scholarly journals Role of thromboxane-A2 and cholinergic mechanisms in bronchoconstriction induced by cigarette smoke in guinea-pigs

1996 ◽  
Vol 9 (12) ◽  
pp. 2468-2473 ◽  
Author(s):  
K. Matsumoto ◽  
H. A Izawa ◽  
H. Inoue ◽  
S. Takata ◽  
M. Shigyo ◽  
...  
Keyword(s):  
Cigarette Smoke ◽  
Guinea Pigs ◽  
Cholinergic Mechanisms

Role of tachykinins in ozone-induced airway hyperresponsiveness to cigarette smoke in guinea pigs

1997 ◽  
Vol 83 (3) ◽  
pp. 958-965 ◽  
Author(s):  
Zhong-Xin Wu ◽  
Robert F. Morton ◽  
Lu-Yuan Lee
Keyword(s):  
Cigarette Smoke ◽  
Guinea Pigs ◽  
Airway Hyperresponsiveness ◽  
Lung Compliance ◽  
Smoke Inhalation ◽  
Before And After ◽  
Sham Exposure ◽  
Inhalation Challenge ◽  
Dynamic Lung Compliance

Wu, Zhong-Xin, Robert F. Morton, and Lu-Yuan Lee. Role of tachykinins in ozone-induced airway hyperresponsiveness to cigarette smoke in guinea pigs. J. Appl. Physiol. 83(3): 958–965, 1997.—Acute exposure to ozone (O3) induces airway hyperresponsiveness to various inhaled bronchoactive substances. Inhalation of cigarette smoke, a common inhaled irritant in humans, is known to evoke a transient bronchoconstrictive effect. To examine whether O3 increases airway responsiveness to cigarette smoke, effects of smoke inhalation challenge on total pulmonary resistance (Rl) and dynamic lung compliance (Cdyn) were compared before and after exposure to O3 (1.5 ppm, 1 h) in anesthetized guinea pigs. Before O3 exposure, inhalation of two breaths of cigarette smoke (7 ml) at a low concentration (33%) induced a mild and reproducible bronchoconstriction that slowly developed and reached its peak (ΔRl= 67 ± 19%, ΔCdyn = −29 ± 6%) after a delay of >1 min. After exposure to O3 the same cigarette smoke inhalation challenge evoked an intense bronchoconstriction that occurred more rapidly, reaching its peak (ΔRl = 620 ± 224%, ΔCdyn = −35 ± 7%) within 20 s, and was sustained for >2 min. By contrast, sham exposure to room air did not alter the bronchomotor response to cigarette smoke challenge. Pretreatment with CP-99994 and SR-48968, the selective antagonists of neurokinin type 1 and 2 receptors, respectively, completely blocked the enhanced responses of Rl and Cdyn to cigarette smoke challenge induced by O3. These results show that O3 exposure induces airway hyperresponsiveness to inhaled cigarette smoke and that the enhanced responses result primarily from the bronchoconstrictive effect of endogenous tachykinins.

Role of superoxide anions in airway hyperresponsiveness induced by cigarette smoke in conscious guinea pigs

Lung ◽  
1996 ◽  
Vol 174 (5) ◽  
Author(s):  
M. Nishikawa ◽  
M. Kudo ◽  
N. Kakemizu ◽  
H. Ikeda ◽  
T. Okubo
Keyword(s):  
Cigarette Smoke ◽  
Guinea Pigs ◽  
Airway Hyperresponsiveness ◽  
Superoxide Anions

Role of adrenergic nervous system in cigarette smoke-induced bronchoconstriction in guinea pigs

1998 ◽  
Vol 358 (1) ◽  
pp. 49-54 ◽  
Author(s):  
Koichiro Matsumoto ◽  
Hisamichi Aizawa ◽  
Hiromasa Inoue ◽  
Shohei Takata ◽  
Mutsumi Shigyo ◽  
...  
Keyword(s):  
Nervous System ◽  
Cigarette Smoke ◽  
Guinea Pigs ◽  
Adrenergic Nervous System

Cigarette smoke-induced bronchoconstriction: causative agents and role of thromboxane receptors

1996 ◽  
Vol 81 (5) ◽  
pp. 2053-2059 ◽  
Author(s):  
Ju-Lun Hong ◽  
Lu-Yuan Lee
Keyword(s):  
Cigarette Smoke ◽  
Guinea Pigs ◽  
Bronchoalveolar Lavage Fluid ◽  
Smooth Muscles ◽  
Lavage Fluid ◽  
Phase Response ◽  
Second Phase ◽  
Causative Agents ◽  
Thromboxane Receptors

