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Oxygen radicals and vascular damage.

H A Kontos, M L Hess

    Advances in Experimental Medicine and Biology
    |January 1, 1983
    PubMed
    Summary
    This summary is machine-generated.

    Oxygen radicals, such as the hydroxyl free radical, cause sustained dilation and damage to cerebral arterioles. These radicals, implicated in brain injury and hypertension, are generated from arachidonate and prostaglandin synthesis.

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    Area of Science:

    • Neuroscience
    • Vascular Biology
    • Biochemistry

    Background:

    • Oxygen radicals are implicated in various physiological and pathological processes.
    • Cerebral arterioles are crucial for regulating brain blood flow.
    • Understanding the role of free radicals in cerebrovascular function is important for neurological health.

    Purpose of the Study:

    • To investigate the effects of oxygen radicals on cerebral arterioles in vivo.
    • To determine the specific free radical responsible for cerebrovascular damage.
    • To explore the role of oxygen radicals in brain injury and hypertension-induced vascular changes.

    Main Methods:

    • Topical application of oxygen radical-generating agents (xanthine oxidase/xanthine, H2O2/ferrous sulfate) to feline cerebral arterioles.

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  • Administration of arachidonate, 15-HPETE, and PGG2 to assess their effects.
  • Use of free radical scavengers (mannitol, SOD, catalase) to identify radical involvement.
  • Induction of experimental concussive brain injury and acute hypertension.
  • Measurement of vascular responses, endothelial/smooth muscle integrity, phospholipase C activation, and prostaglandin levels.

    • Main Results:

    • Oxygen radicals induced sustained dilation, reduced responsiveness to hypocapnia, and endothelial/smooth muscle damage.
    • Arachidonate, 15-HPETE, and PGG2 mimicked these effects.
    • Scavenger studies implicated the hydroxyl free radical, likely formed from superoxide and hydrogen peroxide.
    • Similar vascular abnormalities were observed after brain injury and hypertension.
    • Vascular effects of brain injury and hypertension were mitigated by free radical scavengers.

    Conclusions:

    • The hydroxyl free radical is a key mediator of oxygen radical-induced cerebrovascular damage.
    • Oxygen radicals, generated from arachidonate and prostaglandin synthesis, play a significant role in vascular dysfunction following brain injury and hypertension.