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논문 기본 정보

자료유형
학술저널
저자정보
Shinl, Chang-Yell (Department of Pharmacology, College of Pharmacy, Chung Ang University) Lee, Nam-In (Department of Pharmacology, College of Pharmacy, Chung Ang University) Je, Hyun-Dong (Department of Pharmacology, College of Pharmacy, Chung Ang University) Kim, Jeong-Soo (Department of Pharmacology, College of Pharmacy, Chung Ang University) Sung, Ji-Hyun (Department of Pharmacology, College of Pharmacy, Chung Ang University) Kim, Dong-Seok (Department of Pharmacology, College of Pharmacy, Chung Ang University) Lee, Doo-Won (Department of Pharmacology, College of Pharmacy, Chung Ang University) Bae, Ki-Lyong (Department of Pharmacology, College of Pharmacy, Chung Ang University) Sohn, Uy-Dong (Department of Pharmacology, College of Pharmacy, Chung Ang University)
저널정보
대한약학회 Archives of pharmacal research : a publication of the Pharmaceutical Society of Korea Archives of pharmacal research : a publication of the Pharmaceutical Society of Korea 제25권 제5호
발행연도
2002.1
수록면
697 - 703 (7page)

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We investigated that the role of nitric oxide (NO) on ischemic rats in brain and heart. Ischemia was induced by both common carotid arteries (CCA) occlusion for 24h following reperfusion. Then tissue samples were removed and measured NOx. In brain, NOx was increased by about 40% vs. normal and it was significantly inhibited by aminoguanidine, selective iNOS inhibitor. This result showed that NOx concentration was increased by iNOS. We investigated the role of $Ca^{2+}$ during ischemia. Nimodipine, L-type calcium channel blocker, didn't inhibit the increases of NOx concentration during ischemia. It suggested that increased NOx was due to calcium-independent NOS. MK-801, which N-methyl-D-aspartate (NMDA) receptor antagonist, didn't significantly prevent the increases of NOx. In heart, ischemia caused NOx decrease and it is inconsistent with NOx increase in brain. Aminoguanidine and nimodipine didnt affect on NOx decrease. But MK-801 more lowered NOx concentration than those of ischemia control group. It seemed that $Ca^{2+}$ influx in heart partially occurred via NMDA receptor and inhibited by NMDA receptor antagonist. The mean arterial pressure (MAP) in ischemic rats after 24h of CCA occlusion was decreased when compared to normal value, whereas the heart rates (HR) was not different between two groups. Aminoguanidine or MK801 had no effect on MAP or HR, but nimodipine reduced MAP. There was no difference the effects of aminoguanidine, nimodipine, or MK-801, on MAP and HR between normal rats and ischemic rats. In summary, ischemic model caused an increase of NOx concentration, suggesting that this may be produced via iNOS, which is calcium independent in brain. However in heart, ischemia decreased NOx concentration and NMDA receptor was partially involved. The basal MAP was decreased in ischemic rats but HR was not different from normal control, suggesting that increased NOx in brain of ischemic rat may result in the hypotension.
#Nitric oxide #NO #N-methy-D-aspartate #NMDA #NO #Nitric oxide #NMDA #N-methyl-D-aspartate #NOS #Nitric oxide synthase

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