Role of endogenous nerve growth factor in laryngeal airway hyperreactivity and laryngeal inflammation induced by intermittent hypoxia in rats.

Obstructive sleep apnea, characterized by airway exposure to intermittent hypoxia (IH), is associated with laryngeal airway hyperreactivity (LAH) and laryngeal inflammation. The sensitization of capsaicin-sensitive superior laryngeal afferents (CSSLAs) by inflammatory mediators has been implicated in the pathogenesis of LAH. Nerve growth factor (NGF) is an inflammatory mediator that acts on tropomyosin receptor kinase A (TrkA) and the p75 neurotrophin receptor (p75) to induce lower airway hyperresponsiveness.

Stimulatory effect of methylglyoxal on capsaicin-sensitive lung vagal afferents in rats: role of TRPA1.

Methylglyoxal (MG), a reactive metabolic byproduct of glycolysis, is a causative of painful diabetic neuropathy. Patients with diabetes are associated with more frequent severe asthma exacerbation. Stimulation of capsaicin-sensitive lung vagal (CSLV) afferents may contribute to the pathogenesis of hyperreactive airway diseases such as asthma.

Effect of prolonged mechanical ventilation on cough function and TRPV1 expression.

Cough is a pivotal airway protective reflex, yet the effects of prolonged mechanical ventilation (PMV) on cough function are unknown. This study compared the cough function in subjects with PMV (≥ 21 days, n = 29) and those with short-term mechanical ventilation (SMV, ≤ 7 days, n = 27). Cough reflex sensitivity was measured by capsaicin provocation concentrations after extubation.

Airway hyperresponsiveness induced by intermittent hypoxia in rats.

This study investigated whether intermittent hypoxia (IH) induces airway hyperresponsiveness (AHR) and associated with lung inflammation. Male Brown Norway rats were exposed to 14-day IH or room air (RA) for 6 h/day. One day after the last exposure, total lung resistance to various doses of methacholine was measured as an index of bronchoconstrictive responses.

HIF-1α-Mediated, NADPH Oxidase-Derived ROS Contributes to Laryngeal Airway Hyperreactivity Induced by Intermittent Hypoxia in Rats.

Obstructive sleep apnea, similar to intermittent hypoxia (IH) during sleep, is associated with laryngeal airway hyperreactivity (LAH). IH-induced laryngeal oxidative stress may contribute to LAH, but the underlying mechanism remains unknown. Conscious rats were subjected to repetitive 75 s cycles of IH for 7 or 14 consecutive days.

Inflammatory Role of ROS-Sensitive AMP-Activated Protein Kinase in the Hypersensitivity of Lung Vagal C Fibers Induced by Intermittent Hypoxia in Rats.

Obstructive sleep apnea (OSA), manifested by airway exposure to intermittent hypoxia (IH), is associated with excess reactive oxygen species (ROS) production in airways, airway inflammation, and hyperreactive airway diseases. The cause-effect relationship for these events remains unclear. We investigated the inflammatory role of ROS-sensitive AMP-activated protein kinase (AMPK) in IH-induced airway hypersensitivity mediated by lung vagal C fibers (LVCFs) in rats.

NADPH Oxidase-Derived ROS Induced by Chronic Intermittent Hypoxia Mediates Hypersensitivity of Lung Vagal C Fibers in Rats.

Obstructive sleep apnea (OSA), manifested by exposure to chronic intermittent hypoxia (CIH) and excess production of reactive oxygen species (ROS) in the airways, is associated with hyperreactive airway diseases. ROS, particularly when created by NADPH oxidase, are known to sensitize lung vagal C fibers (LVCFs), which may contribute to airway hypersensitivity pathogenesis. We investigated whether CIH augments the reflex and afferent responses of LVCFs to chemical stimulants and the roles of ROS and NADPH oxidase in such airway hypersensitivity.