Hong, Ju-Lun, and Lu-Yuan Lee. Cigarette smoke-induced bronchoconstriction: causative agents and role of thromboxane receptors. J. Appl. Physiol. 81(5): 2053–2059, 1996.—Inhalation of cigarette smoke induces a biphasic bronchoconstriction in guinea pigs: the first phase is induced by a combination of cholinergic reflex and tachykinins, whereas the second phase involves cyclooxygenase metabolites (J.-L. Hong, I. W. Rodger, and L.-Y. Lee. J. Appl. Physiol. 78: 2260–2266, 1995). This study was carried out to further determine the causative agents in the smoke and the types of prostanoid receptors and endogenous prostanoids mediating the bronchoconstriction. Inhalation of 10 ml of high-nicotine cigarette smoke consistently elicited the biphasic bronchoconstriction in anesthetized and artificially ventilated guinea pigs. Pretreatment with hexamethonium (10 mg/kg iv) significantly reduced the first-phase bronchoconstriction but did not have any measurable effect on the second-phase response. In sharp contrast, gas-phase smoke did not elicit any bronchoconstrictive effect. Furthermore, when the animals were challenged with low-nicotine cigarette smoke, only a single second-phase response was evoked, accompanied by increases in thromboxane (Tx) B2 (a stable metabolite of TxA2), prostaglandin (PG) D2, PGF2α in the bronchoalveolar lavage fluid. The bronchoconstrictive response induced by low-nicotine smoke was completely prevented by pretreatment with SQ-29548 (0.3 mg/kg iv), a TxA2-receptor antagonist. These results indicate that 1) nicotine is the primary causative agent responsible for the first-phase bronchoconstriction and 2) nonnicotine smoke particulates evoke the release of TxA2, PGD2, and PGF2α, which act on TxA2 receptors on airway smooth muscles and induce the second-phase response to cigarette smoke.

Role of tachykinins in airway narrowing induced by cigarette smoke in guinea pigs

1996 ◽  
Vol 1 (4) ◽  
pp. 227-233 ◽  
Author(s):  
Koichiro Matsumoto ◽  
Hisamichi Aizawa ◽  
Mutsumi Shigyo ◽  
Hiromasa Inoue ◽  
Shohei Takata ◽  
...  
Keyword(s):  
Cigarette Smoke ◽  
Guinea Pigs ◽  
Airway Narrowing

scholarly journals Pivotal role of MUC1 glycosylation by cigarette smoke in modulating disruption of airway adherens junctions in vitro

2014 ◽  
Vol 234 (1) ◽  
pp. 60-73 ◽  
Author(s):  
Lili Zhang ◽  
Marianne Gallup ◽  
Lorna Zlock ◽  
Yu Ting Feeling Chen ◽  
Walter E Finkbeiner ◽  
...  
Keyword(s):  
Cigarette Smoke ◽  
Adherens Junctions ◽  
Pivotal Role

Paradoxical effect of salbutamol in a model of acute organophosphates intoxication in guinea pigs: role of substance P release

2007 ◽  
Vol 292 (4) ◽  
pp. L915-L923 ◽  
Author(s):  
Jaime Chávez ◽  
Patricia Segura ◽  
Mario H. Vargas ◽  
José Luis Arreola ◽  
Edgar Flores-Soto ◽  
...  
Keyword(s):  
Substance P ◽  
Guinea Pigs ◽  
Smooth Muscle Contraction ◽  
In Vivo Experiments ◽  
Intracellular Ca ◽  
Neurokinin 1 ◽  
Substance P Release

Organophosphates induce bronchoobstruction in guinea pigs, and salbutamol only transiently reverses this effect, suggesting that it triggers additional obstructive mechanisms. To further explore this phenomenon, in vivo (barometric plethysmography) and in vitro (organ baths, including ACh and substance P concentration measurement by HPLC and immunoassay, respectively; intracellular Ca2+ measurement in single myocytes) experiments were performed. In in vivo experiments, parathion caused a progressive bronchoobstruction until a plateau was reached. Administration of salbutamol during this plateau decreased bronchoobstruction up to 22% in the first 5 min, but thereafter airway obstruction rose again as to reach the same intensity as before salbutamol. Aminophylline caused a sustained decrement (71%) of the parathion-induced bronchoobstruction. In in vitro studies, paraoxon produced a sustained contraction of tracheal rings, which was fully blocked by atropine but not by TTX, ω-conotoxin (CTX), or epithelium removal. During the paraoxon-induced contraction, salbutamol caused a temporary relaxation of ∼50%, followed by a partial recontraction. This paradoxical recontraction was avoided by the M2- or neurokinin-1 (NK1)-receptor antagonists (methoctramine or AF-DX 116, and L-732138, respectively), accompanied by a long-lasting relaxation. Forskolin caused full relaxation of the paraoxon response. Substance P and, to a lesser extent, ACh released from tracheal rings during 60-min incubation with paraoxon or physostigmine, respectively, were significantly increased when salbutamol was administered in the second half of this period. In myocytes, paraoxon did not produce any change in the intracellular Ca2+ basal levels. Our results suggested that: 1) organophosphates caused smooth muscle contraction by accumulation of ACh released through a TTX- and CTX-resistant mechanism; 2) during such contraction, salbutamol relaxation is functionally antagonized by the stimulation of M2 receptors; and 3) after this transient salbutamol-induced relaxation, a paradoxical contraction ensues due to the subsequent release of substance P.

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