Controlled sinus arrhythmia during burst stimulation of the vagus nerve

In experiments on anesthesized cats and rats the desynchronization of the heart rate and burst stimulation of the vagus brought about severe sinus arrhythmia. Analysis of the functional dependence between the P--S interval (atrial wave of the ECG--moment of vagus stimulation) and the P--P interval showed periodical alterations in pacemaker sensitivity to the effect of the vagus during each cardiac cycle. It is supposed that natural vagus arrhythmia is the result of discoordination between heart automacy and efferent vagus bursts of central origin.     

Sensitive control of heart rate in monkeys using burst stimulation of the vagus nerve

Burst vagus stimulation led to synchronization of the cardiac and vagal rhythms at certain frequency ranges. The increase of the number of impulses in a burst from 1 to 16 extended the range of synchronization and shifted it towards lower frequencies forming a total range of exact regulation of the heart rate within 85--40% of the initial rate. It was suggested that vagal effect consists of tonic and synchronizing components.     

The spectrogram of heart rate in cats following burst stimulation of the vagus nerve

Denervation of the heart (bilateral vagotomy and propranolol) in artificially ventilated cats didn't remove respiratory peaks on the spectrogram of heart rate, while burst stimulation of vagus nerve increased or decreased them several times by synchronization of the heart and vagus rhythms, which in its turn was observed under the bradycardia only. At the same time, the desynchronization of rhythms provoked severe sinus arrhythmia which had a distinct periodic character. Under these conditions, there were high non-respiratory peaks appearing at the spectrogram of the heart rate that indicated existence of two vagus chronotropic effects: a well known tonic one and special intracycle synchronizing effect correcting duration of every cardiac cycle.     

Alpha-adrenergic receptor modulation of the intrathoracic efferent sympathetic nervous system regulating the canine heart

The augmentation of ventricular inotropism induced by electrical stimulation of acutely decentralized efferent sympathetic preganglionic axons was reduced, but still present, following administration of hexamethonium (10 mg/kg i.v.). While hexamethonium continued to be administered, the cardiac augmentations so induced were enhanced significantly following administration of the alpha-adrenergic receptor blocking agent, phentolamine myselate (1 mg/kg i.v.). Stimulation of the sympathetic efferent postganglionic axons in cardiopulmonary nerves induced cardiac augmentations that were unchanged following administration of these agents singly or together. The cardiac augmentations induced by stimulation of efferent preganglionic sympathetic axons were unchanged when phentolamine was administered alone. The augmentations of cardiac inotropism induced by efferent postganglionic sympathetic axonal stimulation were decreased following local administration of the beta-adrenergic antagonist timolol into the ipsilateral stellate and middle cervical ganglia. Thereafter, these augmentations were unchanged following the subsequent intravenous administration of phentolamine. It is concluded that the activation of cardiac neurons in the stellate and middle cervical ganglia by stimulation of efferent preganglionic sympathetic axons can be modified by alpha-adrenergic receptors and that these effects are dependent upon beta-adrenergic receptors, not nicotinic ones, in intrathoracic ganglia.     

Control of cardiac rhythm by stimulation of the vagus nerve in bursts in the rat

Burst stimulation of the vagus nerve in rats made it possible to obtain the ranges of the heart rate regulation. The increase of the number of impulses in a burst from 1 to 16 leads to a consistent decrease in the range of regulation from respectively 72.1 and 66.7% to 30.4 and 25% of the initial rate. The maximal range (10.1% of the initial rate) is reached with 4 impulses in a burst. The phenomenon of the regulation is reversed by atropine.     

Types of the peptide modulation of the vagus nerve effect on the heart rhythm

In anaesthetised cats, effects of 24 regulatory peptides upon inhibitory tonic and synchronizing components of vagal chronotropic action, were studied. The findings allowed to divide the peptidergic vagotropic activity into three types: (1) a selective action upon inhibitory tonic vagal effect; (2) a selective modulation of synchronizing vagal effect; (3) opposite changes in the vagal chronotropic effect components. The peptides seem to be able to modulate both the vagal bradycardia and the functional structure of parasympathetic chronotropic effect.     

