China 
Africa 
Explore chapters and articles related to this topic
Carbon Monoxide — From Tool to Neurotransmitter
Published in David G. Penney, Carbon Monoxide, 2019
Nanduri R. Prabhakar, Robert S. Fitzgerald
Stories of carbon monoxide (CO) poisoning can be read every day in newspapers across the world. But two other stories can be told about CO. In the past it has been used as a tool to assess the effects of hypoxia on the cardiorespiratory system. The peripheral chemoreceptors (i.e., the carotid and aortic bodies) are necessary for cardiorespiratory responses to low oxygen. Since CO has a greater effect on aortic than carotid bodies, it has been used as a tool to delineate the relative contribution of the two chemoreceptor systems to cardiorespiratory adaptations to hypoxia. Presently it is becoming evident not only that CO is formed in many different tissues but also that it may function as a transmitter in the nervous system. In fact, it is intriguing that CO may be a chemical messenger in one of the chemoreceptor organs, the carotid body, in which it was previously used as a tool to unravel the mechanisms of oxygen chemoreception.
Oxygen Delivery and Acute Hypoxia: Physiological and Clinical Considerations
Published in Anthony N. Nicholson, The Neurosciences and the Practice of Aviation Medicine, 2017
Peripheral chemoreceptors are located in the carotid bodies at the bifurcation of the common carotid artery. The carotid body contains neuron-like glomus or type 2 cells that are believed to act as the chemoreceptor, surrounded by glial-like type 1 cells. Each carotid body is normally just a few grams in weight, and the afferents join the carotid sinus nerve, which also carries afferents from the arterial baroreceptors in the nearby carotid sinus. The carotid sinus nerve is a branch of the glossopharyngeal nerve via which the afferent information from both chemoreceptors and baroreceptors passes to the nucleus of the tractus solitarius (NTS) in the brainstem. Similar chemoreceptors are found in the aortic bodies scattered around the aortic arch. Afferents from the aortic bodies pass to the NTS via the vagus nerve. Carotid bodies are stimulated by increased arterial PCO2, increased arterial hydrogen ion (reduced pH) and reduced arterial PO2. As discussed above, in humans the reflex ventilatory response to arterial hypoxia and also to acute metabolic acidosis is largely, if not solely, due to the stimulation of the carotid body chemoreceptors.
Toxic and Asphyxiating Hazards in Confined Spaces
Published in Neil McManus, Safety and Health in Confined Spaces, 2018
Chemoreceptor cells located centrally near the respiratory centers and peripherally in carotid and aortic bodies influence the rate and depth of breathing. Of the two types of chemoreceptors, the central are by far the more important. Central chemoreceptors respond to the partial pressure of CO2 through change in the concentration of H+ ions in extracellular fluid in the brain. Peripheral chemoreceptors respond to the partial pressure of O2 and CO2, and to the H+ concentration in arterial blood. Nervous control originates from higher centers in the midbrain and from cerebral centers. In most circumstances, the concentration of carbon dioxide in arterial blood regulates the depth and rate of breathing (Vander et al. 1990).
Plateau effect on driver’s hazard perception response mode: Graph construction approach
Published in Journal of Transportation Safety & Security, 2023
Chenzhu Wang, Mingyu Hou, Fei Chen, Jiayun Zhu, Jianchuan Cheng, Wu Bo, Ping Zhang, Said M. Easa
Known as “the Roof of the World,” the Qinghai–Tibet Plateau in China has an average altitude of more than 4,500 m (H. Sun, 2010), where the partial pressure of oxygen (about 11 kPa) and atmospheric pressure (about 53 kPa) are lower than the those on the plain. Therefore, after entering the plateau, the respiratory center is indirectly stimulated through the peripheral chemoreceptors (mainly the carotid body), resulting in an early increase in ventilation and subsequent altitude sickness. Altitude sickness is the physiological discomfort caused by hypoxia, primarily as headache, dizziness, cardiopalmus, shortness of breath, and even temporary blackout (Anand & Wu, 2004). After being in a plateau area for some time, the body can adapt, with significantly relieved initial hypoxia symptoms and altitude acclimation. Then the body can inhale more oxygen to compensate, during a gradual transition to stable adaptation (around 1 to 3 months; Li et al., 2012).
Into the deep blue sea: A review of the safety of recreational diving in people with diabetes mellitus
Published in European Journal of Sport Science, 2020
Theocharis Koufakis, Spyridon N. Karras, Omar G. Mustafa, Dimos Karangelis, Pantelis Zebekakis, Kalliopi Kotsa
The exact mechanisms mediating these optimal effects remain obscure. In a model of diabetic mice, HBOT was shown to reduce autoimmune diabetes incidence, via increased resting T cells and reduced activation of dendritic cells, with preservation of beta-cell mass related to decreased apoptosis and increased proliferation (Faleo et al., 2012). HBOT has been shown to increase brain glucose utilisation (Contreras, Kadekaro, & Eisenberg, 1988), as well as central nervous system's sensitivity to responding in variations of BG concentrations, in a rat model (Torbati, 1985). Increased activity of carotid bodies (peripheral chemoreceptors that respond to hypoxia) has been demonstrated in T2D animal models (Ribeiro et al., 2013). Carotid bodies are a powerful glucose and insulin sensor and surgical ablation of its nerve inhibits the development of diet-induced metabolic diseases (Ribeiro et al., 2013). Deactivation of carotid body chemoreceptors reduces sympathetic hyperactivity, which contributes to the pathogenesis of T2D, possibly by negatively affecting insulin resistance (Esler et al., 2001). Therefore, functional inhibition of carotid bodies activity by hyperoxia may partially explain the HBOT optimal effects on glycemia (Vera-Cruz et al., 2015).