China
Africa
Explore chapters and articles related to this topic
Primary Stress Damage of the Heart
Published in Felix Z. Meerson, Alexander V. Galkin, Adaptive Protection of The Heart: Protecting Against Stress and Ischemic Damage, 2019
Felix Z. Meerson, Alexander V. Galkin
The disorders in external respiration and in its response to changing oxygen parameters and carbon dioxide tension in blood are usually explained by brain hypoxia.130 However, in the present case the respiration regulatory disorders cannot be simply attributed to a decreased oxygen supply to the brain. As already mentioned, the secondary tissue hypoxia (which develops when the oxygen delivery is inadequate to the tissue demand) is only weakly pronounced upon stress. Moreover, the comparison of the extent of arterial hypoxemia (decreased supply of O2 to the tissue capillaries) found in this study with the well-known hypoxic hypoxia caused by inspiring oxygen-depleted mixtures134 demonstrates that a drop in arterial oxygen tension to 80 to 90 hPa cannot by itself depress respiration. The attenuated O2 delivery due to the lesser blood flow also does not appreciably change the in the tissue capillaries of the organs well supplied with oxygen, which include the brain (see Table 11). All this prompts a suggestion that immobilization stress elicits defects of respiratory regulation which are not directly associated with the stress hypoxia.
Clinical considerations in prolonged aeromedical transfer
Published in Nicholas Green, Steven Gaydos, Hutchison Ewan, Edward Nicol, Handbook of Aviation and Space Medicine, 2019
Nicholas Green, Steven Gaydos, Hutchison Ewan, Edward Nicol
Acceleration/deceleration: Forces associated with takeoff, landing and in-flight manoeuvres can produce rises in intracranial pressure, especially in supine patients.Elevated intracranial pressure reduces cerebral perfusion pressure, resulting in relative brain hypoxia; traumatic brain injuries susceptible to secondary insults from hyperglycaemia and hypoxia.Head-first loading should counter the takeoff acceleration; long, slow landings should mitigate the landing deceleration.Restraint required in accordance with litter/aircraft guidelines to prevent unwanted movement during takeoff, landing, turbulence.
Resuscitation techniques for lifeguards
Published in Mike Tipton, Adam Wooler, The Science of Beach Lifeguarding, 2018
In drowning, the physiological process is different: in general during at least the first one to two minutes underwater, the heart continues to beat and the circulation continues to transport available oxygen reservoirs to the cells. The oxygen reserve in the lungs and blood decreases as a result of the oxygen consumed by the cells and gradually all cells have to deal with hypoxia (lowered oxygen). To the brain, hypoxia initially means a decrease in consciousness. To the heart, it initially means a slower and reduced pumping function, which is reflected in a slower and weaker pulse. At a certain point, the oxygen supply to the cells of the heart muscles becomes so low that the heart stops beating. At that point, the cells in the brain might already have started to suffer hypoxic damage, but this may temporarily be delayed when there has been a rapid decline in brain temperature [16,17]. However, in most cases the preceding and prolonged hypoxia will have caused gradual and severe neurological damage [18,19].
Two Useful Umbilical Biomarkers for Therapeutic Hypothermia Decision in Patients with Hypoxic İschemic Encephalopathy with Perinatal Asphyxia: Netrin-1 and Neuron Specific Enolase
Published in Fetal and Pediatric Pathology, 2022
Ufuk Cakir, Burak Ceran, Cuneyt Tayman
Perinatal asphyxia (PA) results from insufficient availability of oxygen to various organs and tissues of the fetus and newborn in the antenatal and intranatal periods that causes brain hypoxia and ischemia and results in neonatal hypoxic-ischemic encephalopathy (HIE) [1]. Approximately 0.1–0.4% of term newborns experience some degree of PA to PA and may be affected by dramatic complications due to HIE [2]. Brain damage due to asphyxia is the main cause of macrophage infiltration/activation in the perinatal period [3]. The pathogenesis of HIE is highly complex and still poorly understood. Stimulation of pro-inflammatory cascades, neutrophil and monocyte migration, production of cytokines and chemokines into the injured area occurs due to hypoxic-ischemic brain damage. During the hours and days after the injury, leukocyte subsets and local and systemic cytokine production cause injury in the central nervous system (CNS). This immune response is likely to cause secondary injury [4]. Multiorgan dysfunction may develop due to failure to maintain cerebral, cardiac, gastrointestinal, renal, and adrenal perfusion after the perinatal event. There is no current successful and proven therapeutic approach other than moderate therapeutic hypothermia for neuroprotection and targeting immune cells in the developing brain [1,4]. Some studies have shown that the combination of increased cytokines predicts the severity of HIE [5]. Some markers have even been associated with determining the mortality of patients with HIE, their response to hypothermia treatment, and the need for additional treatment [6].
Narirutin-rich fraction from grape fruit peel protects against transient cerebral ischemia reperfusion injury in rats
Published in Nutritional Neuroscience, 2022
Paresh Patel, Kalyani Barve, Lokesh Kumar Bhatt
During brain hypoxia/ ischemia, pathological and cellular mechanisms involved in cerebral function are unclear. Studies have proved that cerebral hypoperfusion results in cognitive and memory dysfunction [23]. A four-year follow-up assessment of stroke survivors in hospitals showed that approximately one-third of the patients met the criteria of dementia [22]. The study carried out by Yan et al. revealed that bilateral common carotid artery occlusion model of global cerebral ischemia caused a marked cognitive and memory dysfunction in rats [24]. Furthermore, global cerebral ischemia has been reported to cause marked decrease in muscle strength of the limbs, which has been demonstrated in rotarod experiments [25,26]. Consistent with the studies mentioned above, a marked decrease in muscle strength was observed in the present study after 30 min of bilateral common carotid artery occlusion followed by 24 h of reperfusion. These effects were significantly attenuated by NRF pretreatment, which suggests that NRF has therapeutic potential against I/R injury. The hippocampus is an area of the brain that is important for the regulation of memory [27]. Global cerebral ischemia causes memory dysfunction because of its influence on hippocampal neurons [20,26]. Results of the present experiment are in line with the above findings, which showed a marked reduction in memory retention in the I/R control rats in elevated plus maze paradigm. NRF pretreatment significantly prevented this decline in memory performance. This suggested potential of NRF against stroke-induced cognitive dysfunction.
LncRNA SNHG1 protects SH-SY5Y cells from hypoxic injury through miR-140-5p/Bcl-XL axis
Published in International Journal of Neuroscience, 2021
Da-Wei Wang, Xiao-Qian Lou, Zuo-Long Liu, Nan Zhang, Li Pang
Hypoxic brain injury can lead to many central nervous system diseases. The brain hypoxia-ischemia insult to cerebellum and brainstem has been shown to cause neurological injury [1]. Hypoxic-ischemic brain injury results in neuronal death and probably leads to multiple human neurological dysfunctions, such as movement and learning disabilities, epilepsy, cerebral palsy, and even death, during which multiple apoptosis-associated signal pathways were involved [2,3]. It has been demonstrated that oxygen and hypothermia therapies are used for the treatment of hypoxic brain damage [4,5]. However, even though the hypothermia therapy has been recognized for years, there are still some controversies and problems needs to be solved, such as the increased risk of interference with blood clotting or infection. Therefore, to reveal the mechanism of the development of hypoxic brain injury and to find new treatment methods and targets are the urgent problems to be solved in the treatment of hypoxic brain injury in the future.