Nerve Stimulation In Rabbits Research Articles

Neuroprotective effects of vagus nerve stimulation on traumatic brain injury.

Previous studies have shown that vagus nerve stimulation can improve the prognosis of traumatic brain injury. The aim of this study was to elucidate the mechanism of the neuroprotective effects of vagus nerve stimulation in rabbits with brain explosive injury. Rabbits with brain explosive injury received continuous stimulation (10 V, 5 Hz, 5 ms, 20 minutes) of the right cervical vagus nerve. Tumor necrosis factor-α, interleukin-1β and interleukin-10 concentrations were detected in serum and brain tissues, and water content in brain tissues was measured. Results showed that vagus nerve stimulation could reduce the degree of brain edema, decrease tumor necrosis factor-α and interleukin-1β concentrations, and increase interleukin-10 concentration after brain explosive injury in rabbits. These data suggest that vagus nerve stimulation may exert neuroprotective effects against explosive injury via regulating the expression of tumor necrosis factor-α, interleukin-1β and interleukin-10 in the serum and brain tissue.

A practical model to induce bradycardia by chemical ablation of sinus node and bilateral vagus nerve stimulation in rabbits, which satisfies the requirement for biopacemaking experiment in vivo

ObjectivesTo investigate the feasibility of the bradyarrhythmia rabbit model built by sinus node ablation and bilateral vagus nerve stimulation.Methods30 two-month-old Japanese white rabbits were randomly and equally divided into three...

Spatiotemporal Properties of Multipeaked Electrically Evoked Potentials Elicited by Penetrative Optic Nerve Stimulation in Rabbits

To investigate the spatiotemporal properties of the cortical responses elicited by intraorbital optic nerve (ON) stimulation with penetrating electrodes as means of designing optimal stimulation strategies for an ON visual prosthesis. The ON of rabbits was exposed by orbital surgery for electrical stimulation. Craniotomy was performed to expose the visual cortex contralateral to the operated eye. Electrically evoked potentials (EEPs) were recorded by an electrode array positioned on the visual cortex. There were primarily four components (N1, P1, P2, P3) in EEPs with implicit times of 8.0 ± 0.6, 11.3 ± 1.3, 20.5 ± 1.4, and 26.9 ± 1.5 ms, respectively, when the ON was stimulated by penetrating electrodes. The thresholds to elicit these components were different, and the higher thresholds were seen with slower cortical components. The corresponding thresholds were 13.8 ± 3.1 μA for N1, 21.8 ± 4.7 μA for P1, 36.4 ± 11.4 μA for P2, and 68.4 ± 17.2 μA for P3. The time courses of the EEP components were also distinct. The locations of EEPs with the maximum P1 amplitude showed a spatial correspondence to the ON stimulation sites. Different profiles of cortical responses could be discriminated when the ON stimulation sites were separated by 150 μm. Multiple components with different properties were elicited in EEPs when the ON was stimulated by penetrating electrodes. Retinotopic and localized stimulation could be achieved with this stimulating approach.

Response properties of electrically evoked potential elicited by multi-channel penetrative optic nerve stimulation in rabbits

Visual prosthesis is a potential way to restore partial vision for the patients with degenerative retinal diseases such as retinitis pigmentosa (RP) and age-related macular degeneration (AMD). Optic nerve stimulation with penetrating microelectrode array has been suggested as a possible method for visual prosthesis. The purpose of this study was to investigate the feasibility and basic response properties of cortical responses elicited by optic nerve stimulation with penetrating electrodes in rabbits. In this study, three triangularly or linearly configured platinum-iridium wire electrodes were inserted into the optic nerves of rabbits for electrical stimulation. The charge-balanced current pulses with amplitudes ranging from 10 to 100 microA at 0.5 ms pulse duration were used as the electrical stimuli. The electrically evoked potentials (EEPs) were recorded with a 16-channel silver-ball electrode array in the rabbit visual cortex. Our experimental results showed that the activities of visual cortex could be effectively evoked by the optic nerve stimulation with penetrating electrodes. The threshold of current and charge density to elicit EEPs under optic nerve stimulation at 0.5 ms pulse duration was 20.3 +/- 7.5 microA and 37.8 +/- 13.9 microC/cm(2), respectively. Current stimuli with cathode-first pulses elicited larger cortical responses than that with anode-first pulses. The amplitude of P1 and extent of EEPs increased as the stimulating current amplitude increased, while the latency of P1 decreased. The spatial distributions of multi-channel EEPs in visual cortex demonstrated distinctively different properties under stimulation with different orientations of the stimulating electrodes.

