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Toxicity of Carbon Monoxide: Hemoglobin vs. Histotoxic Mechanisms
Published in David G. Penney, Carbon Monoxide, 2019
In addition to EAA-mediated oxidative stress, autooxidation or oxidative deamination of catecholamines during reperfusion may also contribute to ROS production (Simonson et al., 1993). ROS production after CO exposure can be inhibited by partially blocking of type B monoamine oxidase (MAO-B) (Piantadosi et al., 1995), which is located predominantly in glia. Glial responses, such as gliosis, previously believed to be a response to tissue damage, may play a role in cellular damage after cerebral hypoxia. Persistent gliosis can precede delayed cell death in vulnerable brain regions after ischemia (Perito et al., 1992). Increased gliosis and MAO-B activity also have been implicated in the pathogenesis of Alzheimer’s disease (Jossan et al., 1991), amyotrophic lateral sclerosis (Ekblom et al., 1993), and Parkinson’s disease (Forno et al., 1992). It should be determined whether gliosis after CO exposure enhances MAO-B activity, and when combined with increased catecholamine release, augments H2O2 production and contributes to delayed degeneration in vulnerable brain regions.
Advances in Portable Neuroimaging and Their Effect on Novel Therapies
Published in Yu Chen, Babak Kateb, Neurophotonics and Brain Mapping, 2017
Eric M. Bailey, Ibrahim Bechwati, Sonal Ambwani, Matthew Dickman, Joseph Fonte, Geethika Weliwitigoda
Ischemic stroke is one of the leading causes of death and disability worldwide. It occurs when an artery delivering blood to the brain becomes occluded causing cerebral hypoxia. About 90% of all strokes are ischemic in nature. Presently, thrombolysis with recombinant tissue plasminogen activator (r-tPA) is the only approved treatment for ischemic stroke. Its chief function is to facilitate blood flow through the occluded region until surgical intervention can alleviate the blockage. However, according to the American Stroke Association, the “benefit of [intravenous r-tPA] therapy is time-dependent and treatment should be initiated as quickly as possible” for a Class I acute stroke (NINDS, 1995; Jauch, 2013; Saver, 2013). In fact, neurons in the order of millions are lost each second during an ischemic event. Ischemic events that are not treated within an hour of symptom onset generally result in either death or long-term disabilities. Even so, only 15%–40% of patients arrive at the hospital early enough to be considered for thrombolysis treatment (Walter, 2012) (Figure 24.11).
Oxygen Delivery and Acute Hypoxia: Physiological and Clinical Considerations
Published in Anthony N. Nicholson, The Neurosciences and the Practice of Aviation Medicine, 2017
The dizziness, lightheadedness, cognitive and visual disturbances are caused by the cerebral vasoconstriction that occurs in the presence of hypocapnia. The cerebral circulation has long been known to be very sensitive to arterial PCO2 (for review, see Ainslie and Duffin, 2009) and cerebral blood flow falls by about 2 per cent for each 1 mm Hg fall in arterial PCO2 until PACO2 reaches about 22 mm Hg, when the fall levels off (Reivich, 1964; Raichle and Plum, 1972). The fall in cerebral blood flow is severe enough to lead to cerebral hypoxia despite arterial oxygen content being maintained or slightly increased. The mechanism of the paraesthesia and muscle spasms is still not completely certain. There is an increased excitability of cutaneous and motor axons, which begins before the paraesthesia and tetany start (Macefield and Burke, 1991). The usual explanation is that the alkalosis causes increased binding of calcium to plasma proteins, leading to a reduction of free ionized calcium, which in turn increases neuronal excitability. However, other mechanisms such as hypophosphataemia have been proposed (Gardner, 1996).
Protective effect of Schisandra chinensis lignans on hypoxia-induced PC12 cells and signal transduction
Published in Journal of Toxicology and Environmental Health, Part A, 2018
Yong-hui Zhang, Zhi-ying Zhao, Bao-jun Wang, Yuan-qing Zhang, Ming Zhang, Yang-yang Gao
Hypoxia in central nervous system (CNS) tissues initiates a series of pathophysiological events that might consequently result in several diseases including stroke, Alzheimer’s or encephalopathy (Gillipsie et al. 2017). Neural tissues and neuronal cells are highly sensitive to hypoxia and reperfusion stress leading to tissue injury and cell apoptosis (Wang et al. 2016). In particular cerebral hypoxia develops when the brain suffers from oxygen shortage due to blockade of blood flow, resulting in extensive neuronal cell death in selective vulnerable areas (Sharp and Bernaudin 2004).Sun et al. (2018) reported that hypoxia produced proliferation, migration, and differentiation of platelet activating factors (PAF) accompanied by hypoxic pulmonary vascular remodeling in rats involving by downregulation of the PI3K/Akt/p70S6K signaling pathway. Jiang et al. (2014) demonstrated that SCL exhibited a protective effect in rats suffering from cerebral ischemia injury. Further, Jiang et al. (2014) found the SCL blocking action was associated with inhibition of neuronal apoptosis and upregulation of the p-Akt protein expression levels in rat brain.