Auguet M, Guillon J M, Delaflotte S, Etiemble E, Chabrier P E, Braquet P
Institut Henri Beaufour Research Labs., Les Ulis, France.
Life Sci. 1991;48(2):189-93. doi: 10.1016/0024-3205(91)90413-6.
The effects of NG-monomethyl-L-arginine (NMMA), a specific inhibitor of nitric oxide (NO) synthesis was tested on the endotoxin-induced alterations of alpha-adrenoceptor function. In isolated aorta, there was no significant difference in the tension induced by phenylephrine (PE, 10 microM) on rings removed from control and endotoxin injected rats (10 mg/kg, ip). However, a lack of tonicity of the contraction was observed in rings of shocked rats (8 +/- 2.9 and 86 +/- 4.6% relaxation at 105 min for sham and shocked rings respectively). The gradual tension decrease to PE was more potent in rings possessing endothelial cells. However, in both preparations, the loss of tonicity was significantly inhibited by NMMA (30 microM). In endothelium-free rings, L-arginine (100 microM) potentiated the loss of tonicity to PE and reversed the inhibitory effect of NMMA. NMMA, like methylene blue, was also able to restore the PE-contraction. The results indicate that the endotoxin-induced alterations of vascular reactivity may be due, in part, to NO formation from L-arginine independent of the endothelium.
检测了一氧化氮（NO）合成的特异性抑制剂NG-单甲基-L-精氨酸（NMMA）对内毒素诱导的α-肾上腺素能受体功能改变的影响。在离体主动脉中，去氧肾上腺素（PE，10微摩尔）对取自对照大鼠和注射内毒素大鼠（10毫克/千克，腹腔注射）的血管环所诱导的张力没有显著差异。然而，在休克大鼠的血管环中观察到收缩张力缺乏（假手术组和休克组血管环在105分钟时分别松弛8±2.9%和86±4.6%）。在有内皮细胞的血管环中，对PE的张力逐渐降低更为明显。然而，在两种制剂中，NMMA（30微摩尔）均能显著抑制张力的丧失。在无内皮的血管环中，L-精氨酸（100微摩尔）增强了对PE的张力丧失，并逆转了NMMA的抑制作用。NMMA与亚甲蓝一样，也能够恢复PE收缩。结果表明，内毒素诱导的血管反应性改变可能部分归因于L-精氨酸生成的NO，且不依赖于内皮。