Endogenous endothelins and the response to electrical renal nerve stimulation in anaesthetized rabbits

The influence of endogenous endothelins on the neural control of renal function is poorly understood. We therefore studied the effects of endothelin blockade (combined ET(A) and ET(B) receptor antagonism using TAK-044) on the acute and prolonged effects of renal nerve stimulation in rabbits, measuring renal blood flow, glomerular filtration rate (GFR), urine flow and sodium excretion. Brief (3 min) stimulation over 0.5-8 Hz produced frequency-dependent reductions in total renal blood flow, cortical blood flow and, less markedly, medullary blood flow. TAK-044 did not significantly alter basal total renal blood flow or cortical blood flow, or their responses to nerve stimulation, but significantly increased basal medullary blood flow (P<0.01) and increased the slope of the stimulation frequency-medullary blood flow relationship (P<0.05). Prolonged (20 min) stimulation at 0, 0.5 and 2 Hz produced frequency-dependent reductions in total renal blood flow, GFR, urine flow and sodium excretion, but not medullary blood flow. Pretreatment with TAK-044 did not significantly alter these responses. Thus, endogenous endothelins do not appear to either augment or lessen the effects of renal nerve activation on total renal blood flow, cortical blood flow, GFR or sodium excretion. The apparent ability of TAK-044 to enhance medullary blood flow responses to renal nerve stimulation may reflect an action of endogenous endothelins to blunt neurally mediated vasoconstriction in the medullary circulation. Alternatively, it may simply be secondary to the effects of endogenous endothelins on basal medullary blood flow.

Effect of renal perfusion pressure on responses of intrarenal blood flow to renal nerve stimulation in rabbits.

1. We investigated how sympathetic nerve activity and renal perfusion pressure (RPP) interact in controlling renal haemodynamics in pentobarbitone-anaesthetized rabbits. 2. Renal blood flow (RBF) was reduced by electrical renal nerve stimulation (0.5-8 Hz), with RPP set using an extracorporeal circuit to 65, 100 and 135 mmHg. 3. Responses of RBF and cortical laser Doppler flux to renal nerve stimulation were blunted by increased RPP. For example, 4 Hz stimulation reduced RBF by 68 +/- 7% with baseline perfusion pressure approximately 65 mmHg, but only by 22 +/- 3% at approximately 135 mmHg. Medullary laser Doppler flux was less responsive than cortical laser Doppler flux to renal nerve stimulation and its response was not dependent on perfusion pressure. 4. When perfusion pressure was clamped at its baseline level during renal nerve stimulation, responses of RBF and cortical laser Doppler flux, but not medullary laser Doppler flux, were still blunted with increased baseline perfusion pressure. 5. A frequency rich stimulus was applied to assess the effects of perfusion pressure on dynamic neural control of RBF. Renal blood flow responded similarly at each level of perfusion pressure, as a low-pass filter with a pure time delay. 6. Our results suggest that, in the rabbit extracorporeal circuit model, increased RPP blunts the ability of steady state renal nerve stimulation to reduce cortical, but not medullary perfusion. However, in this model the level of RPP appears to have little impact on dynamic neural control of RBF.

