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At least 37 records · Page 2Linked to original sources
PubMed1986

[Absence of a role for the parasympathetic nervous system in the hemodynamic response to atriopeptin III in the normotensive rat].

The influence of the parasympathetic nervous system on the cardiovascular response to a synthetic atrial peptide (atriopeptin III) was examined in conscious normotensive rats utilizing the technique of radiolabelled microspheres. Atriopeptin III was infused intravenously for 30 min at a rate of 1 microgram/min in rats pretreated with a bolus intravenous injection of atropine, 150 micrograms (n = 8), or of its vehicle (n = 8). Additional animals (n = 9) received the vehicle of both atropine and atriopeptin III. The atrial peptide decreased mean blood pressure to similar extent in rats pretreated with atropine (from 124 +/- 4.5 to 108 +/- 5.3 mmHg, mean +/- SEM, p less than 0.05) and in the controls (from 123 +/- 3.8 to 105 +/- 3.8 mmHg, p less than 0.05). Heart rate rose significantly after administration of atropine. After the 30 minute infusion, cardiac index was significantly lower (p less than 0.05) in both groups infused with atriopeptin III (23.4 +/- 2.3 after atropine pretreatment and 25.1 +/- 2.2 ml/min X 100 g without atropine) than in the group of rats given only the vehicle of both atropine and atriopeptin III (32.4 +/- 2.8 ml/min X 100 g). There was no significant difference in regional blood flow distribution within the three groups of rats. These data therefore indicate that in conscious rats atriopeptin III reduces blood pressure and cardiac output without concomitantly modifying regional blood flow distribution. They also suggest that the parasympathetic nervous system does not contribute to the hemodynamic response to atriopeptin III.

Animals↗
PubMed1986

Induction of coronary artery spasm by acetylcholine in patients with variant angina: possible role of the parasympathetic nervous system in the pathogenesis of coronary artery spasm.

We injected acetylcholine (ACh), the neurotransmitter of the parasympathetic nervous system, into the coronary arteries of 28 patients with variant angina. Injection of 10 to 80 micrograms ACh into the coronary artery responsible for the attack induced spasm together with chest pain and ST segment elevation or depression on the electrocardiogram in 30 of the 32 arteries of the 25 of the 27 patients. The injection of 20 to 100 micrograms ACh into the coronary artery not responsible for the attack in 18 patients resulted in various degrees of constriction in most of them, but no spasm in any of them. After intravenous injection of 1.0 to 1.5 mg atropine sulfate, the injection of ACh into the coronary artery responsible for the attack did not induce spasm or attack in any of the nine coronary arteries injected in eight patients. We conclude that the intracoronary injection of ACh induces coronary spasm and attack in patients with variant angina and that the activity of the parasympathetic nervous system may play a role in the pathogenesis of coronary spasm. We also conclude that the intracoronary injection of ACh is a useful test for provocation of coronary spasm.

Acetylcholine↗
PubMed1979

Asystole and its treatment: the possible role of the parasympathetic nervous system in cardiac arrest.

Parasympathetic tone may be high during ventricular asystole because of reflex vagal stimulation from a number of sources. Eight patients in cardiac arrest were treated with cardiopulmonary resuscitation. All eight patients had ventricular asystole as the initial rhythm or as the result of defibrillation. Six patients failed to respond to 5 cc to 20 cc of 1:10,000 epinephrine intravenously (IV). In all eight cases a regular rhythm (sinus in seven, idioventricular in one) appeared within 30 seconds of administration of the last dose of atropine (1 mg to 2 mg IV). Five patients (62.5%) lived 12 hours, three (37.5%) were discharged from the hospital. These results suggest that atropine may be of value in the treatment of ventricular asystole.

Adult↗
PubMed1988

The parasympathetic nervous system and glucocorticoid-mediated hyperinsulinaemia in the genetically obese (fa/fa) Zucker rat.

Lean (Fa/-) and genetically obese (fa/fa) Zucker rats were adrenalectomized at 18 days of age (3 days before weaning) before the onset of hyperinsulinaemia. At 40-41 days of age, basal and glucose-stimulated insulin concentrations did not differ significantly between lean and obese rats. Plasma insulin and glucose concentrations were higher in both phenotypes 24 h after administration of corticosterone (2.0 mg at 12-h intervals). Corticosterone-treated obese rats had higher basal and glucose-stimulated insulin levels than similarly treated lean animals, although plasma glucose concentrations did not differ between phenotypes. The basal plasma insulin concentration of obese rats treated with corticosterone for 24 h was reduced 15, 30 and 45 min after injection of atropine (0.3 mg) without any significant change in the plasma glucose level. Injection of atropine (0.3 mg) 20 min before a glucose load prevented the greater increment in plasma insulin concentration of corticosterone-treated obese rats compared with similarly treated lean animals. Atropine administration (0.3 mg) to intact obese rats at 40 days of age reduced, but did not abolish, their hyperinsulinaemia compared with intact lean animals. It is concluded that (1) pre-weaning adrenalectomy prevents the development of hyperinsulinaemia in genetically obese rats, (2) corticosterone replacement for only 24 h restores the hyperinsulinaemia of obese rats, (3) the differential effects of corticosterone on insulin secretion by lean and obese rats are mediated by the parasympathetic nervous system and (4) the parasympathetic nervous system contributes to, but is not the only cause of, hyperinsulinaemia in intact obese rats.

