Carbon Monoxide Poisoning

Probable/Hypothesized Mechanisms of Brain Damage:

  • Reduced brain oxygen delivery resulting in tissue hypoxemia.

  • Generalized hypotension - cerebral blood flow becomes purely blood pressure dependent due to loss of autoregulatory control leading to ischemia (oligemia).

  • Role of the limited vasodilatory capability of some portions of the cerebral arterial architecture (ie. anatomy).

  • Hypoxic/Ischemic-induced hyperglycemia.

  • Metabolic acidosis resulting in edema, metabolic shut-down, membrane damage, etc.

  • Hemoconcentration leading to decreased blood flow (i.e. impaired rheology).

  • Binding of CO to intracellular components (e.g. cytochromes, myoglobin) inhibiting metabolic energy release.

  • Stimulation of free radical formation (ie. reactive oxygen species = ROS), eg. superoxide anion, O2-; hydrogen peroxide, H2O2; and hydroxyl radical, OH..

  • Release by nerve cells of excitatory amino acids (EAA) (glutamate & other dicarboxylic amino acids) which have neurotoxic properties.

  • Release of catecholamines (CAT = epinephrine, norepinephrine).

  • Excessive uptake of Ca++ by nerve cells.

  • Excessive stimulation of NMDA (N-methyl-D-aspartic acid), AMPA (D-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid), and KA (kainic acid) receptors.

  • Damage to mitochondria and energy generating machinery of the cell by above mechanisms (??).

  • Interference with the normal vasoregulatory control of the blood supply involving endogenous NO and CO (eg. increased nitric oxide synthase = NOS).

    ...... last changed 10/05/00

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