Generation of nitric oxide and superoxide during reperfusion after focal cerebral ischemia in rats
Generation of nitric oxide and superoxide during reperfusion after focal cerebral ischemia in rats
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DOI：
10.1152/ajpcell.1996.270.3.c748
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发表时间：
1996-03-01
影响因子：
5.5
通讯作者：
Kosaka, H
中科院分区：
文献类型：
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作者：
Kumura, E;Yoshimine, T;Kosaka, H
我们通过电子自旋共振 (ESR) 光谱法研究了大脑中动脉闭塞期间和之后大鼠颈血中亚硝酰血红蛋白 (HbNO) 的水平。将血浆一氧化氮 (NO) 最终产物（亚硝酸盐和硝酸盐）的水平与 HbNO 的水平进行比较。在假手术大鼠 (n = 4) 和 2 小时闭塞大鼠 (n = 4) 中检测到少量 HbNO，而亚硝酸盐和硝酸盐仅在后者中增加（P < 0.01；与假手术相比）。闭塞 2 小时后再灌注，再灌注 15 分钟 (n = 4) 和 30 分钟 (n = 6) 后，HbNO 和亚硝酸盐加硝酸盐均明显增加（P < 0.01；与闭塞相比）。施用超氧化物歧化酶 (5 mg/kg) 显着增加 HbNO (P < 0.05)，但不增加血浆亚硝酸盐和硝酸盐 (n = 5)。再灌注 30 分钟后 HbNO 和亚硝酸盐加硝酸盐的增加可通过给予 N-G-硝基-L-精氨酸甲酯（20 mg/kg；n = 4，P < 0.01）来抑制，并且这种抑制可以通过 L-精氨酸（200 mg/kg）来逆转（n = 4）。本研究清楚地表明，局灶性脑缺血后再灌注期间L-精氨酸-NO合酶途径被激活，并表明在再灌注早期期间涉及NO和超氧化物之间的反应。
We investigated the levels of nitrosyl hemoglobin (HbNO) in rat jugular blood by electron spin resonance (ESR) spectroscopy during and after middle cerebral artery occlusion. The levels of plasma nitric oxide (NO) end products, nitrite plus nitrate, were compared with the levels of HbNO. Small amounts of HbNO were detected in sham-operated rats (n = 4) and those subjected to 2 h of occlusion (n = 4), whereas nitrite plus nitrate was increased only in the latter (P < 0.01; vs. sham). Upon reperfusion after 2 h of occlusion, both HbNO and nitrite plus nitrate clearly increased after 15 min (n = 4) and 30 min (n = 6) reperfusion (P < 0.01; vs. occlusion). Administration of superoxide dismutase (5 mg/kg) significantly increased HbNO (P < 0.05) but not plasma nitrite plus nitrate (n = 5). The increase in HbNO and nitrite plus nitrate after 30 min of reperfusion was suppressed by administration of N-G-nitro-L-arginine methyl ester (20 mg/kg; n = 4, P < 0.01), and this suppression could be reversed by L-arginine (200 mg/kg) (n = 4). The present study clearly showed that the L-arginine-NO synthase pathway was activated during reperfusion after focal cerebral ischemia and indicated the involvement of a reaction between NO and superoxide during early reperfusion.