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Weaver reports serving as an expert witness for both the plaintiff and defense in cases involving carbon monoxide and receiving grants for carbon monoxide research from the Centers for Disease Control and Prevention and the Deseret Foundation. No other potential conflict of interest relevant to this article was reported. An of this article is available at NEJM.org. I thank William W. Orrison, M.D., of Nevada Imaging Centers, Las Vegas, for providing the brain MRI images, and Kayla Deru, of Intermountain Healthcare, Salt Lake City, for assistance with a previous version of the manuscript. Figure 1 Spectrum of Symptoms and Effects of Exposure to Carbon Monoxide, According to the Level and Duration of Exposure. In all humans, small amounts of carbon monoxide are present and are important for multiple physiologic functions, including neurotransmission.

Exogenous exposure to amounts of carbon monoxide above physiologic levels can result in a protective or adaptive response, but exposure to even higher levels results in toxic effects. Toxic exposures can cause inflammation, followed by hypoxia, although there is uncertainty regarding the range of carbon monoxide exposures above which inflammation occurs (as indicated by the dashed line).

The signs and symptoms of poisoning are highly variable, depending on the acuity and duration of the exposure. Figure 2 Pathophysiological Mechanisms of Carbon Monoxide Poisoning. Carbon monoxide (CO) diffuses quickly into the blood by way of the lungs and causes injury and an adaptive response that continue after carboxyhemoglobin levels have returned to normal.

CO causes hypoxemia through the formation of carboxyhemoglobin and a leftward shift of the oxyhemoglobin dissociation curve. CO binds to heme proteins such as cytochrome c oxidase (CCO), impairing mitochondrial function and thereby contributing to hypoxia. Brain hypoxia elevates levels of excitatory amino acids, increasing brain nitrite levels and causing subsequent injury. Brain hypoxia causes oxidative stress, necrosis, and apoptosis, contributing to inflammation and injury. CO also causes inflammation by increasing levels of cytosolic heme and the heme oxygenase-1 (HO-1) protein, resulting in intracellular oxidative stress. CO binds to platelet heme proteins, causing the release of nitric oxide (•NO). Point Facture Serial Crack For Adobe.

Excess •NO produces peroxynitrite (ONOO −), impairing mitochondrial function, which contributes to hypoxia. CO causes platelet-to-neutrophil aggregation and neutrophil degranulation, involving the release or production of myeloperoxidase (MPO), proteases, and reactive oxygen species — which cause oxidative stress, lipid peroxidation, and apoptosis. Proteases interact with xanthine dehydrogenase (XD) in endothelial cells, forming xanthine oxidase (XO), which inhibits endogenous mechanisms against oxidative stress.

Lipid-peroxidation products form adducts with myelin basic protein, altering its structure, triggering a lymphocytic immunologic response, increasing microglia activation and activity, and causing neuropathologic effects. Finally, CO induces cellular stress responses such as the activation of hypoxia-inducible factor 1α (HIF-1α), which can induce gene regulation. This gene regulation can be protective or can result in injury, depending on the CO dose and on host factors, which remain largely unknown.

NMDA denotes N-methyl-D-aspartate, and nNOS neuronal nitric oxide synthase.