一氧化氮（NO）在眼部炎症中的作用。

Role of nitric oxide (NO) in ocular inflammation.

作者信息

Wang Z Y, Håkanson R

机构信息

Department of Pharmacology, University of Lund, Sweden.

出版信息

Br J Pharmacol. 1995 Nov;116(5):2447-50. doi: 10.1111/j.1476-5381.1995.tb15094.x.

DOI:10.1111/j.1476-5381.1995.tb15094.x

PMID:8581283

原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1909062/

Abstract

The actions of nitric oxide (NO) have been investigated in the rabbit eye, with particular emphasis on the relationship between NO and C-fibres and on those effects of NO that may be of importance in the inflammatory response to C-fibre stimulation. 2. The NO synthase inhibitor, NG-nitro-L-arginine (L-NAME; 10-200 mg kg-1), but not the inactive analogue D-NAME (200 mg kg-1), was found to block the inflammatory response induced by infrared irradiation of the iris in a dose-dependent manner. The inhibitory effects of L-NAME (200 mg kg-1) were partially reversed by L-arginine (500 mg kg-1), but not by D-arginine (500 mg kg-1). 3. L-NAME (200 mg kg-1) virtually abolished the ocular effects of intravitreal injection of calcitonin gene-related peptide (CGRP) (0.3 nmol). 4. The concentration of CGRP in aqueous humour from untreated rabbit eyes was 0.1 +/- 0.001 nmol l-1. Irradiation of the iris raised the CGRP concentration to 8.9 +/- 1.5 nmol l-1. L-NAME (200 mg kg-1) greatly suppressed the irradiation-evoked release of CGRP, the concentration in the aqueous humour being 1.2 +/- 0.2 nmol l-1 (P < 0.001). L-Arginine reversed the L-NAME-induced inhibition of release of CGRP, the concentration of CGRP in the aqueous humour being 9.7 +/- 0.6 nmol l-1. 5. In addition, a NO donor, sodium nitroprusside (0.9 mumol), was found to raise the concentration of CGRP in the aqueous humour (14.8 +/- 0.8 nmol l-1) and to induce symptoms of ocular inflammation. The elevation in concentration of CGRP induced by sodium nitroprusside was not affected by L-NAME (200 mg kg-1) (14.5 +/- 1.2 nmol l-1). Ocular responses were not inhibited by L-NAME. 6. Our findings suggest that NO plays an important role in ocular inflammation by activating C-fibres (directly or indirectly) and by mediating CGRP-induced responses.

摘要

一氧化氮（NO）在兔眼中的作用已得到研究，特别着重于NO与C纤维之间的关系以及NO在对C纤维刺激的炎症反应中可能具有重要意义的那些作用。2. 发现NO合酶抑制剂NG-硝基-L-精氨酸（L-NAME；10 - 200 mg kg⁻¹），而非无活性类似物D-NAME（200 mg kg⁻¹），能以剂量依赖方式阻断虹膜红外线照射诱导的炎症反应。L-NAME（200 mg kg⁻¹）的抑制作用可被L-精氨酸（500 mg kg⁻¹）部分逆转，但不能被D-精氨酸（500 mg kg⁻¹）逆转。3. L-NAME（200 mg kg⁻¹）实际上消除了玻璃体内注射降钙素基因相关肽（CGRP）（0.3 nmol）的眼部效应。4. 未处理兔眼房水中CGRP的浓度为0.1±0.001 nmol l⁻¹。虹膜照射使CGRP浓度升高至8.9±1.5 nmol l⁻¹。L-NAME（200 mg kg⁻¹）极大地抑制了照射诱发的CGRP释放，房水中浓度为1.2±0.2 nmol l⁻¹（P < 0.001）。L-精氨酸逆转了L-NAME诱导的CGRP释放抑制，房水中CGRP浓度为9.7±0.6 nmol l⁻¹。5. 此外，发现一种NO供体硝普钠（0.9 μmol）能提高房水中CGRP的浓度（14.8±0.8 nmol l⁻¹）并诱发眼部炎症症状。硝普钠诱导的CGRP浓度升高不受L-NAME（200 mg kg⁻¹）影响（14.5±1.2 nmol l⁻¹）。眼部反应未被L-NAME抑制。6. 我们的研究结果表明，NO通过（直接或间接）激活C纤维以及介导CGRP诱导的反应在眼部炎症中起重要作用。