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Query: UMLS:C0085383 (hypocapnia)
 1,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Superoxide production was measured as the superoxide dismutase (SOD)-inhibitable portion of nitro blue tetrazolium (NBT) reduction after cerebral ischemia-reperfusion in anesthetized cats equipped with cranial windows. Significant superoxide production was found in the early reperfusion period and continued for more than 1 h after ischemia. Superoxide was not detected in control animals not subjected to ischemia, during ischemia, and at 120 min of reperfusion. After ischemia, the vasoconstrictor response to arterial hypocapnia was reduced. This effect was prevented by pretreatment with SOD plus catalase or by deferoxamine. The response to topical acetylcholine was converted to vasoconstriction after ischemia. The normal vasodilator response reappeared spontaneously at 120 min of reperfusion. The vasodilator response to acetylcholine was preserved in animals pretreated with SOD plus catalase. Blood-brain barrier permeability to labeled albumin and horseradish peroxidase was increased after ischemia. These effects were minimized by pretreatment with SOD and catalase. We conclude that superoxide generation occurs during reperfusion after cerebral ischemia for a fairly long period and that superoxide and its derivatives are responsible at least in part for the vasodilation and the abnormal reactivity as well as for the increase in blood-brain barrier permeability to macromolecules seen after ischemia. Furthermore, the findings suggest that the agent responsible for the vascular abnormalities is hydroxyl radical generated via the iron-catalyzed Haber-Weiss reaction.
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PMID:Oxygen radicals in cerebral ischemia. 133 9

The appearance of superoxide anion radicals in cerebral extracellular space during and after experimental fluid-percussion brain injury was investigated in anesthetized cats equipped with cranial windows. Superoxide was detected by demonstrating the presence of superoxide dismutase (SOD)-inhibitable reduction of nitroblue tetrazolium (NBT). The SOD-inhibitable rate of reduction of NBT was 3.52 +/- 0.72 nM/min/sq cm during brain injury and 4.11 +/- 0.74 nM/min/sq cm 1 hour after injury. No significant superoxide production was detected in control animals. The sustained arteriolar dilation and reduced responsiveness to the vasoconstrictor effects of arterial hypocapnia observed 30 minutes after brain injury were eliminated by after-treatment with topical SOD (60 U/ml) and catalase (40 U/ml). The results show that experimental brain injury causes the generation and appearance in extracellular fluid space of superoxide. Superoxide production continues for at least 1 hour following injury. The sustained dilation and abnormal responsiveness of cerebral arterioles after injury are due to the continued generation of superoxide and other radicals derived from it. These functional changes can be reversed by after-treatment with appropriate scavenging agents.
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PMID:Superoxide production in experimental brain injury. 300 36

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

The effects of topical application of agents which produce oxygen radicals on cerebral arterioles were studied in anesthetized cats. Xanthine oxidase plus xanthine, which produced superoxide anion radical, hydrogen peroxide, and hydrogen peroxide plus ferrous sulfate, which produced the free hydroxyl radical, induced sustained dilation, reduced responsiveness to the vasoconstrictor effect of hypocapnia, and destructive lesions of the endothelium and of the vascular smooth muscle. Similar effects were produced by arachidonate, 15-HPETE, and PGG2. The effect of arachidonate was inhibited by mannitol, a free hydroxyl radical scavenger, the effect of PGG2 was inhibited by SOD, the effect of 15-HPETE was inhibited by either catalase or SOD. These results suggest that these cerebral vascular abnormalities were produced by a single destructive free radical, probably the hydroxyl free radical, generated via interaction of superoxide and hydrogen peroxide. Cerebral vascular abnormalities similar to those produced by oxygen radicals were also seen after experimental concussive brain injury or after acute hypertension. After brain injury, activation of phospholipase C and increased brain prostaglandin concentration were demonstrated. The vascular effects of brain injury and acute hypertension were inhibited by free radical scavengers. The results suggest that, in these conditions, vascular damage is induced by oxygen radicals generated from arachidonate in association with increased prostaglandin synthesis.
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PMID:Oxygen radicals and vascular damage. 640 99

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

The effects of topical application of 15-hydroperoxy-eicosatetraenoic acid (15-HPETE, 200 micrograms/ml) on cerebral arterioles were studied in anesthetized cats equipped with cranial windows. 15-HPETE induced arteriolar dilation during application, sustained dilation 1 h after washout, and reduced responsiveness to the vasoconstrictive effects of hypocapnia. Electron microscopy of cerebral arterioles disclosed discrete endothelial lesions and focal morphological abnormalities of the vascular smooth muscle. Topical application of superoxide dismutase or catalase or the combination of the two inhibited the functional and morphological abnormalities induced by 15-HPETE. The results show that the vascular effects of 15-HPETE are mediated by superoxide anion radical and hydrogen peroxide or by other radicals derived from them, such as the hydroxyl radical. The results, together with earlier findings, support the view that the oxygen radicals responsible for these cerebral vascular effects are generated via the prostaglandin hydroperoxidase reaction.
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PMID:Effects of 15-hydroperoxy-eicosatetraenoic acid (15-HPETE) on cerebral arterioles of cats. 643 43