Reaction of the hypothalamo-hypophyseal system of cats to stimulation of the cervical sympathetic nerve and the afferent fibers of the vagus nerve]

Data are presented on the functional morphology of the hypothalamo-hypophysial neurosecretory system of cats in stimulation of the cervical sympathetic nerve and of the afferent fibers of the vagus. Stimulation of the sympathetic nerve selectively activated the supraoptic nucleus and caused the discharge of the neurohormones from the posterior lobe of the hypophysis, whereas its infundibular portion contained much neurosecretory material. In response to the stimulation of the vagus all the portions of the neurohypophysis were released of the Gomori-positive substance; both the supraoptic and the paraventricular nucleus were activated.     

Norepinephrine release from the lung by sympathetic nerve stimulation inhibition by vagus and methacholine

A procedure to isolate the sympathetic nerve supply to the lung has been developed in the rabbit. Electrical stimulation (50V, 1ms, 10Hz) of these nerves released norepinephrine (NE) which could be measured in the outflows from lungs perfused via the pulmonary artery. On the average 19 ng NE/stimulation period were found in the perfusates. The release of NE from the lung by nerve stimulation is thereby demonstrated by direct measurement of the amine. Infusion of methacholine (1 or 10 ug/ml) and excitation of the vagus nerves inhibited the output of NE. These data suggest existence of a sympathetic-parasympathetic presynaptic balance in the lung.     

迷走神经和交感神经系统不同活动状态对心率变异性的影响

实验在氯醛糖加氨基甲酸乙酯麻醉的新西兰兔上进行。记录血压、心率、心电图并对心电Ｒ－Ｒ间期（ＲＲＩ）作功率谱密度（ＰＳＤ）分析。以单调性电刺激和低频率的波动性电刺激分别刺激减压神经、疑核和右侧迷走神经外周端,观察到低频率的波动性刺激对增加ＰＳＤ中低频成分（ＬＦ）的作用比单调性电刺激更大（Ｐ〈０．０５）。注射新福林仅在头一个２５６个心动周期时间内引起总变异性（ＴＶ）、ＬＦ、ＰＳＤ中高频成分（ＨＦ）。Ｌ     

Effect of sympathetic nerve stimulation on myocardial reactive hyperemia

It has been established in experiments on 25 dogs that the peak of reactive hyperemia (RH) of the myocardium cannot be regarded as an absolute criterion of the coronary dilatory reserves. Stimulation of the stellate ganglion under the conditions of arterial blood pressure stabilization increased the peak of RH. After-effect of the sympathetic nerve stimulation also led to a rise in the peak of RH as compared with control.     

迷走神经刺激对记忆的影响

迷走神经刺激(vagus nerve stimulation, VNS)用于终止癫痫发作已经有二十年的历史.期间VNS也用于难治性抑郁的治疗.在治疗过程中研究者发现VNS 对癫痫、抑郁患者的学习和记忆能力有改善作用,这种改善作用在一些动物和人体实验中也得到证实.但VNS在记忆形成的哪个阶段起作用以及如何起作用的具体机制尚不十分清楚.因此,进一步了解VNS对记忆的影响及作用机制有利于探讨记忆形成的生理机制,也为临床治疗特异性记忆障碍和相关神经精神疾病提供新的思路和有益补充.本文综述了近十几年来VNS对记忆的影响及相关机制.     

The effect of sulfinpyrazone on the response to sympathetic nervous system stimulation

The purpose of this study was to determine if sulfinpyrazone has a direct action on sympathetic nerve endings to prevent release of the transmitter. Pre-synaptic and post-synaptic events as well as direct sympathetic nervous system stimulation were tested in 15 α-chloralose anesthetized cats before and 1 hour after sulfinpyrazone (100 mg·kg⁻¹, i.v.). Heart rate response to cardiac accelerator nerve stimulation or to increasing doses of isoproterenol was not significantly depressed by sulfinpyrazone. In addition, no alteration in the reflex activation of the sympathetic nervous system in response to histamine was observed following sulfinpyrazone. Both norepinephrine and epinephrine levels were similar to those levels reported previously by Smith and Robinson (7) for untreated cats. We conclude sulfinpyrazone has no direct depressing effect on the sympathetic nerve endings and that this mechanism cannot explain the reported beneficial effect of sulfinpyrazone on coronary occlusion induced arrhythmias.