Peripheral chemoreceptors in the carotid body play important roles in the transduction of chemical stimuli in the arterial blood to the central for eliciting the chemoreflex, which mediates the ventilatory and circulatory responses to hypoxia. The activity of carotid chemoreceptor is modulated and significantly contributes to the ventilatory acclimatization at high altitude. In addition, the carotid chemoreceptor activity is augmented in patients with sleep-disordered breathing, notably in central or obstructive sleep apnea, and also in experimental animals. Thus, the carotid body functions to maintain the oxygen homeostasis, whereas anomalous carotid chemoreceptor activities could be both adaptive and pathogenic in sleep apnea. This review aims to summarize the cellular and molecular mechanisms that could mediate the augmented chemoreceptor activity induced by intermittent hypoxia. Our recent findings suggest a pathogenic role of inflammation mediated by an upregulation of renin-angiotensin system in the carotid body in the over-activity of the chemoreflex. These locally regulated mechanisms are proposed to be a significant part of the hypoxia-mediated maladaptive changes of the carotid body function, which could play a role in the pathophysiology of sleep apnea.
Acclimatization ; Animals ; Carotid Body ; cytology ; Chemoreceptor Cells ; pathology ; Humans ; Hypoxia ; physiopathology ; Renin-Angiotensin System ; Sleep Apnea Syndromes ; physiopathology

The carotid body can transduce hypoxia and other blood-borne stimuli, perhaps including hypoglycaemia, into afferent neural discharge that is graded for intensity and which forms the afferent limb of a cardiorespiratory and neuroendocrine reflex loop. Hypoxia inhibits a variety of K(+) channels in the type I cells of the carotid body, in a seemingly species-dependent manner, and the resultant membrane depolarisation is sufficient to activate voltage-gated Ca(2+) entry leading to neurosecretion and afferent discharge. The ion channels that respond to hypoxia appear to do so indirectly and recent work has therefore focussed upon identification of other proteins in the type I cells of the carotid body that may play key roles in the oxygen sensing process. Whilst a role for mitochondrial and/or NADPH-derived reactive oxygen species (ROS) has been proposed, the evidence for their signalling hypoxia in the carotid body is presently less than compelling and two alternate hypotheses are currently being tested further. The first implicates haemoxygenase 2 (HO-2), which may control specific K(+) channel activation through O(2)-dependent production of the signalling molecule, carbon monoxide. The second hypothesis suggests a role for the cellular energy sensor, AMP-activated protein kinase (AMPK), which can inhibit type I cell K(+) channels and increase afferent discharge when activated by hypoxia-induced elevations in the AMP: ATP ratio. The apparent richness of O(2)-sensitive K(+) channels and sensor mechanisms within this organ may indicate a redundancy system for this vital cellular process or it may be that each protein contributes differently to the overall response, for example, with different O(2) affinities. The mechanism by which low glucose is sensed is not yet known, but recent evidence suggests that it is not via closure of K(+) channels, unlike the hypoxia transduction process.
AMP-Activated Protein Kinases ; metabolism ; Animals ; Carotid Body ; physiology ; Chemoreceptor Cells ; physiology ; Heme Oxygenase (Decyclizing) ; metabolism ; Humans ; Hypoxia ; physiopathology ; Potassium Channels ; metabolism ; Reactive Oxygen Species ; metabolism

The sensory function of the trigeminal nerve is to provide tactile, proprioceptive, and nociceptive afference by chemical stimulation. Various physical responses of the trigeminal nerve to stimuli help to defend against harmful substances. Recently, many studies have been conducted on solitary chemoreceptor cells innervated by trigeminal nerve. Most volatile organic compounds stimulate both the olfactory and trigeminal nervous systems. In general, the trigeminal nervous system is less sensitive than the olfactory nervous system. Studies have shown that sensation of the trigeminal nerve by chemical stimulation results in inhibition of olfaction. This indicates that the olfactory and trigeminal nerves interact with each other in the central nervous system. It is important to study various noxious stimuli acting on the trigeminal nerve in modern society where environmental concerns are intensifying.
Central Nervous System ; Chemoreceptor Cells ; Nervous System ; Sensation ; Smell ; Stimulation, Chemical ; Trigeminal Nerve ; Volatile Organic Compounds

Paragangliomas are neoplasms that arise from extra-adrenal paraganglia, microscopic islands of cells derived from the neural crest. In the head and neck region, paraganglionic tissue is distributed in the superior and inferior paraganglia, the carotid body, the vagal body, and the jugulotympanic region. Approximately 10% of patients with a paraganglioma have a family history of such tumors. Multiple lesions can be found in 26% of patients with family history. Patients with multiple paragangliomas have a higher risk of having functional pheochromocytoma and should undergo a pretreatment screening for vasopressor substances. Similarly, patients with a family history should undergo four-vessel arteriography to rule out any multiple and clinically unrecognized lesions. The authors have experienced three cases of multiple paragangliomas, which were managed surgically. Two cases were bilateral carotid body tumors and two cases were accompanied by glomus jugulare. Of these, one case had family history. We report three cases of multiple paragangliomas with a review of literatures.
Angiography ; Aortic Bodies ; Carotid Body ; Carotid Body Tumor ; Glomus Jugulare ; Head ; Humans ; Islands ; Mass Screening ; Neck ; Neural Crest ; Paraganglioma* ; Pheochromocytoma

