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Nitric oxide dependent and independent effects of in vitro incubation or endotoxin on vascular reactivity in rat aorta

机译：一氧化氮对体外培养或内毒素的依赖性和独立性对大鼠主动脉血管反应性的影响

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We sought to delineate contributions of nitric oxide (NO) and other mechanisms to impairment of contraction and endothelium-dependent relaxation following prolonged in vitro incubation, endotoxin and interleukin-1 exposure in isolated rat aorta. Responses from freshly-dissected (control) rings +/- endothelium were compared with those from rings incubated in sterile, antibiotic containing medium +/- E. Coli endotoxin (LPS, 100 mug/ml) +/- interleukin-1 (IL-1,40 ng/ml) at 37 degrees C for 20-24 h. In some experiments, medium included dexamethasone (DEX, 1 mug/ml), cycloheximide (10 mug/ml), or N-G-nitro-L-arginine (NNLA, 10(-4)M). After incubation, medium nitrite was measured. Incubation alone, without addition of inflammatory mediators, impaired contraction in an agonist-specific manner, by both NO-dependent and NO-independent mechanisms. Either LPS or IL-1 diminished contraction further, in a similarly heterogeneous manner. For example, contractions were changed in LPS-incubated endothelium-intact rings (vs. fresh controls) by -85%, + 115%, -15%, -96%, and -37% for phenylephrine (PE), serotonin, prostaglandin F-2 alpha angiotensin Il, and U46619, respectively. NO synthase inhibition with NNLA either following, or during LPS incubation only partially normalized subsequent PE contractions, an effect which was smaller than that of DEX. Nitrite accumulation was inversely proportional to PE response, even though NO was not the sole mediator of LPS-impaired contraction. LPS and IL-1 nearly abolished ACh-induced relaxation, which was only mildly impaired by incubation alone. We conclude that prolonged incubation impaired vasoconstriction via both NO synthase induction and NO-independent mechanisms. LPS or IL-1 incubation impaired vasoconstriction further, primarily by NO-independent mechanisms. Moreover, vasoconstrictor responses following LPS varied with the agonist's ability to modulate endothelial NO release. These results are in accord with the failure of NO synthase inhibition to fully restore systemic vascular resistance indices in experimental endotoxemia or in hyperdynamic septic patients. (C) 2001 Elsevier Science Inc. All rights reserved. [References: 37]
机译：我们试图描述一氧化氮（NO）和其他机制对延长的体外温育，内毒素和白细胞介素-1暴露于离体大鼠主动脉后收缩和内皮依赖性松弛的损害的作用。将新鲜解剖的（对照）环+/-内皮的反应与在无菌的，含抗生素的+/- E培养基中孵育的环的反应进行比较。大肠杆菌内毒素（LPS，100杯/毫升）+/-白介素-1（IL- 1,40 ng / ml）在37摄氏度下放置20-24小时。在一些实验中，培养基包括地塞米松（DEX，1杯/毫升），环己酰亚胺（10杯/毫升）或N-G-硝基-L-精氨酸（NNLA，10（-4）M）。温育后，测量中等亚硝酸盐。单独的温育，不添加炎性介质，通过NO依赖性和NO依赖性机制以激动剂特异性方式损害了收缩。 LPS或IL-1以类似的异质性方式进一步减少了收缩。例如，对于苯肾上腺素（PE），5-羟色胺，前列腺素，在LPS孵育的内皮完整环（相对于新鲜对照）中收缩改变为-85％，+ 115％，-15％，-96％和-37％。 F-2α血管紧张素II和U46619分别。在LPS孵育后或在LPS孵育过程中，NNLA对NO合酶的抑制作用仅使随后的PE收缩部分标准化，其作用小于DEX。亚硝酸盐积累与PE反应成反比，即使NO不是LPS受损收缩的唯一介体。 LPS和IL-1几乎消除了ACh诱导的松弛，仅通过温育即可轻微减弱。我们得出的结论是，长时间孵育会通过NO合酶诱导和NO独立机制削弱血管收缩。 LPS或IL-1的孵育主要通过NO依赖性机制进一步损害了血管收缩。而且，LPS后的血管收缩反应随激动剂调节内皮NO释放的能力而变化。这些结果与NO合酶抑制不能完全恢复实验性内毒素血症或高动力性脓毒症患者的全身血管阻力指数不符。 （C）2001 Elsevier Science Inc.保留所有权利。 [参考：37]

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