Nevzorova V A, Eliseeva E V, Zuga M V, Protopopova M Iu, Gel'tser B I
Ter Arkh. 1998;70(3):13-8.
Assessment of NO-synthase (NOS) activity in bronchial asthma (BA) basing on cytochemical identification and quantitation of NADPN-diaphorase.
Operative samples from 12 BA patients and biopsies from 8 patients free of bronchial inflammation or obstruction. Experimental data on control and BA rat males injected either with NOS agonist acetyl choline (AC) or beta-2-agonist fenoterol (F).
A direct relationship was found between BA severity and activity of NADPN-diaphorase resultant from activation of inducible NOS (iNOS) mediating constrictive effect via different cellular and humoral mechanisms. AC treatment caused bronchial relaxation and severe constriction in control and BA rats, respectively, though NADPN-diaphorase activity was enhanced in both groups. Introduction of F brought about bronchial relaxation in both groups. However, there were some cases of constriction in the bronchi with impaired epithelium and high baseline iNOS activity.
In intact bronchial epithelium, administration of cholino- and adrenoreceptors agonists induced bronchial myocyte relaxation due to activation of constitutive NOS. In impaired bronchial epithelium, AC stimulates iNOS induction provoking severe constriction of small bronchi.
基于烟酰胺腺嘌呤二核苷酸磷酸黄递酶（NADPN - diaphorase）的细胞化学鉴定和定量分析，评估支气管哮喘（BA）中的一氧化氮合酶（NOS）活性。
取自12例BA患者的手术样本以及8例无支气管炎症或阻塞患者的活检样本。关于对照大鼠和BA雄性大鼠的实验数据，这些大鼠分别注射了NOS激动剂乙酰胆碱（AC）或β - 2激动剂非诺特罗（F）。
发现BA的严重程度与诱导型NOS（iNOS）激活所产生的NADPN - 黄递酶活性之间存在直接关系，iNOS通过不同的细胞和体液机制介导收缩效应。AC处理分别导致对照大鼠和BA大鼠出现支气管舒张和严重收缩，尽管两组中NADPN - 黄递酶活性均增强。F的注入使两组均出现支气管舒张。然而，在上皮受损且基线iNOS活性较高的支气管中存在一些收缩病例。
在完整的支气管上皮中，胆碱能和肾上腺素能受体激动剂的给药通过组成型NOS的激活诱导支气管肌细胞舒张。在受损的支气管上皮中，AC刺激iNOS的诱导，引发小支气管的严重收缩。
