TY - JOUR
T1 - Prostaglandins in physiological and in certain pathological responses of the cerebral circulation
AU - Kontos, H. A.
AU - Wei, E. P.
AU - Ellis, E. F.
AU - Dietrich, W. D.
AU - Povlishock, J. T.
PY - 1981
Y1 - 1981
N2 - The most abundant prostaglandin produced by brain tissue varies from species to species. The most abundant prostaglandin produced by brain microvessels is PGI 2. PGG 2, PGH 2, PGI 2, PGE 2, PGD 2, 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 PGG 2 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.
AB - The most abundant prostaglandin produced by brain tissue varies from species to species. The most abundant prostaglandin produced by brain microvessels is PGI 2. PGG 2, PGH 2, PGI 2, PGE 2, PGD 2, 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 PGG 2 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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M3 - Article
C2 - 7238914
AN - SCOPUS:0019861575
VL - 40
SP - 2326
EP - 2330
JO - Federation Proceedings
JF - Federation Proceedings
SN - 0014-9446
IS - 8
ER -