channels is critical to these systemic responses. Here, we have investigated the effect of capsaicin [transient receptor potential (TRP) vanilloid 1 (TRPV1) agonist], AITC [TRP ankyrin 1 (TRPA1) agonist], and ATP (P2X2/3 agonist) on bronchopulmonary sensory activity and cardiovascular responses of conscious Sprague-Dawley (SD) rats. Single fiber recordings show that allyl isothiocyanate (AITC) and capsaicin selectively activate C fibers, whereas subpopulations of both A and C fibers are activated by stimulation of P2X2/3 receptors. Inhalation of the agonists by conscious rats caused significant bradycardia, atrioventricular (AV) block, and prolonged PR intervals, although ATP-induced responses were lesser than those evoked by AITC or capsaicin. Responses to AITC were inhibited by the TRP channel blocker ruthenium red and the muscarinic antagonist atropine. AITC inhalation also caused a biphasic blood pressure response: a brief hypertensive phase followed by a hypotensive phase. Atropine accentuated the hypertensive phase, while preventing the hypotension. AITC-evoked bradycardia was not abolished by terazosin, the α1-adrenoceptor inhibitor, which prevented the hypertensive response. Anesthetics had profound effects on AITC-evoked bradycardia and AV block, which was abolished by urethane, ketamine, and isoflurane. Nevertheless, AITC inhalation caused bradycardia and AV block in paralyzed and ventilated rats following precollicular decerebration. In conclusion, we provide evidence that activation of ion channels expressed on nociceptive airway sensory nerves causes significant cardiovascular effects in conscious SD rats via reflex modulation of the autonomic nervous system.

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Section: Discussionmentioning

confidence: 99%

Characterization of cardiovascular reflexes evoked by airway stimulation with allylisothiocyanate, capsaicin, and ATP in Sprague-Dawley rats

Hooper

Hadley

Morris

et al. 2016

Journal of Applied Physiology

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“…In piglets, pentylenetetrazole-induced seizures coincided with alterations in HR, hypertension, increased ventilation, and decreased cardiac output (70). Systemic KA administration in rats has also been associated with increased HR and QTc prolongation as well as elevated sympathetic nerve activity and decreased vagal tone (24,25,57). In addition, Metcalf et al (47) also looked at VSE in rats following status epilepticus and found that the VSE ratio (iHR/HR) dropped from 0.98 to 0.87 at 7 days, suggesting sympathetic dominance.…”

Section: Discussionmentioning

confidence: 99%

Progressive development of cardiomyopathy following altered autonomic activity in status epilepticus

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McCann

Millen

et al. 2015

American Journal of Physiology-Heart and Circulatory Physiology

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Seizures are associated with altered autonomic activity, which has been implicated in the development of cardiac dysfunction and structural damage. This study aimed to investigate the involvement of the autonomic nervous system in seizure-induced cardiomyopathy. Male Sprague-Dawley rats (320 -350 g) were implanted with EEG/ECG electrodes to allow simultaneous telemetric recordings during seizures induced by intrahippocampal (2 nmol, 1 l/min) kainic acid and monitored for 7 days. Seizure activity occurred in conjunction with increased heart rate (20%), blood pressure (25%), and QTc prolongation (15%). This increased sympathetic activity was confirmed by the presence of raised plasma noradrenaline levels at 3 h post-seizure induction. By 48 h post-seizure induction, sympathovagal balance was shifted in favor of sympathetic dominance, as indicated by both heart rate variability (LF/HF ratio of 3.5 Ϯ 1.0) and pharmacological autonomic blockade. Functional cardiac deficits were evident at 7 and 28 days, as demonstrated by echocardiography showing a decreased ejection fraction (14% compared with control, P Ͻ 0.05) and dilated cardiomyopathy present at 28 days following seizure induction. Histological changes, including cardiomyocyte vacuolization, cardiac fibrosis, and inflammatory cell infiltration, were evident within 48 h of seizure induction and remained present for up to 28 days. These structural changes most probably contributed to an increased susceptibility to aconitine-induced arrhythmias. This study confirms that prolonged seizure activity results in acute and chronic alterations in cardiovascular control, leading to a deterioration in cardiac structure and function. This study further supports the need for modulation of sympathetic activity as a promising therapeutic approach in seizure-induced cardiomyopathy.

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“…Autonomic dysregulation and bradyarrythmias occur in many pathological conditions including ischemic stroke, inflammation, seizure and traumatic injury (Hotta et al, 2009; Mameli et al, 2001; Saritemur et al, 2013). Seizures may elicit brain acidosis and vagally-mediated bradyarrhythmias that may lead to sudden death (Hotta et al, 2009). Moreover, bradycardia and metabolic acidosis are concurrent in propofol-infusion syndrome (Fudickar and Bein, 2009).…”

Section: Discussionmentioning

confidence: 99%

“…Inflammation, ischemic stroke, traumatic brain injury, and epileptic seizure are conditions in which protons over-accumulate, leading to brain acidosis (Chu and Xiong, 2012). Several pathological conditions associated with acidosis are accompanied by autonomic dysregulation and bradyarrhythmia (Hotta et al, 2009; Mameli et al, 2001; Mameli et al, 2006; Saritemur et al, 2013); nevertheless, the function of ASIC in central cardiovascular control has not been explored.…”

Section: Introductionmentioning

confidence: 99%

Evidence for role of acid-sensing ion channels in nucleus ambiguus neurons: essential differences in anesthetized versus awake rats

et al. 2014

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Acid-sensing ion channels (ASIC) are widely expressed in several brain regions including medulla; their role in physiology and pathophysiology is incompletely understood. We examined the effect of acidic pH of 6.2 on the medullary neurons involved in parasympathetic cardiac control. Our results indicate that retrogradely-labeled cardiac vagal neurons of nucleus ambiguus are depolarized by acidic pH. In addition, acidic saline of pH 6.2 increases cytosolic Ca2+ concentration by promoting Ca2+ influx in nucleus ambiguus neurons. In vivo studies indicate that microinjection of acidic artificial cerebrospinal fluid (pH 6.2) into the nucleus ambiguus decreases the heart rate in conscious rats, whereas it has no effect in anesthetized animals. Pretreatment with either amiloride or benzamil, two widely used ASIC blockers, abolishes both the in vitro and in vivo effects elicited by pH 6.2. Our findings support a critical role for ASIC in modulation of cardiac vagal tone and provide a potential mechanism for acidosis-induced bradycardia, while identifying important differences in the response to acidic pH between anesthetized and conscious rats.

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Vagus nerve stimulation-induced bradyarrhythmias in rats

Cited by 31 publications

References 29 publications

Characterization of cardiovascular reflexes evoked by airway stimulation with allylisothiocyanate, capsaicin, and ATP in Sprague-Dawley rats

Characterization of cardiovascular reflexes evoked by airway stimulation with allylisothiocyanate, capsaicin, and ATP in Sprague-Dawley rats

Progressive development of cardiomyopathy following altered autonomic activity in status epilepticus

Evidence for role of acid-sensing ion channels in nucleus ambiguus neurons: essential differences in anesthetized versus awake rats

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