Characteristics of laryngeal late responses to superior laryngeal nerve stimulation in rabbits

Characteristics of laryngeal late responses to superior laryngeal nerve stimulation in rabbits

P-548 - Role of nitric oxide in norepinephrine release induced by renal nerve stimulation in rabbits

P-548 - Role of nitric oxide in norepinephrine release induced by renal nerve stimulation in rabbits

Influence of hypoglycaemic sulphonylureas on the electrophysiological parameters of the heart

The effects of different ATP-sensitive potassium channel blocker sulphonylurea drugs (0.01-1000 mumol/l, or kg) were investigated in vitro on the electrical threshold, conduction time, effective refractory period and automaticity of left atrium, right ventricle and Purkinje fibers as well as in vivo on strophanthidin-, ischaemia- and reperfusion-induced arrhythmias and on vagal nerve stimulation in rabbits, rats and dogs. They proved to exert different actions not only quantitatively but also qualitatively. In vitro, glibenclamide diminished the electrical activity of the heart muscle preparations, while chlorpropamide stimulated it, whereas glimepiride does not seem to affect it markedly. In vivo, glibenclamide and glimepiride decrease, while gliclazide and tolbutamide increase, the amount of strophanthidin- and ischaemia-induced ventricular ectopic beats and the duration of ventricular fibrillation. In the case of glimepiride the effect was dependent on the metabolic state. The different actions of sulphonylureas on the electrophysiological properties of the heart cannot be explained solely by their ATP-dependent potassium channel blocking potencies.

Effects of some neuropeptides on the uvea

This lecture summarizes studies on the effects of some of the neuropeptides which seem to be present in somatosensory and autonomic nerves in the uvea. Release of these peptides is likely to explain nerve induced effects in the eye which are not due to classical transmitters. Trigeminal nerve fibres in the eye seem to contain substance P (SP), calcitonin gene-related peptide (CGRP), and cholecystokinin (CCK), parasympathetic nerve fibers from the facial nerve seem to contain vasoactive intestinal polypeptide (VIP), and peptide with histidine and isoleucine terminals (PHI), and sympathetic nerves seem to contain neuropeptide Y (NPY). Retrograde trigeminal nerve stimulation in rabbits causes hyperemia, miosis, a breakdown of the blood-aqueous barrier to plasma proteins and a rise in intraocular pressure (IOP). There is release of SP and CGRP or related peptides. The miosis seems to be due to SP and the other effects to CGRP and small amounts of arachidonic acid metabolites released by the peptides. SP has no miotic effect in monkeys and cats. However, CCK is a potent miotic in monkeys and causes contraction of the human pupillary sphincter muscle. It has no such effect in the lower species. The effect of CCK in primates seems to derive from the presence of CCK receptors of the A-type on the pupillary sphincter muscle, and can be blocked by lorglumide. Miosis can be produced in cats by the peptide endothelin; this effect is due to release of arachidonic acid metabolites. Facial nerve stimulation causes vasodilation in the uvea of rabbits, cats and monkeys. The effect cannot be abolished by muscarinic blocking agents.(ABSTRACT TRUNCATED AT 250 WORDS)

Temporal and spatial summation caused by aortic nerve stimulation in rabbits. Effects of stimulation frequencies and amplitudes

