Figure 3: In the left panel, noncartilaginous guinea pig airways obtained from controls (a–c), ovalbumin-exposed (d–f), and ovalbumin-exposed animals treated with L-NAME (g–i) or 1400 W (j–l), a specific and highly selective iNOS inhibitor. We noted a weak yellow-greenish birefringence of the walls in the tissue section from control animals (b), coincident with the maintenance of the histoarchitecture of the extracellular matrix in H&E preparations (arrows) (a) and scant elastic fibers (c). In contrast, the airways of animals with airway inflammations induced by ovalbumin show an intense bronchoconstriction associated with peribronchial edema (d), an increase of birefringence in the airway wall (e) and in the elastic fibers content (f). L-NAME treatment decreased peribronchial edema (g), coincident with the increase of collagen content in the ECM (h), without interference in the elastic content (i). In contrast, 1400 W treatment attenuated the inflammatory cell infiltrate (j), collagen (k), and elastic (l) fiber deposition in airway walls without influencing peribronchial edema (original magnification in (b, c, e, f, h, i, k, l) ×200; (g) ×400; (a, d, j) ×1,000). In the right panel, the mean values of the total area (A), collagen (B), and elastic fibers (C) content in the airway walls of animals exposed to ovalbumin that received treatment with vehicle, L-NAME or 1400 W. * 𝑃 < . 0 5 compared with controls (open bars); ** 𝑃 < . 0 5 compared with ovalbumin-exposed animals treated with vehicle and with 1400 W; and 𝑃 < . 0 5 compared with ovalbumin-exposed animals treated with vehicle and L-NAME (closed bars). Reproduced with permission from Prado et al. [48].