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Results for “Parasympathetic Nervous System”

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At least 127 records · Page 7Linked to original sources
PubMedDate not supplied

The effect of parasympathetic nervous system on hydrodynamics of intraocular fluids and distribution of electrolytes and amino acids.

Tonographic determinations Po and C), cannulation of the anterior chamber and measurements of the secreted aqueous humor volume by the method of posterior-anterior chamber perfusion with inulin solution were carried out in normal eyes, in eyes after parasympathetic denervation and during the action of a cholinergic neurotransmitter under the conditions of postdenervation hyperexcitability. Parasympathetic denervation of the eyeball was obtained by excision of the ciliary ganglion. Additonally, pharmacological blockade of the adrenergic neurons was applied. In the aqueous humor from the posterior and anterior chamber osmolality, as well as concentrations of sodium potassium, calcium, magnesium and total alpha-amino nitrogen were determined. The cholinergic effect on the volume of secreted aqueous humor and on the channels of its outflow was described. This effect was enhanced by the postdenervation hyperexcitability state, indicating a stimulating parasympathetic influence on the passage of electrolytes and amino acids into the intraocular fluids.

Amino Acids↗
PubMed2000

[Treatment of tachycardic atrial fibrillation by catheter-assisted electrical stimulation of the cardiac parasympathetic nervous system].

UNLABELLED: Treatment of tachycardic atrial fibrillation (AF) is difficult in patients with congestive heart failure because many drugs which exert negative dromotropic effects (beta-blockers, calcium channel antagonists) may depress ventricular contractility and/or decrease arterial blood pressure. We have identified 2 intravascular sites in the superior (SVC) and inferior vena cava (IVC) where parasympathetic nerves, which innervate the atrioventricular node, can be stimulated electrically. In 8 dogs, a 7-F catheter with an expandable electrode basket at its tip was non-fluoroscopically positioned in the SVC and in the proximal IVC (time for positioning: 3-5 minutes). High-frequency electrical parasympathetic stimulation (PS) with 20 Hz at an impulse duration of 0.1 ms was performed during pacing induced AF. RESULTS: With increasing stimulus strength, a graded ventricular rate slowing was observed during PS in the SVC and IVC (P < 0.01, ANOVA). The negative dromotropic effect started instantaneously after onset of PS and ceased immediately after termination of PS. During ventricular pacing at a constant rate, no decrease of the arterial blood pressure was observed during PS. PS in the IVC yielded significantly lower stimulation thresholds than in the SVC. CONCLUSIONS: Transvenous parasympathetic stimulation for ventricular rate control during AF can easily be achieved in the SVC and IVC in dogs. This procedure may provide a foundation for investigating the usefulness of PS in humans. If the results translate to patients, PS may be very beneficial in the treatment of AF in patients with congestive heart failure.

Animals↗
PubMed2002

[Mechanism of synergism of the sympathetic and parasympathetic nervous system in regulating cardiac and gastric activity].

The authors studied the mechanism of the higher vagus suppression of cardiac performance, which occurs when irritation of the sympathetic nerve is added to that of the vagus and when gastric motility occurring with the irritation of the sympathetic trunk is stimulated. Preganglionic serotonic fibers synaptically connected with serotoninergic intramural neurons are involved in showing these mechanisms.

Animals↗
PubMed1988

Endogenous opioid involvement in the cardiovascular effects of clonidine in rats: role of the parasympathetic nervous system.

The interaction between intravenously administered clonidine and naloxone on blood pressure and heart rate was studied in urethane-anesthetized, normotensive Sprague-Dawley rats. In rats pretreated with propranolol, 1 mg/kg i.v., to eliminate sympathetic tone in the heart clonidine, 5 micrograms/kg i.v. produced hypotension and bradycardia which were inhibited by naloxone, 2 mg/kg i.v. These effects were similar to effects observed in earlier studies in the absence of propranolol. In contrast, in rats pretreated with atropine, 5 mg/kg i.v., to eliminate the effects of changes in vagal tone, the hypotensive and bradycardic effects of clonidine were not influenced by naloxone. These findings are interpreted to indicate that an endogenous opioid is involved in the clonidine-induced increase in parasympathetic outflow to the myocardium.

