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Airway hyperresponsiveness to bronchoconstrictor challenge after wood smoke exposure in guinea pigs.
Life Sci. 2001 May 18; 68(26):2945-56.LS

Abstract

Prior airway exposure to wood smoke induces an increase in airway responsiveness to subsequent smoke inhalation in guinea pigs (Life Sci. 63: 1513, 1998; 66: 971, 2000). To further characterize this airway hyperreactivity, we investigated and compared the airway responsiveness to bronchoconstrictor challenge before and 30 min after sham air exposure or wood smoke exposure in anesthetized and artificially ventilated guinea pigs. Various doses of substance P (0.8-6.4 microg/kg), capsaicin (0.2-3.2 microg/kg), prostaglandin F2alpha (30-3000 microg/kg), histamine (1-8 microg/kg), or acetylcholine (5-20 microg/kg) were intravenously injected at 2-min intervals in successively increasing doses to obtain the dose required to provoke a 200% increase in baseline total lung resistance (ED200). Wood smoke exposure significantly lowered the ED200 of substance P, capsaicin, and prostaglandin F2alpha whereas sham air exposure failed to do so. Furthermore, wood smoke exposure did not significantly alter the ED200 of histamine or acetylcholine. Pretreatment with phosphoramidon (2 mg/kg), an inhibitor of the neutral endopeptidase (the major degradation enzyme of substance P), before smoke exposure did not significantly affect the smoke-induced reduction in ED200 of substance P. Sectioning both cervical vagi before smoke exposure did not significantly alter the smoke-induced reduction in ED200 of capsaicin or prostaglandin F2alpha. These results suggest that airway exposure to wood smoke acutely produces airway hyperresponsiveness to substance P, capsaicin, and prostaglandin F2alpha, but not to histamine or acetylcholine. Since the combination of phosphoramidon and wood smoke exposure did not result in an additive potentiation of smoke-induced airway hyperresponsiveness to substance P, it is suggested that an inhibition of the degradation enzyme of substance P may contribute to this increase in airway reactivity. Furthermore, vagally-mediated bronchoconstriction does not play a vital role in enhanced airway responsiveness to capsaicin or prostaglandin F2alpha.

Authors+Show Affiliations

Institute of Physiology, School of Medicine and Life Science, National Yang-Ming University, Taipei, Taiwan.No affiliation info available

Pub Type(s)

Journal Article
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

11411794

Citation

Hsu, T H., and Y R. Kou. "Airway Hyperresponsiveness to Bronchoconstrictor Challenge After Wood Smoke Exposure in Guinea Pigs." Life Sciences, vol. 68, no. 26, 2001, pp. 2945-56.
Hsu TH, Kou YR. Airway hyperresponsiveness to bronchoconstrictor challenge after wood smoke exposure in guinea pigs. Life Sci. 2001;68(26):2945-56.
Hsu, T. H., & Kou, Y. R. (2001). Airway hyperresponsiveness to bronchoconstrictor challenge after wood smoke exposure in guinea pigs. Life Sciences, 68(26), 2945-56.
Hsu TH, Kou YR. Airway Hyperresponsiveness to Bronchoconstrictor Challenge After Wood Smoke Exposure in Guinea Pigs. Life Sci. 2001 May 18;68(26):2945-56. PubMed PMID: 11411794.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Airway hyperresponsiveness to bronchoconstrictor challenge after wood smoke exposure in guinea pigs. AU - Hsu,T H, AU - Kou,Y R, PY - 2001/6/20/pubmed PY - 2001/7/6/medline PY - 2001/6/20/entrez SP - 2945 EP - 56 JF - Life sciences JO - Life Sci VL - 68 IS - 26 N2 - Prior airway exposure to wood smoke induces an increase in airway responsiveness to subsequent smoke inhalation in guinea pigs (Life Sci. 63: 1513, 1998; 66: 971, 2000). To further characterize this airway hyperreactivity, we investigated and compared the airway responsiveness to bronchoconstrictor challenge before and 30 min after sham air exposure or wood smoke exposure in anesthetized and artificially ventilated guinea pigs. Various doses of substance P (0.8-6.4 microg/kg), capsaicin (0.2-3.2 microg/kg), prostaglandin F2alpha (30-3000 microg/kg), histamine (1-8 microg/kg), or acetylcholine (5-20 microg/kg) were intravenously injected at 2-min intervals in successively increasing doses to obtain the dose required to provoke a 200% increase in baseline total lung resistance (ED200). Wood smoke exposure significantly lowered the ED200 of substance P, capsaicin, and prostaglandin F2alpha whereas sham air exposure failed to do so. Furthermore, wood smoke exposure did not significantly alter the ED200 of histamine or acetylcholine. Pretreatment with phosphoramidon (2 mg/kg), an inhibitor of the neutral endopeptidase (the major degradation enzyme of substance P), before smoke exposure did not significantly affect the smoke-induced reduction in ED200 of substance P. Sectioning both cervical vagi before smoke exposure did not significantly alter the smoke-induced reduction in ED200 of capsaicin or prostaglandin F2alpha. These results suggest that airway exposure to wood smoke acutely produces airway hyperresponsiveness to substance P, capsaicin, and prostaglandin F2alpha, but not to histamine or acetylcholine. Since the combination of phosphoramidon and wood smoke exposure did not result in an additive potentiation of smoke-induced airway hyperresponsiveness to substance P, it is suggested that an inhibition of the degradation enzyme of substance P may contribute to this increase in airway reactivity. Furthermore, vagally-mediated bronchoconstriction does not play a vital role in enhanced airway responsiveness to capsaicin or prostaglandin F2alpha. SN - 0024-3205 UR - https://www.unboundmedicine.com/medline/citation/11411794/Airway_hyperresponsiveness_to_bronchoconstrictor_challenge_after_wood_smoke_exposure_in_guinea_pigs_ L2 - https://linkinghub.elsevier.com/retrieve/pii/S0024320501010888 DB - PRIME DP - Unbound Medicine ER -