TY - JOUR
T1 - Prostaglandin E2 enhances chemical and mechanical sensitivities of pulmonary C fibers the rat
AU - Ho, C. Y.
AU - Gu, Q.
AU - Hong, J. L.
AU - Lee, L. Y.
PY - 2000
Y1 - 2000
N2 - It has been recently reported that pulmonary reflex responses to injection or inhalation challenge of capsaicin are enhanced by exogenous Prostaglandin E2 (PGE2). The present study was carried out to determine whether PGE2 enhances the stimulatory effects of chemical stimulants and lung inflation on vagal pulmonary C fibers, and if so, whether the excitabilities of other types of lung afferents are also augmented by PGE2. In anesthetized, open-chest rats, administration of PGE2 (1.5 μg/kg/min for 2 min) did not significantly change the baseline activity of vagal pulmonary C fibers, but it markedly enhanced the stimulatory effects of both low (0.25 μg/kg) and high doses (0.5 μg/kg) of capsaicin on these fibers. Similarly, potentiating effects of PGE2 were found on the pulmonary C-fiber responses to injections of lactic acid and adenosine, although considerable variability existed in the degrees of potentiation between the different stimulants. Furthermore, PGE2 infusion also significantly enhanced the C-fiber response to constant-pressure lung inflation (tracheal pressure [Pt] = 30 cm H2O). In contrast, PGE2 did not alter the responses of either slowly adapting pulmonary receptors or rapidly adapting pulmonary receptors to lung inflation. In summary, these results show that the sensitivity of pulmonary C-fiber afferents to both mechanical and chemical stimuli is enhanced by PGE2, suggesting that endogenous release of this autocoid may play a part in the airway irritation and dyspneic sensation associated with airway inflammation.
AB - It has been recently reported that pulmonary reflex responses to injection or inhalation challenge of capsaicin are enhanced by exogenous Prostaglandin E2 (PGE2). The present study was carried out to determine whether PGE2 enhances the stimulatory effects of chemical stimulants and lung inflation on vagal pulmonary C fibers, and if so, whether the excitabilities of other types of lung afferents are also augmented by PGE2. In anesthetized, open-chest rats, administration of PGE2 (1.5 μg/kg/min for 2 min) did not significantly change the baseline activity of vagal pulmonary C fibers, but it markedly enhanced the stimulatory effects of both low (0.25 μg/kg) and high doses (0.5 μg/kg) of capsaicin on these fibers. Similarly, potentiating effects of PGE2 were found on the pulmonary C-fiber responses to injections of lactic acid and adenosine, although considerable variability existed in the degrees of potentiation between the different stimulants. Furthermore, PGE2 infusion also significantly enhanced the C-fiber response to constant-pressure lung inflation (tracheal pressure [Pt] = 30 cm H2O). In contrast, PGE2 did not alter the responses of either slowly adapting pulmonary receptors or rapidly adapting pulmonary receptors to lung inflation. In summary, these results show that the sensitivity of pulmonary C-fiber afferents to both mechanical and chemical stimuli is enhanced by PGE2, suggesting that endogenous release of this autocoid may play a part in the airway irritation and dyspneic sensation associated with airway inflammation.
UR - http://www.scopus.com/inward/record.url?scp=0033845835&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0033845835&partnerID=8YFLogxK
U2 - 10.1164/ajrccm.162.2.9910059
DO - 10.1164/ajrccm.162.2.9910059
M3 - Article
C2 - 10934082
AN - SCOPUS:0033845835
SN - 1073-449X
VL - 162
SP - 528
EP - 533
JO - American Journal of Respiratory and Critical Care Medicine
JF - American Journal of Respiratory and Critical Care Medicine
IS - 2 I
ER -