Animals↗
PubMedDate not supplied

[Antifibrillatory effect of antiarrhythmic drugs of various classes under conditions of activation of the parasympathetic nervous system].

The experiments on anesthetized rats under the conditions of a 7-min occlusion of the anterior descending branch of the left coronary artery followed by reperfusion showed that drugs belonging to various classes of antiarrhythmic agents (ethacizine, IC; cardiocyclide, III; verapamil, IV; bradizol, V) produce a pronounced antifibrillatory and antiarrhythmic effects. The cholinomimetic carbacholine produced practically the same effect. Cardiocyclide, verapamil, and bradizol retained their antifibrillatory properties upon combined administration with carbacholine, while the effect of ethacizine administered jointly with carbacholine was decreased.

Animals↗
PubMed1982

Peripheral inhibition of the parasympathetic nervous system by angiotensin.

1. The effects of angiotensin II and angiotensin III ([des-1-Asp]-angiotensin II) on the actions of the peripheral vagus were studied in several preparations. 2. In the anaesthetized dog and in the spontaneously beating guinea-pig isolated atrial preparation the decrease in heart rate evoked by stimulation of the peripheral end of the vagus nerve was attenuated in the presence of angiotensin II and angiotensin III. These effects persisted after sympathetic beta-blockade. 3. In the anaesthetized rabbit vagally-stimulated increases in tension in a segment of the gastric wall were also attenuated in the presence of angiotensin II and angiotensin III.

Angiotensins↗
PubMed1982

Age-related protective role of parasympathetic nervous system against hypercalcaemia-induced ventricular arrhythmias in the rat.

Time of appearance of extrasystoles, ventricular fibrillation, and cardiac arrest were monitored in urethane-anaesthetized rats of different ages following CaCl2 infusion. Ca++ required to produce ventricular arrhythmias was significantly higher in younger than in older animals. Bilateral vagotomy or atropine treatment significantly reduced Ca++ requirements for production of arrhythmias in younger but not in older animals. These findings support the hypothesis of vagally mediated age-related antagonism toward Ca++-induced ventricular arrhythmias. This suggests that young subjects are less prone to develop ventricular rhythm disturbances as a result of hypercalcaemic states.

Age Factors↗
PubMed1991

The parasympathetic nervous system and the diurnal variation of lung mechanics in asthma.

In a placebo-controlled double-blind experiment the effects of cholinergic blockade with 30 micrograms kg-1 atropine administered by intravenous injection have been studied in nocturnal asthma. Cholinergic blockade at night reversed the changes in indices of airflow in small airways and of gas trapping to the values seen after administration of atropine during the daytime. However, the improvement in indices of airflow in large airways was not complete, reaching only the daytime placebo levels. No changes were seen in any aspect of breathing pattern. The results are discussed in relation to the literature.

Adult↗
PubMed1982

[Role of the parasympathetic nervous system in cell proliferation of the corneal epithelium of rats after submandibular gland injury].

A study was made of the effect of cholinergic nerves on proliferation of epithelial cells of the cornea. Two series of experiments on 89 anesthetized Wistar rats were made to define that the blockade of the cholinergic neurons with botulinum toxin and that of tissue M-cholinoreceptors with atropine increased the mitotic index. Upon formation of humoral growth stimulators during submaxillary gland injury (SGI), the stimulating effect of atropine was further potentiated. At the same time stimulation of M-cholinoreceptors with pilocarpine lowered the magnitude of the mitotic index of the cornea cells. During SGI injury administration of pilocarpine noticeably decreased the proliferation rate. Thus the stimulation of cholinergic innervation inhibited the rate of tissue proliferation. It is suggested that during operations on the internal organs and vegetative dystonia the proliferation pattern of the cornea cell might vary which should be taken into consideration in experimental and clinical studies.

Animals↗
PubMedDate not supplied

[The effect of qualitatively different nutrition on various indicators of the functional status of the parasympathetic nervous system and blood proteins in students during an examination period].