Adrenalectomy↗
PubMed1985

Role of the parasympathetic nervous system in acute lung response to ozone.

We conducted an ozone (O3) exposure study using atropine, a muscarinic receptor blocker, to determine the role of the parasympathetic nervous system in the acute response to O3. Eight normal subjects with predetermined O3 responsiveness were randomly assigned an order for four experimental exposures. For each exposure a subject inhaled either buffered saline or atropine aerosol followed by exposure either to clean air or 0.4 ppm O3. Measurements of lung mechanics, ventilatory response to exercise, and symptoms were obtained before and after exposure. O3 exposure alone resulted in significant changes in specific airway resistance, forced vital capacity (FVC), forced expiratory flow rates, tidal volume (VT), and respiratory rate (f). Atropine pretreatment prevented the significant increase in airway resistance with O3 exposure and partially blocked the decrease in forced expiratory flow rates but did not prevent a significant fall in FVC, changes in f and VT, or the frequency of reported respiratory symptoms after O3. These results suggest that the increase in pulmonary resistance during O3 exposure is mediated by a parasympathetic mechanism and that changes in other measured variables are mediated, at least partially, by mechanisms not dependent on muscarinic cholinergic receptors of the parasympathetic nervous system.

Adolescent↗
PubMed1989

The parasympathetic nervous system and the thermic effect of glucose/insulin infusions in humans.

The thermic effect of glucose/insulin infusions was investigated in seven healthy young men before and during either inhibition (atropine sulphate 10 micrograms/kg bolus; 10 micrograms/kg/h) or stimulation (edrophonium chloride, 10 mg bolus; 0.75 mg/min starting rate) of the parasympathetic nervous system. The thermic effects of glucose/insulin were 6.2% +/- 0.4% and 5.6% +/- 0.7% before atropine and edrophonium, respectively, and increased to 7.1% +/- 0.5% (NS) with atropine and 7.5% +/- 1.2% (P less than .05) with edrophonium. In four subjects atropine or edrophonium was infused before the hyperinsulinemic, euglycemic clamp. A significant increase in resting metabolic rate and plasma norepinephrine concentrations was observed with edrophonium alone. When the thermic effects of glucose/insulin were calculated with respect to the metabolic rates observed during the drug infusions alone, they were 5.9% +/- 1.4% and 3.6% +/- 0.6% (NS) for the clamp + atropine and clamp + edrophonium, respectively. These results demonstrate that the increases in the thermic effect of glucose/insulin infusions observed during inhibition or stimulation of the parasympathetic nervous system were due to atropine or edrophonium increasing the resting metabolic rate rather than increasing the thermic response to glucose-insulin infusions. However, because it has been shown that atropine can decrease the thermic effect of an orally administered meal by approximately 60%, it would appear that the parasympathetic nervous system can influence the thermic effect of food by affecting the rate of digestion, absorption and storage of the ingested nutrients.

Adult↗
PubMed1997

Long-term carvedilol therapy increases parasympathetic nervous system activity in chronic congestive heart failure.

To determine the effect of beta blockade on parasympathetic nervous system activity, we assessed RR variability during 24-hour Holter monitoring in 10 patients with congestive heart failure before and after 3 to 4 months of treatment with the beta blocker carvedilol. High-frequency power increased from 26 to 64 ms2, root-mean-square of successive differences in RR interval increased from 14.3 to 23.7 ms2, and percentage of absolute differences >50 ms between successive normal RR intervals increased from 0.8% to 4.7%, all p <0.01, indicating a substantial increase in parasympathetic modulation of RR intervals.

Adrenergic beta-Antagonists↗
PubMed1993

Endothelin-3 increases transmission in the rabbit pulmonary parasympathetic nervous system.

The effect of endothelin-3 (ET-3) on the response to parasympathetic nerve stimulation of rabbit isolated bronchus was examined. The site of action of ET-3 in the pulmonary parasympathetic nervous system was also investigated. ET-3 induced a concentration-dependent increase in the response to electrical field stimulation. The response was atropine sensitive and therefore cholinergically mediated. At a concentration of 10 nM, ET-3 increased the response to field stimulation to 205 +/- 42% of the initial response. The effect was concentration-related, as 100 nM further increased this response to 315 +/- 69%. The responsiveness of the tissue to exogenous acetylcholine was not affected by ET-3. Therefore ET-3 has a neuromodulatory role on cholinergic parasympathetic transmission in rabbit airways exerted at a prejunctional site.

