Hypoxia in Acute Chemical Emergencies: Toxicity, Mechanism, and Treatment



Hypoxia is a pathological condition in which the whole body or a particular region of the body suffers from oxygen deprivation. There are various kinds of hypoxia viz. hypoxemic hypoxia (e.g., high-altitude pulmonary edema, high-altitude cerebral edema, etc.), anemic hypoxia (e.g., chronic anemia, carbon monoxide (CO) poisoning, etc.), stagnant hypoxia (heart failure, vasodilatory shock, etc.), and histotoxic hypoxia. In histotoxic hypoxia, the quantity of oxygen reaching the cells is normal, but the cells are unable to utilize the oxygen efficiently. This is due to inactivation of enzymes involved in oxidative phosphorylation. This causes profound reduction in adenosine triphosphate production by the mitochondria, leading to various cellular perturbations, and possibly cell death. The gases considered as chemical asphyxiants act either by decreasing the oxygen-carrying capacity of the blood (CO) or by interfering with cellular utilization of oxygen (cyanide and hydrogen sulfide). Regardless of mode of action, chemical asphyxiants can cause severe hypoxia (chemical hypoxia), which is detrimental for the living organisms. Acute chemical emergencies can be encountered during industrial disasters, occupational exposures, accidents, use of chemical warfare agents, and acts of terrorism. This chapter discusses the toxicity, molecular mechanism(s) of action, and treatment modalities of chemical asphyxiants. Possible implication of organophosphorus compounds in producing chemical hypoxia is also addressed. This information will be useful for medical management of hypoxia-related chemical emergencies.


Lactic Acidosis Mitochondrial Permeability Transition Pore Mitochondrial Permeability Transition Pore Cyanide Poisoning Chemical Hypoxia 
These keywords were added by machine and not by the authors. This process is experimental and the keywords may be updated as the learning algorithm improves.



Authors acknowledge Dr. B.K. Bhattacharya, Head, Division of Biochemistry and Biotechnology, and Dr. Pravin Kumar, Head, Division of Pharmacology and Toxicology, DRDE, Gwalior, for their valuable suggestions. Authors also thank Mr. Shiv Kumar Yadav and Ms. Poonam Singh, Research Scholars, Division of Pharmacology and Toxicology, DRDE, Gwalior, for their excellent technical support in preparation of this manuscript.


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Copyright information

© Springer India 2014

Authors and Affiliations

  1. 1.Defence Research and Development EstablishmentGwaliorIndia

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