The investigations were conducted on two groups of students of the Baku Naval School (15 subjects in each group). It was shown that in the presence of traditional nutrition containing mainly meat and grain products and characterized by insufficient content of animal protein and milk products, the psychoemotional and mental stress by the end of the examination session, as compared to the period of the current studies, resulted in a significant growth of acetylcholine-like substances, alpha- and gamma-globulins, a tendency to an increased acetylcholinesterase concentration in their blood, most manifest on the day of passing the 3d examination, and a tendency to elevated cholinesterase activity on the day of passing the 4th examination; a significant decrease of protein content and albumin levels. Due to nutrition correction (mainly by the protein component) shifts in the content of protein and albumin levels, alpha- and gamma-globulins, acetylcholine-like substances in the blood were recorded by the end of the examination session, and were appreciably close to the values in the period of the current studies.

Adolescent↗
PubMed2005

Miotic tolerance to sarin vapor exposure: role of the sympathetic and parasympathetic nervous systems.

O-isopropyl methylphosphonofluoridate, also known as sarin or GB, is a highly toxic organophosphorous compound that exerts its effect by inhibiting the enzyme acetylcholinesterase. While the effects of a single exposure to GB vapor are well characterized, the effects of multiple exposures to GB vapor are less clear. Previous studies in the rat and guinea pig have demonstrated that multiple exposures result in tolerance to the miotic effect of nerve agents. The aim of the present study was to examine potential mechanisms responsible for tolerance to the miotic effect of GB vapor that has been observed in the rat after multiple exposures. Multiple whole-body inhalation exposures to GB vapor were conducted in a dynamic airflow chamber. Exposures lasted 60 min and each of the three exposures occurred at 24-h intervals. The results of the present study demonstrate that the alpha-adrenergic antagonist phentolamine and the beta-adrenergic receptor antagonist propranolol did not affect the development of tolerance to the miotic effect of GB vapor, suggesting that enhanced sympathetic tone to the eye is not responsible for the observed tolerance. Administration of atropine before the first exposure prevented the tolerance to the miotic effect of GB vapor after the third exposure, suggesting that the tolerance is the result of muscarinic receptor desensitization secondary to receptor stimulation. The present study extends the findings of previous studies to strengthen the hypothesis that the miotic tolerance observed in the rat upon repeated exposure to nerve agents is due to desensitization of muscarinic acetylcholine receptors located on the pupillary sphincter.

Adrenergic alpha-Antagonists↗
PubMed1989

Role of acetylcholine in pyridostigmine-induced myocardial injury: possible involvement of parasympathetic nervous system in the genesis of cardiomyopathy.

Although acetylcholine is known to be involved in the genesis of skeletal muscle disturbance, its effect on cardiac muscle has been scarcely studied. In the present paper, using pyridostigmine, a cholinesterase inhibitor, the possible role of acetylcholine in the genesis of cardiomyopathy was investigated. In a mortality study, it was shown that pyridostigmine (100 mg/kg) caused death of 9/10 rats within 8 h, and that the lethality of such a dose could be significantly diminished by the subsequent administration of a total dose of 4 mg/kg atropine. In all other experiments, rats were divided into three groups; the control, untreated group; the pyridostigmine + atropine group in which atropine (2 mg/kg) was administered 5 min after pyridostigmine (60 mg/kg) administration; and the pyridostigmine group in which pyridostigmine (60 mg/kg) was administered orally. Rats were killed 3 h after pyridostigmine administration, and hearts were isolated. Heart mitochondrial electron transport activity (NADH-cytochrome c reductase, succinate-cytochrome c reductase, and cytochrome c oxidase) were measured enzymatically, and mitochondrial respiratory rates and control indices were measured polarographically. Structural changes in cardiac muscles of each group were observed by electron microscopy of cardiac sections. Acetylcholine levels of left ventricle were measured by high performance liquid chromatography. Activities of NADH-cytochrome c reductase and succinate-cytochrome c reductase were not affected by pyridostigmine administration; however, cytochrome c oxidase activity was significantly reduced in the pyridostigmine group. Atropine markedly lessened this reduction in activity. A protective effect of atropine was also observed morphologically. A protective effect of atropine was also observed morphologically. In the pyridostigmine group and the pyridostigmine + atropine group, left ventricular acetylcholine levels were increased significantly compared with the control.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1998

Lineage and development of the parasympathetic nervous system of the embryonic chick heart.

