Serotonin-induced apnea.

J Am Pharm Assoc Am Pharm Assoc

Published: March 1960

Download full-text PDF

Source

Publication Analysis

Top Keywords

serotonin-induced apnea
4
serotonin-induced
1

Similar Publications

Intracerebroventricular injections of dronabinol, a cannabinoid receptor agonist, does not attenuate serotonin-induced apnea in Sprague-Dawley rats.

J Negat Results Biomed

May 2016

Center for Narcolepsy, Sleep and Health Research, University of Illinois at Chicago, 845 South Damen Avenue (M/C 802), Chicago, IL, 60612, USA.

Background: Evidence suggests that vagal nerve activity may play a role in sleep apnea induction. In anesthetized rats, dronabinol, a cannabinoid (CB) receptor agonist, injected into the nodose ganglia attenuates reflex apnea and increases genioglossus activity, and reflex apnea attenuation is blocked by systemic pre-treatment with cannabinoid type 1 and/or type 2 receptor antagonists. However, it is unclear whether dronabinol has similar effects in the central nervous system; CB receptors are widely distributed in the brain, especially on neuronal circuitry important for respiration and upper airway activation.

View Article and Find Full Text PDF

Cannabinoid type 1 and type 2 receptor antagonists prevent attenuation of serotonin-induced reflex apneas by dronabinol in Sprague-Dawley rats.

PLoS One

January 2016

Center for Narcolepsy, Sleep and Health Research, University of Illinois at Chicago, Chicago, Illinois, United States of America; Department of Biobehavioral Health Science, University of Illinois at Chicago, Chicago, Illinois, United States of America; Department of Medicine, University of Illinois at Chicago, Chicago, Illinois, United States of America.

The prevalence of obstructive sleep apnea (OSA) in Americans is 9% and increasing. Increased afferent vagal activation may predispose to OSA by reducing upper airway muscle activation/patency and disrupting respiratory rhythmogenesis. Vagal afferent neurons are inhibited by cannabinoid type 1 (CB1) or cannabinoid type 2 (CB2) receptors in animal models of vagally-mediated behaviors.

View Article and Find Full Text PDF

Intranodose ganglion injections of dronabinol attenuate serotonin-induced apnea in Sprague-Dawley rat.

Respir Physiol Neurobiol

January 2014

Center for Narcolepsy, Sleep and Health Research, University of Illinois at Chicago, Chicago, IL, USA; Department of Biobehavioral Health Science, University of Illinois at Chicago, Chicago, IL, USA. Electronic address:

Obstructive sleep apnea represents a significant public health concern. Afferent vagal activation is implicated in increased apnea susceptibility by reducing upper airway muscle tone via activation of serotonin receptors in the nodose ganglia. Previous investigations demonstrated that systemically administered cannabinoids can be used therapeutically to decrease the apnea/hypopnea index in rats and in humans.

View Article and Find Full Text PDF

Study Objective: Animal data suggest that Δ(9)-TetraHydroCannabinol (Δ(9)THC) stabilizes autonomic output during sleep, reduces spontaneous sleep-disordered breathing, and blocks serotonin-induced exacerbation of sleep apnea. On this basis, we examined the safety, tolerability, and efficacy of dronabinol (Δ(9)THC), an exogenous Cannabinoid type 1 and type 2 (CB1 and CB2) receptor agonist in patients with Obstructive Sleep Apnea (OSA).

Design And Setting: Proof of concept; single-center dose-escalation study of dronabinol.

View Article and Find Full Text PDF

Cardio-respiratory reflex effects of an exogenous serotonin challenge are suggested to be modulated by activation of the peripheral 5HT2 and 5HT3 receptors. In the present experiments the blocking effects of serotoninergic active drugs: ketanserin and tropanserin (MDL 72222) were studied in six pentobarbitone-chloralose anaesthetized cats. Bolus injection of serotonin (0.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!