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Zapytanie:
ARMSTEAD
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Tytuł oryginału:
NOC/oFQ activates PKC and generates superoxide to impair hypotensive cerebrovasodilation after hypoxia/ischemia.
Autorzy:
Armstead
William M.
Źródło:
Med. Sci. Monitor 2002: 8 (1) s.BR8-BR14, il., bibliogr. 19 poz.
Sygnatura GBL:
313,278
Hasła klasyfikacyjne GBL:
neurologia
Typ dokumentu:
praca doświadczalna
tytuł obcojęzyczny
Wskaźnik treści:
zwierzęta
Świnie
płeć męska
płeć żeńska
Streszczenie angielskie:
Previous studies have observed that hypotensive pial artery dilation was blunted following global cerebral ischemia in the piglet. In unrelated studies, superoxide (O-2) contributed to impaired hypotensive cerebrovasodilation following traumatic brain injury in the rat while the opioid nociceptin/orphanin FQ (NOC/oFQ) generated O-2 via activation of protein kianse C in the piglet. This study determined the contribution of NOC/oFQ, PKC activation and O-2 generation in hypoxic ischemic hypotensive cerebrovasodilation impairment. Anesthetized newborn pigs equipped with a closed cranial window were used. Global cerebral ischemia was produced via elevated intracranial pressure. Hypoxia, via inhalation of nitrogen, decreased P02 to 34 ń mmHg. Topical NOC/oFQ(10**-10 M), the CSF concentration following hypoxia/ischemia, had to effecton pial artery diameter by itself but attenuated hypotension (mean arterial blood pressure decrease of 44 ń 2 p.c.) induced pial artery dilation (33 ń 1 vs 19ń 2 p.c.). Coadministration of the PKC inhibiator chelerythrine (10**-7 M) or the O-2 scavenger polyethylene glycol superoxide dismutase and catalase (SODCAT) with NOC/oFQ (10**-10 M) partially prevented hypotensive pial dilation impariment (34 ń 2 vs 28 ń 1 p.c. fopr SODCAT). Hypotensive pial artery dilation was blunted by hypoxia/ischemia but such dilation was partially protected by the NOC/oFQ receptor antagonist [F/G] NOC/oFQ (1-13) NH2 (10**-6 M), chelerythine or SODCAT (34 ń 1 vs 7 + 2 vs 21 ń 2 p.c. for sham, H/I and H/I + SODCAT, respectively).
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