Effect of superoxide anion scavenger on rat hearts with chronic intermittent hypoxia.

Only very limited information regarding the protective effects of the superoxide anion scavenger on chronic intermittent hypoxia-induced cardiac apoptosis is available. The purpose of this study is to evaluate the effects of the superoxide anion scavenger on cardiac apoptotic and prosurvival pathways in rats with sleep apnea. Forty-two Sprague-Dawley rats were divided into three groups, rats with normoxic exposure (Control, 21% O2, 1 mo), rats with chronic intermittent hypoxia exposure (Hypoxia, 3-7% O2vs.

Role of TRPA1 and TRPV1 in the ROS-dependent sensory irritation of superior laryngeal capsaicin-sensitive afferents by cigarette smoke in anesthetized rats.

Background: Laryngeal exposure to cigarette smoke (CS) evokes sensory irritation, but the mechanisms are largely unclear. The TRPA1 and TRPV1 receptors are two types of Ca(2+)-permeant channels located at the terminals of airway capsaicin-sensitive afferents. We investigated the mechanisms underlying the airway reflex evoked by laryngeal CS exposure in anesthetized rats.

Perivagal antagonist treatment in rats selectively blocks the reflex and afferent responses of vagal lung C fibers to intravenous agonists.

The terminals of vagal lung C fibers (VLCFs) express various types of pharmacological receptors that are important to the elicitation of airway reflexes and the development of airway hypersensitivity. We investigated the blockade of the reflex and afferent responses of VLCFs to intravenous injections of agonists using perivagal treatment with antagonists (PAT) targeting the transient receptor potential vanilloid 1, P2X, and 5-HT(3) receptors in anesthetized rats. Blockading these responses via perivagal capsaicin treatment (PCT), which blocks the neural conduction of C fibers, was also studied.

Hypersensitivity of lung vagal C fibers induced by acute intermittent hypoxia in rats: role of reactive oxygen species and TRPA1.

Obstructive sleep apnea, manifested by intermittent hypoxia and excess production of reactive oxygen species (ROS) in airways, is associated with hyperreactive airway diseases, but the mechanism remains unclear. Sensitization of lung vagal C fibers (LVCFs) contributes to the airway hypersensitivity. We investigated the mechanisms underlying the sensitization of LVCFs with acute intermittent hypoxia (AIH), by 10 episodes of exposure to 30 s of hypoxic air (0%, 5%, or 10% O(2)) followed by 30 s of room air in anesthetized, open-chest, and artificially ventilated rats.

Reactive oxygen species are the cause of the enhanced cardiorespiratory response induced by intermittent hypoxia in conscious rats.

This study was carried out to investigate the role of reactive oxygen species (ROS) in the elevation of cardiorespiratory responses during the development of intermittent hypoxia (IH)-induced hypertension. Rats were exposed to either 30 days of IH [(30s N₂)+(45 s room air (RA)] or RA for 6 h/day. After 5 days of exposure, stable mean arterial pressure, normalized low-frequency power of pulses interval spectrogram (a marker of cardiac sympathetic outflow), and minute ventilation (an index for arterial chemoreflex activation) were significantly increased throughout the observation period in IH-exposed rats, but not in RA-exposed rats.

Involvement of sympathetic function in the sleep-related change of gastric myoelectrical activity in rats.

The gastric myoelectrical activity (GMA) fluctuates across sleep-wake states as a result of modulation by the brain-gut axis. The role of the autonomic nervous system in this phenomenon, however, was not elucidated fully. Through simultaneous recording and subsequent continuous power spectral analysis of electroencephalogram, electromyogram, electrocardiogram and electrogastromyogram (EGMG) in 16 freely moving Wistar rats, the sleep-wake states of the animals were defined and indices of cardiac autonomic regulation and GMA were calculated.

Asymmetry in sympathetic and vagal activities during sleep-wake transitions.

Study Objectives: To explore the role of autonomic nervous system in initiation of sleep-wake transitions.

