Application of a Model of Exertional Heatstroke Pathophysiology to Cocaine Intoxication
Abstract
We would like to propose a novel cellular model of cocaine intoxication which originates from work on heatstroke pathophysiology. This model emphasizes the role of heat, hypohydration (hypernatremia), and increased neuromuscular activity (i.e. accelerated energy consumption, ion flux, and heat production) in activating the sodium pump. A vicious circle is described which leads to increased intracellular sodium concentration, cell swelling, hyperthermia, energy depletion, metabolic cascades, and irreversible cell damage. Named The Energy Depletion Model, it shifts emphasis from hyperthermia alone to a potential cellular mechanism implicating anaerobic glycolysis and lactacidosis as consequences of the total energy drain on the cell. For the following reasons, we propose that this model is applicable to cocaine intoxication. 1) Exertional heatstroke and cocaine intoxication share many of the same symptoms, strongly implicating common pathways during the evolution of each disorder. The symptoms of both illnesses (e.g. elevated serum ALT, AST, CPK; myoglobinuria) suggest increased ion flux, membrane permeability to macromolecules, and thereby a potential increase in permeability to smaller molecular species such as monovalent and divalent cations.
Document Details
- Document Type
- Technical Report
- Publication Date
- Jan 11, 1989
- Accession Number
- ADA206033
Entities
People
- L. E. Armstrong
- R. W. Hubbard
Organizations
- United States Army Research Institute of Environmental Medicine