Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020440 (hypercapnia)
 7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Effects of topical application of hydrogen peroxide (H2O2) on pial arteriolar diameter and cerebral prostanoid synthesis were examined in newborn pigs. H2O2 (10 mM) caused initial constriction during the 1st min, followed by prolonged (20 min) dilation that was reversed on removal of the H2O2 in piglets treated with deferoxamine. H2O2 also caused an increase in cortical periarachnoid 6-ketoprostaglandin F1 alpha, thromboxane (TX) B2, and prostaglandin (PG) E2. Indomethacin pretreatment or coadministration of SQ 29548 (PGH2/TXA2 receptor antagonist) with H2O2 blocked the constriction due to H2O2 but did not alter the dilation. The constriction, the dilation, and the increased prostanoids caused by H2O2 were not affected by topical and systemic deferoxamine (an iron chelator) or simultaneous application of FeSO4 and FeCl3. Neither prior treatment with H2O2 nor with H2O2 plus FeSO4 and FeCl3 altered pial arteriolar dilation in response to hypercapnia. Therefore the initial constriction caused by H2O2 appears to result from stimulation of prostanoid synthesis and activation of PGH2/TXA2 receptors, whereas the dilation is not caused by prostanoids. H2O2 alone does not produce detectable residual alteration of pial arteriolar responsiveness or cerebral prostanoid synthesis.
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PMID:H2O2 effects on cerebral prostanoids and pial arteriolar diameter in piglets. 233 73

The most abundant prostaglandin produced by brain tissue varies from species to species. The most abundant prostaglandin produced by brain microvessels is PGI2, PGG2, PGH2, PGI2, PGE2, PGD2, and arachidonic acid dilated cerebral arterioles. Cyclooxygenase inhibitors (indomethacin, AHR-5850), in doses that reduced prostaglandin synthesis substantially, did not affect resting vascular caliber and did not influence the responses of cerebral arterioles to arterial hypoxia, arterial hypercapnia, or arterial hypocapnia, suggesting that prostaglandins are not involved in the mediation of these responses. The vasodilator action of vasoactive intestinal peptide on cerebral arterioles was blocked by these cyclooxygenase inhibitors. The cerebral arteriolar damage induced by fluid-percussion brain injury was inhibited by pretreatment with cyclooxygenase inhibitors, or with free radical scavengers. Topical application of arachidonic acid or PGG2, reproduced the damage seen with brain injury. These findings show that prostaglandins are mediators of the cerebral arteriolar damage due to brain injury and that their mechanism of action is dependent on the generation of free oxygen radicals.
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PMID:Prostaglandins in physiological and in certain pathological responses of the cerebral circulation. 723 14