BALLOON INJURY AND INTERLEUKIN-1-BETA INDUCE NITRIC-OXIDE SYNTHASE ACTIVITY IN RAT CAROTID ARTERIES
BALLOON INJURY AND INTERLEUKIN-1-BETA INDUCE NITRIC-OXIDE SYNTHASE ACTIVITY IN RAT CAROTID ARTERIES
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DOI：
10.1161/01.res.71.2.331
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发表时间：
1992-08-01
影响因子：
20.1
通讯作者：
VANHOUTTE, PM
中科院分区：
文献类型：
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作者：
JOLY, GA;SCHINI, VB;VANHOUTTE, PM
实验研究球囊损伤是否诱导血管壁一氧化氮合酶活性。比较球囊插管损伤后即刻(t=0)、术后6小时或24小时切除的大鼠左侧颈动脉对苯肾上腺素的收缩反应，并与对照组(有无内皮)的右侧颈动脉进行比较。去甲肾上腺素在球囊损伤(t=0)和对照无内皮颈动脉引起类似的浓度依赖性收缩，而在有内皮对照动脉引起收缩抑制。在球囊损伤的颈动脉(6小时和24小时)，苯肾上腺素的浓度-收缩曲线与球囊损伤的动脉相比右移(t=0)。在球囊损伤的颈动脉(6小时)，超氧化物歧化酶增强了对苯肾上腺素的低反应性。在球囊损伤的颈动脉(24小时)，硝基-L精氨酸和亚甲蓝可完全恢复收缩，而超氧化物歧化酶则加强对苯肾上腺素的低反应性。抑制的收缩伴随着cGMP基础水平的升高；这种产生被硝基-L-精氨酸取消。白介素1β(4小时)对苯肾上腺素的浓度-收缩曲线的抑制和cGMP组织水平的升高，在球囊损伤的动脉(24小时)比无内皮的对照动脉更明显。硝基-L-精氨酸可抑制IL-1β的作用。这些观察表明，在体大鼠颈动脉内皮损伤可诱导血管壁上L-精氨酸产生一氧化氮，这种作用可被白介素1β增强。
Experiments were performed to investigate whether balloon injury induces nitric oxide synthase activity in the blood vessel wall. Contractions to phenylephrine were compared in left carotid arteries of the rat, previously injured by balloon catheterization and excised either immediately (t=0), 6, or 24 hours after the procedure, with those in control right carotid arteries (with and without endothelium). Phenylephrine evoked comparable concentration-dependent contractions in balloon-injured (t=0) and control carotid arteries without endothelium, whereas those in control arteries with endothelium were depressed. In the balloon-injured carotid arteries (6 and 24 hours), the concentration-contraction curves to phenylephrine were shifted to the right compared with those observed in balloon-injured arteries (t=0). In balloon-injured carotid arteries (6 hours), the hyporeactivity to phenylephrine was enhanced by superoxide dismutase. In balloon-injured carotid arteries (24 hours), nitro-L-arginine and methylene blue restored full contractions, whereas superoxide dismutase potentiated the hyporesponsiveness to phenylephrine. The depressed contractions were associated with a concomitant increase in the basal level of cGMP; this production was abolished by nitro-L-arginine. The depression of the concentration-contraction curves to phenylephrine and the increase of the tissue level of cGMP induced by interleukin-1 beta (4 hours) were more pronounced in balloon-injured arteries (24 hours) than in control arteries without endothelium. The effects of interleukin-1 beta were inhibited by nitro-L-arginine. These observations indicate that in vivo endothelial injury of the rat carotid arteries induces the production of nitric oxide from L-arginine in the blood vessel wall, an effect which is potentiated by interleukin-1 beta.