We were interested in the contribution of the cardiac neural crest to the complete anterior and posterior nerve plexus of the chick heart. This includes the pathways by which these cardiac neural crest-derived neuronal precursors enter the heart. As lineage techniques we used the traditional quail-chick chimera in combination with the newly introduced technique of retroviral reporter gene transfer to premigratory cardiac neural crest cells. Retrovirally infected embryos (n=23) and quail-chick chimeras (n=19) between stages HH27 and 40, were immunohistochemically evaluated, using the lineage markers LacZ (retroviral reporter) and QCPN (anti-quail nuclear marker), respectively and the neuronal differentiation markers HNK-1, RMO-270 and DO-170. Between stages HH27 and 33, quail-derived and LacZ positive cells were situated around the arterial cardiac vagal branches at the arterial pole, and vagal branches along the anterior cardinal veins and the sinal vagal branch at the venous pole. From stage HH35 onward, QCPN/LacZ-positive cardiac ganglia were observed throughout the anterior and posterior plexus and were mainly concentrated in the subepicardium near the distal ends of the arterial cardiac vagal branches and the sinal cardiac vagal branch respectively. From stage HH36 both the anterior and posterior plexus contained a population of large cardiac ganglion cells and a population of smaller cells along nerve branches as well as in the cardiac ganglia, which means that differentiation starts in both plexus at the same time. Furthermore only nerve fiber connections between the anterior and posterior plexus were observed. These results show that the cardiac neural crest contributes to the cardiac ganglion cells from both the entire anterior and posterior plexus. Furthermore these results suggest that these precursor cells enter the arterial pole via the arterial cardiac vagal branches and the venous pole via the sinal cardiac vagal branch without intermixing. Finally we show that in addition to the cardiac ganglia, the cardiac neural crest contributes to small myocardial glia or undifferentiated cells along nerve fibers, and some myocardial nerve fibers as well as nerve tissue in the adventitia of the large veins at the venous pole and in the adventitia of the coronary arteries.

Animals↗
PubMed1988

Parasympathetic nervous system in nocturnal asthma.

To investigate the effect of vagal blockade with atropine on nocturnal fall in peak expiratory flow rate 10 patients with asthma who had a diurnal variation in peak expiratory flow rate of greater than 20% were given 30 micrograms/kg of intravenous atropine or a placebo at 4 am and 4 pm. Vagal blockade caused significant bronchodilatation at 4 am and 4 pm (peak expiratory flow rate rose from 260 to 390 l/min at 4 am and 400 to 440 l/min at 4 pm) and significantly increased the pulse rate from 60 to 121 beats/minute at 4 am and from 76 to 122 beats/minute at 4 pm. Nocturnal asthma was almost totally reversed, implying that vagal mechanisms are fundamental in its pathophysiology. Other mechanisms--diurnal changes in plasma adrenaline concentration, the activity of non-adrenergic non-cholinergic nerves, and circadian rhythms of inflammatory mediator activity--may also be implicated.

Adult↗
PubMedDate not supplied

[The role of the parasympathetic nervous system in the regulation of microsomal monooxygenase activity in the liver of rats].

The effect of vegetative nervous system activation or depression (subdiaphragmatic vagotomy, atropine, proserine and acetylcholine treatments) on the hepatic microsomal enzymes activities has been studied on Wistar male rats. It is found, that hepatic denervation and atropine treatment decreased cytochrome P450 content and aniline hydroxylase activity. Proserine and acetylcholine induced an opposite effect. It is considered that these different changes in the microsomal enzyme activities with variations in the vegetative nervous system state have proved the nervous control of these processes.

Aniline Hydroxylase↗