R. Sorkness et al., VIRUS-INDUCED AIRWAY-OBSTRUCTION AND PARASYMPATHETIC HYPERRESPONSIVENESS IN ADULT-RATS, American journal of respiratory and critical care medicine, 150(1), 1994, pp. 28-34
Citations number
35
Categorie Soggetti
Emergency Medicine & Critical Care","Respiratory System
Viral respiratory infections in humans have been associated with exace
rbations of late allergic responses and asthma, as well as with airway
abnormalities that persist after resolution of the acute infection. W
e hypothesized that augmented parasympathetic contractile mechanisms m
ay contribute to postviral airway dysfunction. We studied airway physi
ology in anesthetized rats at 1 to 8 wk after inoculation with Parainf
luenza 1 virus or vehicle. The virus groups had airway obstruction (ab
normal lung mechanics, gas exchange, and residual volume), and increas
ed sensitivity to intravenous methacholine at 1 to 4 wk, although meth
acholine hypersensitivity was minimal in vagotomized rats; these abnor
malities were absent at 7 to 8 wk after inoculation. Airway responses
to vagal parasympathetic nerve stimulation were enhanced markedly at 1
to 4 wk, and significantly at 7 to 8 wk, after viral inoculation. Dys
function of M(2) muscarinic autoreceptors during acute viral infection
was indicated by a significant attenuation of gallamine-induced augme
ntation of airway parasympathetic responses; in contrast, gallamine-au
gmentation of parasympathetic responses at 2 to 8 wk after viral inocu
lation was not different from noninfected control animals. We conclude
that respiratory virus infection in rats produces airway dysfunction
that remains for weeks after resolution of the acute infection, and th
at is caused in part by parasympathetic hyperresponsiveness, associate
d both with M(2) autoreceptor malfunction and with M(2)-independent me
chanism(s).