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Parasympathetic dysfunction and antiarrhythmic effect of vagal nerve stimulation following myocardial infarction.

ABSTRACT: Myocardial infarction causes sympathetic activation and parasympathetic dysfunction, which increase risk of sudden death due to ventricular arrhythmias. Mechanisms underlying parasympathetic dysfunction are unclear. The aim of this study was to delineate consequences of myocardial infarction on parasympathetic myocardial neurotransmitter levels and the function of parasympathetic cardiac ganglia neurons, and to assess electrophysiological effects of vagal nerve stimulation on ventricular arrhythmias in a chronic porcine infarct model. While norepinephrine levels decreased, cardiac acetylcholine levels remained preserved in border zones and viable myocardium of infarcted hearts. In vivo neuronal recordings demonstrated abnormalities in firing frequency of parasympathetic neurons of infarcted animals. Neurons that were activated by parasympathetic stimulation had low basal firing frequency, while neurons that were suppressed by left vagal nerve stimulation had abnormally high basal activity. Myocardial infarction increased sympathetic inputs to parasympathetic convergent neurons. However, the underlying parasympathetic cardiac neuronal network remained intact. Augmenting parasympathetic drive with vagal nerve stimulation reduced ventricular arrhythmia inducibility by decreasing ventricular excitability and heterogeneity of repolarization of infarct border zones, an area with known proarrhythmic potential. Preserved acetylcholine levels and intact parasympathetic neuronal pathways can explain the electrical stabilization of infarct border zones with vagal nerve stimulation, providing insight into its antiarrhythmic benefit.

SUBMITTER: Vaseghi M

PROVIDER: S-EPMC5621871 | biostudies-other | 2017 Aug

REPOSITORIES: biostudies-other

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Parasympathetic dysfunction and antiarrhythmic effect of vagal nerve stimulation following myocardial infarction.

Vaseghi Marmar M Salavatian Siamak S Rajendran Pradeep S PS Yagishita Daigo D Woodward William R WR Hamon David D Yamakawa Kentaro K Irie Tadanobu T Habecker Beth A BA Shivkumar Kalyanam K

JCI insight 20170817 16

Myocardial infarction causes sympathetic activation and parasympathetic dysfunction, which increase risk of sudden death due to ventricular arrhythmias. Mechanisms underlying parasympathetic dysfunction are unclear. The aim of this study was to delineate consequences of myocardial infarction on parasympathetic myocardial neurotransmitter levels and the function of parasympathetic cardiac ganglia neurons, and to assess electrophysiological effects of vagal nerve stimulation on ventricular arrhyth ...[more]

PMID: 28814663

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Project description:Abstract The aim of this prospective study was to investigate autonomic function in Parkinson’s disease with a multidimensional approach including clinical evaluation tools, head-up tilt test and morphological studies of the vagus nerve. Head-up tilt test parameters including high frequency power of the heart frequency interval, the ratio of low frequency power of the distance between two consecutive R waves in electrocardiogram (RR interval) to the high frequency and low frequency power of systolic blood pressure were used to evaluate parasympathetic, cardiac sympathetic and vasomotor sympathetic functions, respectively, in 80 patients with Parkinson's disease. We examined the cross-sectional area of the vagus nerves bilaterally using nerve ultrasound and compared mean values with a control group of healthy subjects (n = 40) as well as patients with chronic inflammatory demyelinating polyneuropathy (n = 76). The cross-sectional area of right/left vagus nerve of Parkinson's patients was significantly lower compared to the right/left vagus nerve of the control group and of chronic demyelinating polyneuropathy patients. Furthermore, the cross-sectional area of the right vagus nerve was significantly larger from the one of the left vagus nerve for all groups. Based on tilt test, 43 patients (disease duration 7 ± 5, age at evaluation 71 ± 9, Hoehn and Yahr score 2.8 ± 8) were diagnosed with autonomic dysfunction (orthostatic hypertension n = 11, chronotropic incompetence n = 31, postural orthostatic tachycardia syndrome n = 1). Patients with orthostatic hypotension showed significantly higher Unified Parkinson’s Disease Rating Scale-III values than those with chronotropic incompetence. The cross-sectional area of the vagus nerve correlated inversely with heart rate in rest and supine position and positively with tilt test parameters representing parasympathetic modulation through vagal activity [high frequency power of the distance between two consecutive R waves in electrocardiogram (RR interval)] at rest. We demonstrate for the first time that morphological characteristics of the vagus nerve correlate with parameters of parasympathetic function from the spectral analysis of cardiovascular parameters in tilt test for Parkinson's patients. This correlation reveals the impact of the atrophy of vagal atrophy for autonomic function in Parkinson's disease. Nerve ultrasound of the vagus nerve could potentially be used as an adjunct to tilt table examination to diagnose autonomic dysfunction. Huckemann et al. report that the mean and right cross-sectional area of the vagus nerve in patients with Parkinson's syndrome was reduced compared to the control group and patients with inflammatory demyelinating neuropathy as a sign of degeneration. Furthermore, it correlated with markers of parasympathetic dysfunction in head-up tilt test. Graphical Abstract Graphical abstract

Project description:BACKGROUND:This study aimed to evaluate effects of electric vagal nerve stimulation on early postoperation cognitive dysfunction in aged rats. METHODS:A total of 33 male Sprague Dawley rats were selected and assigned randomly to three groups, control group (C, n?=?10), splenectomy group (S, n?=?10) and splenectomy+vagal nerve stimulation group (SV, n?=?13). Behavior and memory of rats were evaluated by Open Field Test and Morris Water Maze. Levels of TNF-?, IL-6 and IL-10 in serum were measured by ELISA. The level of TNF-? protein in hippocampus was assessed by Western blotting. rt-PCR was used to detect mRNA expression of NF-?B in hippocampus. RESULTS:During anesthesia/operation, vital life signs of rats were stable. In SV group, vagal nerve stimulation decreased heart rate lower than 10% of basic level and kept it at a stable range by regulating stimulation intensity. After stimulation stop, heart rate returned to the basic level again. This indicated that the model of vagal nerve stimulation was successful. Serum levels of TNF-? and IL-6 increased by the operation/anesthesia, but they decreased with vagal nerve stimulation (all P?<?0.05). TNF-? protein and mRNA expression of NF-?B in hippocampus were also eliminated by vagal nerve stimulation compared to S group (P?<?0.05). Results of Morris Water Maze showed escape latency of postoperation in S group was significantly longer than C group (P?<?0.05), and times of crossing platform in S group was lower than that of C group (P?<?0.05). Although escape latency of postopration in SV group was shorter than that of S group, there was no significant difference between two groups. Meanwhile there were no significant differences of behavior test in Open Field test between three groups, although vagal nerve stimulation improved partly active explore behavior compared to S group. CONCLUSION:The inflammation caused by operation and general anesthesia was an important reason of early postoperation cognitive dysfunction, and electric vagal nerve stimulation could inhibit the inflammation. Meanwhile, vagal nerve stimulation could ameliorate early postoperation cognitive dysfunction partly, but its protective effects were not enough and should be studied and improved in future.

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Parasympathetic dysfunction and antiarrhythmic effect of vagal nerve stimulation following myocardial infarction.

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Parasympathetic dysfunction and antiarrhythmic effect of vagal nerve stimulation following myocardial infarction.

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