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在体外吲哚美辛诱导的小鼠空肠炎症过程中,传入神经敏感性通过一种依赖诱导型一氧化氮合酶的机制降低。

Afferent nerve sensitivity is decreased by an iNOS-dependent mechanism during indomethacin-induced inflammation in the murine jejunum in vitro.

作者信息

Xue B, Hausmann M, Müller M H, Pesch T, Karpitschka M, Kasparek M S, Hu W C, Sibaev A, Rogler G, Kreis M E

机构信息

Department of Pathophysiology, Shandong University Medical School, Shandong, China.

出版信息

Neurogastroenterol Motil. 2009 Mar;21(3):322-34. doi: 10.1111/j.1365-2982.2008.01225.x. Epub 2008 Dec 5.

DOI:10.1111/j.1365-2982.2008.01225.x
PMID:19077108
Abstract

Evidence exists that visceral afferent sensitivity is subject to regulatory mechanisms. We hypothesized that afferent sensitivity is decreased in the small intestine during intestinal inflammation by an inducible nitric oxide synthase (iNOS)-dependent mechanism. C57BL/6 mice were injected twice with vehicle or 60 mg kg(-1) indomethacin subcutaneously to induce intestinal inflammation. Afferent sensitivity was recorded on day 3 from a 2-cm segment of jejunum in vitro by extracellular multi-unit afferent recordings from the mesenteric nerve bundle. In subgroups (n = 6), iNOS was inhibited selectively by L-N6-(1-iminoethyl)-lysine (L-NIL) given either chronically from day 1-3 (3 mg kg(-1) twice daily i.p.) or acutely into the organ bath (30 micromol L(-1)). The indomethacin-induced increase of macroscopic and microscopic scores of intestinal inflammation (both P < 0.05) were unchanged after pretreatment with L-NIL. Peak afferent firing following bradykinin (0.5 micromol L(-1)) was 55 +/- 8 impulse s(-1) during inflammation vs 97 +/- 7 impulse s(-1) in controls (P < 0.05). Normal firing rate was preserved following L-NIL pretreatment (112 +/- 16 impulse s(-1)) or acute administration of L-NIL (108 +/- 14 impulse s(-1)). A similar L-NIL dependent reduction was observed for 5-HT (250 micromol L(-1)) and mechanical ramp distension from 20 to 60 cmH(2)O (both P < 0.05). Intraluminal pressure peaks were decreased to 0.66 +/- 0.1 cmH(2)O during inflammation compared to 2.51 +/- 0.3 in controls (P < 0.01). Afferent sensitivity is decreased by an iNOS-dependent mechanism during intestinal inflammation which appears to be independent of the inflammatory response. This suggests that iNOS-dependent nitric oxide production alters afferent sensitivity during inflammation by interfering with signal transduction to afferent nerves rather than by attenuating intestinal inflammation.

摘要

有证据表明内脏传入敏感性受调节机制影响。我们推测在肠道炎症期间,小肠的传入敏感性通过一种诱导型一氧化氮合酶(iNOS)依赖性机制而降低。将C57BL/6小鼠皮下注射两次溶剂或60 mg kg⁻¹消炎痛以诱导肠道炎症。在第3天,通过对肠系膜神经束进行细胞外多单位传入记录,在体外记录2厘米空肠段的传入敏感性。在亚组(n = 6)中,iNOS被L-N6-(1-亚氨基乙基)-赖氨酸(L-NIL)选择性抑制,L-NIL从第1天至第3天长期给药(3 mg kg⁻¹,每日两次腹腔注射)或急性注入器官浴(30 μmol L⁻¹)。用L-NIL预处理后,消炎痛诱导的肠道炎症宏观和微观评分增加(均P < 0.05)未改变。缓激肽(0.5 μmol L⁻¹)刺激后的传入放电峰值在炎症期间为55 ± 8冲动 s⁻¹,而对照组为97 ± 7冲动 s⁻¹(P < 0.05)。L-NIL预处理后(112 ± 16冲动 s⁻¹)或急性给予L-NIL后(108 ± 14冲动 s⁻¹),正常放电率得以保留。对于5-羟色胺(250 μmol L⁻¹)和从20至60 cmH₂O的机械斜坡扩张,观察到类似的L-NIL依赖性降低(均P < 0.05)。与对照组的2.51 ± 0.3相比,炎症期间腔内压力峰值降至0.66 ± 0.1 cmH₂O(P < 0.01)。在肠道炎症期间,传入敏感性通过iNOS依赖性机制降低,这似乎与炎症反应无关。这表明iNOS依赖性一氧化氮生成在炎症期间通过干扰向传入神经的信号转导而非通过减轻肠道炎症来改变传入敏感性。

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