Frequency-modulated stimulus patterns, controlled by heart rate or blood pressure feed-back, are proposed for therapeutic use of electrical stimulation of the carotid sinus nerves (CSNS). Continuous CSNs with equidistant pulses is applied in hypertensive or angina pectoris patients who are refractory to therapy. Frequency modulation simulates transmission properties of single baroreceptors, while modulation of stimulus amplitudes simulates recruitment of baroreceptors by pressure pulses in the carotid sinus. Using aortic nerves in the anesthetized rabbit as a model, it was investigated if amplitude modulation could substitute frequency modulation in electrical stimulation. First, 'step stimulation' was applied (protocol 1): starting from a basal low frequency with the basal amplitude set at a level of 10% between threshold and the maximum, either the frequency or the amplitude of pulses was increased in a single step for 20 s (frequency step, FS; amplitude step, AS). The blood pressure response and its course of recovery was analyzed. Fifteen different basal stimulus frequencies (1, 2, ...15 Hz) were investigated. For FS, each given frequency was increased 10-fold (10, 20, ...150 Hz) while the basal amplitude level was kept constant. For AS, the basal amplitude level was increased to the maximum, while each given frequency was kept constant. Depressor responses to AS were equivalent to FS at a 10-fold higher frequency. After step stimulation it was either stopped immediately (type A), or was resumed for 90 s with a basal low frequency and the basal low amplitude level (type B). After type A and B stimulations, the recovery time of blood pressure response was found to be longer after cessation of AS, compared to FS. In further experiments (protocol 2), an 'electronic baroreceptor analog' generated stimulus patterns which were feed-back controlled by the blood pressure signal. Either frequencies (FM) or amplitudes (AM) of stimuli were modulated by the pressure pulse signal. Since in feed-back controlled stimulation the mean electrical current flow is reduced by depressor responses, stimulus current flow in relation to the blood pressure response served to compare the efficacy of different stimulus patterns. Equidistant stimulation (EDS) was also applied for comparison. Both feed-back controlled stimulus patterns (FM and AM) were more effective than EDS. It is suggested that AS predominantly activated C-fibers, whereas low level stimulation predominantly excited A-fibers.(ABSTRACT TRUNCATED AT 400 WORDS)

Effects of hexamethonium, biperiden and phentolamine on the vasoconstrictive effects of oculomotor nerve stimulation in rabbits

Abstract In rabbits intracranial stimulation of the oculomotor nerve causes vasoconstriction in the anterior uvea and vasodilation in the choroid and an attempt has been made to analyze the mechanism involved in the vasoconstrictive response to stimulation. The oculomotor nerve was stimulated unilaterally, and regional blood flow was determined in both eyes using radioactively labelled microspheres. Hexamethonium bromide, in a dose of 40–80 mg/kg body weight, completely abolished the vasoconstrictive response in the iris and the ciliary processes. The blood flow in all parts of the uvea tended to be higher on the stimulated side than on the control side. The parasympatholytic agent biperiden lactate, in a dose of 2·5–5 mg/kg body weight, reduced the response in the iris, but no significant change was observed in the ciliary processes. The alpha-adrenergic blocking agent phentolamine chloride, in a dose of 10–15 mg/kg body weight had no significant effect on the response in the iris but reversed the effect in the ciliary processes. A combination of biperiden and phentolamine totally abolished the vasoconstrictive response in the iris, and there was increased blood flow in the ciliary processes on the stimulated side. The results indicate that intracranial stimulation of the oculomotor nerve and possibly of adjacent structures caused a release of vasodilating and vasoconstricting agents in the uvea. The vasoconstrictive effect was partly muscarinic, possibly due to miosis, and partly due to stimulation of receptors sensitive to phentolamine. A ganglion or ganglion-like receptors, somewhere between the site of stimulation and the effector cells, seem to be involved in the transmission of the vasoconstrictive impulses.

Increase in aqueous humour protein concentration induced by oculomotor nerve stimulation in rabbits

Abstract The oculomotor nerve was stimulated intracranially with a stereotactic technique in rabbits. Paracentesis was performed after 15 or 30 min of stimulation and the protein concentration of the aqueous humour was measured. The protein content of the aqueous humour increased about twofold in the stimulated eye as compared with the control eye. This increase was not due to the increased tension of the extraocular muscles during stimulation. Neither was the change dependent on the stimulation intensity above the threshold for intense miosis. Pretreatment with indomethacin was always ineffective in preventing the increase in protein concentration. Blockade of the muscarinic receptors with biperiden abolished most of this increase during stimulation. Thus, the increase in protein concentration of the aqueous humour during oculomotor nerve stimulation seems to be due to a cholinergic mechanism.