Jugulotympanic paragangliomas (JTPs) known as glomus tumors, are neoplasms of variable invasiveness that arise from the paraganglia situated around the jugular bulb or middle ear. We now report a rare case of JTP in an 18-year-old male. Preoperative diagnoses through external auditory canal biopsy and radiologic examination both failed. Even using a frozen section, an informative finding was not obtained because mostly granulation tissue was present along with associated squeezing artifacts. On permanent histologic examination, small cell nests between many ectatic small vessels and fibrotic stroma were seen, and those cells were positive for CD56, synaptophysin and chromogranin. Because JTPs are rare and have rather different histologic findings - higher vascularity, smaller and less uniform tumor cells than other paragangliomas - they are easy to misdiagnose. However, remembering those differences may help the physician avoid missing JTPs.
Adolescent ; Artifacts ; Biopsy ; Ear Canal ; Ear, Middle ; Frozen Sections ; Glomus Jugulare ; Glomus Tumor ; Glomus Tympanicum ; Granulation Tissue ; Humans ; Male ; Paraganglioma ; Paraganglioma, Extra-Adrenal ; Synaptophysin

Jugulotympanic paragangliomas (JTPs) known as glomus tumors, are neoplasms of variable invasiveness that arise from the paraganglia situated around the jugular bulb or middle ear. We now report a rare case of JTP in an 18-year-old male. Preoperative diagnoses through external auditory canal biopsy and radiologic examination both failed. Even using a frozen section, an informative finding was not obtained because mostly granulation tissue was present along with associated squeezing artifacts. On permanent histologic examination, small cell nests between many ectatic small vessels and fibrotic stroma were seen, and those cells were positive for CD56, synaptophysin and chromogranin. Because JTPs are rare and have rather different histologic findings - higher vascularity, smaller and less uniform tumor cells than other paragangliomas - they are easy to misdiagnose. However, remembering those differences may help the physician avoid missing JTPs.
Adolescent ; Artifacts ; Biopsy ; Ear Canal ; Ear, Middle ; Frozen Sections ; Glomus Jugulare ; Glomus Tumor ; Glomus Tympanicum ; Granulation Tissue ; Humans ; Male ; Paraganglioma ; Paraganglioma, Extra-Adrenal ; Synaptophysin

The aim of the present study was to observe whether protein tyrosine kinase (PTK) within the nucleus tractus solitarius (NTS) was involved in the regulation of ventilatory responses of peripheral chemoreflex. The experiments were performed on anesthetized, immobilized and artificially ventilated rabbits. Peripheral chemoreflex was elicited by ventilating the animal with 10% O2-balance 90% N2. Changes in the peak amplitude and frequency of integrated phrenic nerve activity were observed. The ventilatory responses of peripheral chemoreflex following 0.1 microl microinjection within the NTS of either PTK inhibitor genistein (10 mol/L), AMPA glutamate receptor inhibitor CNQX (10 mol/L),or inactive PTK inhibitor daidzein (10 mol/L) were recorded. The results are as follows: Both genistein and CNQX attenuated the ventilatory responses of peripheral chemoreflex, while no changes occurred following daidzein. The amplitude of integrated phrenic nerve discharge and the phrenic burst frequency were decreased by (-21.77+/-6.93)% and (-24.70+/-7.61)% respectively after administration of genistein. CNQX resulted in similar decreases in the amplitude of phrenic nerve discharge (-27.13+/-7.63)% and the burst frequency (-21.34+/-4.88)%. In addition, the inhibitory effects of CNQX and genistein were the same whether they were applied alone or one after another, indicating that they had no cooperative effects. The results obtained suggest that PTK within the NTS regulates the peripheral chemoreflex control of respiration and that this regulation of PTK may be mediated through the phosphorylation of AMPA receptors in NTS neurons.
Animals ; Brain Stem ; enzymology ; physiology ; Chemoreceptor Cells ; physiology ; Female ; Male ; Protein-Tyrosine Kinases ; physiology ; Rabbits ; Receptors, AMPA ; physiology ; Respiration ; Solitary Nucleus ; enzymology

No abstract available.
Glomus Tympanicum*

Congestive heart failure is a syndrome that is usually initiated by a reduction in pump function of the heart, i.e. a decrease in cardiac output. Initially, a reduction in cardiac output leads to unloading of baroreceptor reflex that, in turn, increases heart rate through vago-sympathetic mechanisms and total peripheral resistance via an increase in sympathetic outflow to vascular beds. In this review we are thinking on how baroreceptor reflex plays a role in the abnormal control of the circulation in heart failure. This review and our recent studies suggest that: (1) baroreceptor reflex is blunted in heart failure; (2) central angiotensin II and reactive oxygen species play an important role in blunted baroreceptor reflex; (3) cardiac sympathetic afferent stimulation and chemoreceptor reflex inhibit baroreceptor reflex; and (4) exercise training normalizes abnormal reflexes in the heart failure state.
Angiotensin II ; metabolism ; Animals ; Baroreflex ; physiology ; Cardiac Output ; physiology ; Chemoreceptor Cells ; physiology ; Exercise ; physiology ; Heart Failure ; physiopathology ; Humans ; Reactive Oxygen Species ; metabolism ; Sympathetic Nervous System ; physiology ; Vascular Resistance ; physiology

The therapeutic options for glomus tumor management are either palliative (ie, radiation, embolization or a combination) or definitive (ie, surgery or combinations of surgery-radiation, radiation-surgery or embolization-surgery). Of these, surgical excision is the standard treatment modality for glomus tympanicum tumors. As glomus tympanicum tumor has highly vascular nature, profuse hemorrhage may be intermittently induced during its removal. Preoperative embolization is used frequently to reduce intraoperative bleeding. We report a case of glomus tympanicum tumor which was removed completely with the help of direct inject of HistoacrylR into the mass during the operation. This method allows almost bloodless ablation of the entire tumor.
Enbucrilate ; Glomus Tumor ; Glomus Tympanicum Tumor* ; Glomus Tympanicum* ; Hemorrhage