Design: Changes in cardiovascular variability during sleep-wake transitions of adult male Wistar-Kyoto rats on their normal daytime sleep were analyzed.

Interventions: A 6-h daytime sleep-wakefulness recording session was performed.

Regression analysis between heart rate variability and baroreflex-related vagus nerve activity in rats.

Introduction: Many previous studies have suggested that the high-frequency (HF) power of the heart rate variability may represent cardiac vagal activity although direct evidence of a correlation between the HF and vagal neuronal activity is still lacking. In the present study, we performed a regression analysis of the HF and vagal neurograms.

Methods And Results: Experiments were carried out on adult male Sprague-Dawley rats anesthetized with a continuous infusion of pentobarbital sodium.

The involvement of hydroxyl radical and cyclooxygenase metabolites in the activation of lung vagal sensory receptors by circulatory endotoxin in rats.

Circulatory endotoxin can stimulate vagal pulmonary C fibers and rapidly adapting receptors (RARs) in rats, but the underlying mechanisms are not clear. We investigated the involvement of hydroxyl radicals and cyclooxygenase metabolites in the stimulation of C fibers and RARs by circulatory endotoxin (50 mg/kg) in 112 anesthetized, paralyzed, and artificially ventilated rats. In rats pretreated with the vehicle, endotoxin stimulated C fibers and RARs and caused a slight increase in total lung resistance (Rl) and a decrease in dynamic lung compliance.

Changes in sleep patterns in spontaneously hypertensive rats.

Study Objectives: To explore whether spontaneous hypertension is associated with a change in sleep pattern in rats.

Design: Adult male spontaneously hypertensive rats (SHR) were compared to normotensive Wistar-Kyoto rats (WKY) on their normal daytime sleep pattern.

Participants: Ten WKY and 10 SHR.

Sleep-related sympathovagal imbalance in SHR.

The role of the autonomic nervous system in spontaneous hypertension during each stage of the sleep-wake cycle remains unclear. The present study attempted to evaluate the differences in cardiac autonomic modulations among spontaneously hypertensive rats (SHR), normotensive Wistar-Kyoto rats (WKY), and Sprague-Dawley rats (SD) across sleep-wake cycles. Continuous power spectral analysis of electroencephalogram, electromyogram, and heart rate variability was performed in unanesthetized free moving rats during daytime sleep.

Relationship between electroencephalogram slow-wave magnitude and heart rate variability during sleep in rats.

To explore whether depth of sleep is related to changes in autonomic control in rats, continuous power-spectral analysis of electroencephalogram (EEG) and heart rate variability (HRV) was performed in unanesthetized rats during normal daytime sleep. Quiet sleep (QS) was associated with an increase in high-frequency power of HRV (0.6-2.

A low-noise flexible integrated system for recording and analysis of multiple electrical signals during sleep-wake states in rats.

A low-noise flexible system for the simultaneous recording and analysis of several electrical signals (EEG, ECG, EMG, and diaphragm EMG) from the same rat was constructed for studying changes in physiological functions during the sleep-wake cycle. The hardware in the system includes a multichannel amplifier, a video camera, a timer code generator, and a PC. A miniature buffer headstage with high-input impedance connected to a 6-channel amplifier was developed.

Activation of lung vagal sensory receptors by circulatory endotoxin in rats.

Although endotoxin is known to induce various pulmonary responses that are linked to the function of lung vagal sensory receptors, its effects on these pulmonary receptors are still not clear. This study investigated the effects of circulatory endotoxin on the afferent activity of lung vagal sensory receptors in rats. We recorded afferent activity arising from vagal pulmonary C fibers (CFs), rapidly adapting receptors (RARs), tonic pulmonary stretch receptors (T-PSRs), and phasic pulmonary stretch receptors (P-PSRs) in 64 anesthetized, paralyzed, and artificially ventilated rats.