Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085383 (hypocapnia)
 1,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Xanthine oxidase and xanthine, a combination that produces hydrogen peroxide and superoxide anion radical, applied topically in anesthetized cats equipped with cranial windows caused arteriolar dilation during application, sustained dilation 1 h after washout, and reduced reactivity to the vasoconstrictive effects of arterial hypocapnia, discrete lesions of the endothelium, and morphological abnormalities of the vascular smooth muscle by electron microscopy. Similar effects were seen in small, but not in large, arterioles during topical application of hydrogen peroxide or hydrogen peroxide plus ferrous sulfate, a combination that produces free hydroxyl radical. The functional changes caused by xanthine oxidase plus xanthine were inhibited completely by superoxide dismutase plus catalase. Superoxide dismutase or catalase, each by itself, eliminated the residual effects seen after washout and reduced the dilation during application of xanthine oxidase. The results show that superoxide anion radical and hydrogen peroxide produce reversible arteriolar dilation and that consistent vascular damage is produced in the presence of both superoxide anion radical and hydrogen peroxide.
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PMID:Effects of oxygen radicals on cerebral arterioles. 391 62

Topical application of sodium arachidonate (50-200 micrograms/ml) or bradykinin (0.1-10 micrograms/ml) on the brain surface of anesthetized cats caused dose-dependent cerebral arteriolar dilation. This dilation was blocked by 67-100% in the presence of superoxide dismutase and catalase. These enzymes did not affect the changes in arteriolar diameter caused by alterations in arterial blood PCO2, or the arteriolar dilation from topical acetylcholine. Enzymes inactivated by heat had no effect on the vasodilation from arachidonate or bradykinin. Superoxide dismutase alone or catalase alone reduced the dilation during application of 200 micrograms/ml of arachidonate for 15 minutes; they also completely prevented the residual dilation seen 1 hour after washout, as well as the reduction in the vasoconstrictive effects of arterial hypocapnia observed at this time. The results show that superoxide anion radical and hydrogen peroxide, or radicals derived from them, such as the hydroxyl radical, are mediators of the cerebral arteriolar dilation from sodium arachidonate or bradykinin. These radicals are not the endothelium-derived relaxant factor released by acetylcholine. The presence of both superoxide anion radical and hydrogen peroxide is required for the production of the vascular damage seen during prolonged application of high concentrations of sodium arachidonate.
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PMID:Oxygen radicals mediate the cerebral arteriolar dilation from arachidonate and bradykinin in cats. 643 60