Prostaglandin E2 enhances chemical and mechanical sensitivities of pulmonary C fibers in the rat

被引:95
作者
Ho, CY
Gu, QH
Hong, JL
Lee, LY
机构
[1] Univ Kentucky, Med Ctr, Dept Physiol, Lexington, KY 40536 USA
[2] Vet Gen Hosp, Dept Otolaryngol, Taipei, Taiwan
[3] Natl Yang Ming Univ, Taipei 112, Taiwan
关键词
D O I
10.1164/ajrccm.162.2.9910059
中图分类号
R4 [临床医学];
学科分类号
1002 ; 100602 ;
摘要
It has been recently reported that pulmonary reflex responses to injection or inhalation challenge of capsaicin are enhanced by exogenous Prostaglandin E-2 (PCE2). The present study was carried out to determine whether PCE2 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 PCE2. In anesthetized, open-chest rats, administration of PCE2 (1.5 mu g/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 mu g/kg) and high doses (0.5 mu g/kg) of capsaicin on these fibers. Similarly, potentiating effects of PGE(2) 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, PGE(2) infusion also significantly enhanced the C-fiber response to constant-pressure lung inflation (tracheal pressure [Pt] = 30 cm H2O). In contrast, PGE(2) 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 PGE(2), suggesting that endogenous release of this autocoid may play a part in the airway irritation and dyspneic sensation associated with airway inflammation.
引用
收藏
页码:528 / 533
页数:6
相关论文
共 31 条
[1]  
BARNES PJ, 1991, LUNG BIOL HLTH DIS S, V49, P385
[2]   SENSITIVITY OF THE HUMAN COUGH REFLEX - EFFECT OF INFLAMMATORY MEDIATORS PROSTAGLANDIN-E2, BRADYKININ, AND HISTAMINE [J].
CHOUDRY, NB ;
FULLER, RW ;
PRIDE, NB .
AMERICAN REVIEW OF RESPIRATORY DISEASE, 1989, 140 (01) :137-141
[3]  
COLEMAN RA, 1994, PHARMACOL REV, V46, P205
[4]  
Coleridge H M, 1978, Adv Exp Med Biol, V99, P291
[5]   AFFERENT VAGAL-C FIBER INNERVATION OF THE LUNGS AND AIRWAYS AND ITS FUNCTIONAL-SIGNIFICANCE [J].
COLERIDGE, JCG ;
COLERIDGE, HM .
REVIEWS OF PHYSIOLOGY BIOCHEMISTRY AND PHARMACOLOGY, 1984, 99 :1-110
[6]   CHARACTERISTICS OF PROSTAGLANDIN INDUCED COUGH IN MAN [J].
COSTELLO, JF ;
DUNLOP, LS ;
GARDINER, PJ .
BRITISH JOURNAL OF CLINICAL PHARMACOLOGY, 1985, 20 (04) :355-359
[7]   CYCLIC-AMP MEDIATES THE PROSTAGLANDIN E(2)-INDUCED POTENTIATION OF BRADYKININ EXCITATION IN RAT SENSORY NEURONS [J].
CUI, M ;
NICOL, GD .
NEUROSCIENCE, 1995, 66 (02) :459-466
[8]   PGE(2) modulates the tetrodotoxin-resistant sodium current in neonatal rat dorsal root ganglion neurones via the cyclic AMP-protein kinase A cascade [J].
England, S ;
Bevan, S ;
Docherty, RJ .
JOURNAL OF PHYSIOLOGY-LONDON, 1996, 495 (02) :429-440
[9]   HYPERALGESIC EFFECTS OF PROSTACYCLIN AND PROSTAGLANDIN-E2 [J].
FERREIRA, SH ;
NAKAMURA, M ;
CASTRO, MSDA .
PROSTAGLANDINS, 1978, 16 (01) :31-37
[10]   PURINOCEPTORS IN THE NERVOUS-SYSTEM [J].
FREDHOLM, BB .
PHARMACOLOGY & TOXICOLOGY, 1995, 76 (04) :228-239