Kaneko T, Ikeda H, Fu L, Nishiyama H, Matsuoka M, Yamakawa H O, Okubo T
First Department of Internal Medicine, Yokohama City University School of Medicine, Japan.
Am J Respir Crit Care Med. 1994 Sep;150(3):724-8. doi: 10.1164/ajrccm.150.3.8087343.
We investigated whether neural pathways are involved in mediating ozone (O3)-induced airway inflammation. To determine this, we studied the contribution of adrenergic and cholinergic pathways to the O3-induced increase in airway vascular permeability, an indicator of airway inflammation, by measuring vascular permeability after giving guinea pigs propranolol or atropine to block these pathways. We also studied the contribution to O3-induced airway inflammation of neuropeptides localized in unmyelinated airway sensory nerves, by measuring vascular permeability after giving capsaicin to deplete neuropeptides from these nerves. We found that capsaicin reduced but did not abolish the increase in airway vascular permeability induced by 3 ppm O3 for 30 min. Propranolol and atropine had no effect on airway vascular permeability. These results indicate that neuropeptides released from sensory nerves, presumably by acting through the axon reflex, partly mediate O3-induced airway inflammation, and that adrenergic and cholinergic pathways are not involved.