Acetylcholine↗
PubMed1975

The role of the parasympathetic nervous system in the maintenance of chronic airway obstruction in asthmatic children.

To evaluate the role of the parasympathetic nervous system in the mediation and maintenance of reversible airway obstruction in perennially asthmatic children, we measured pulmonary function in 18 patients before and after the administration of atropine sulfate aerosol. The bronchodilatory effects of atropine were compared with those of isoproterenol hydrochloride and placebo aerosols. Placebo aerosol did not change any of the pulmonary functions tested. Atropine and isoproterenol aerosols improved forced expiratory flows, airway resistance, and specific airway conductance significantly and to the same degree. Hyperinflation was significantly lessened by atropine, but not by isoproterenol. Because atropine is not a direct smooth muscle relaxant, but rather a selective blocker of cholinergically induced smooth muscle tone, any significant improvement in the lung function of chronically asthmatic children by atropine suggests that at least some of their reversible airway obstruction is induced and maintained by parasympathetically mediated bronchial smooth muscle constriction.

Airway Obstruction↗
PubMed1993

Effect of cervical vagotomy on catecholaminergic neurons in the cranial division of the parasympathetic nervous system.

This study provides evidence of catecholaminergic neurons in the cranial division of the parasympathetic nervous system. Presumptive catecholaminergic preganglionic neurons in the dorsal motor nucleus of the vagus (DMX) were revealed by a clearcut depletion of intracellular catecholamine-synthesizing enzyme immunoreactivity induced by unilateral cervical vagotomy and identified on tissues immunocytochemically processed for tyrosine hydroxylase (TH), dopamine beta-hydroxylase (D beta H) or phenylethanolamine N-methyltransferase (PNMT). This experimental design was essential because of the recent failure in two species to reproduce data previously obtained in double-label (combined immunocytochemical-retrograde transport) studies. Vagotomy data confirmed three spatially-segregated populations of catecholaminergic visceromotor neurons in the DMX. These cell bodies were morphologically identical to preganglionic neurons observed on alternate tissues stained for Nissl substance or immunostained for choline acetyltransferase (ChAT), the enzyme biosynthesizing acetylcholine. Neurons in the central and medial DMX demonstrated fall-off of TH-like immunoreactivity (LI) ipsilateral to the vagotomy at levels caudal to the obex. This cell group is assumed to be predominantly dopaminergic since relatively few neurons at this level of the DMX expressed D beta H-LI and none were immunostained for PNMT. A second population of immunoreactive neurons, concentrated in the rostral-lateral region of the DMX, was depleted of D beta H-LI on the ipsilateral side but did not express PNMT. These visceromotor neurons may, therefore, biosynthesize noradrenaline and belong to the rostral pole of the A2 area. A third population of presumptive adrenergic vagal dorsomotor neurons in the rostral-medial DMX was depleted of TH-, D beta H- and PNMT-LI at levels of the ipsilateral nucleus anterior to obex. Patterns of depletion of cytoplasmic enzyme-immunoreaction product were identical in all cases irrespective of the site of the transection or the postoperative survival period. Quantitative analysis demonstrated statistically significant loss of immunolabeled neurons in rostral and caudal subgroups of the DMX on the side ipsilateral to the vagotomy. It is concluded that catecholaminergic processes in the vagus nerve, as previously identified by the aldehyde-induced histofluorescence method, may partly arise from the lower brainstem.

Animals↗
PubMedDate not supplied

Vagal attenuation in panic disorder: an assessment of parasympathetic nervous system function and subjective reactivity to respiratory manipulations.

We examined the effects of hyperventilation and other manipulations of respiratory pace on parasympathetic nervous system function and subjective reactivity in 15 patients with panic disorder, 15 patients with social phobia, and 15 healthy control subjects. After a 30-minute rest period subjects completed a 2.5-minute trial of each of hypoventilation, normoventilation, and hyperventilation. Trials were separated by a 3 minute inter-trial interval. Incidence of panic attacks, symptom severity, vagal tone, heart rate, end-tidal carbon dioxide level, and respiratory frequency were measured throughout. Resting physiological measures did not differ between groups. Each respiratory manipulation resulted in the expected physiological changes (e.g., hyperventilation attenuated vagal tone), however, groups did not exhibit differential physiological reactivity to the manipulations. There were no panic attacks reported during either the hypoventilation or normoventilation phases; however, two social phobic subjects (13.3%) and two panic disorder patients (13.3%) reported panic attacks during hyperventilation. Although both groups of anxiety patients reported greater severity of hyperventilation-induced symptoms than did control subjects, symptom severity did not correlate significantly with vagal tone or heart rate. These results suggest that parasympathetic function is unlikely to be aberrant in PD patients and that diminished parasympathetic activity is not sufficient for the experience of panic attacks.

Adult↗