Article date: July 1995
By: A. Rudolf C. Ladenius, Gert Folkerts, Henk J. Linde, Frans P. Nijkamp, in Volume 115, Issue 6, pages 1048-1052
We investigated whether virus‐induced airway hyperresponsiveness in guinea‐pigs could be modulated by pretreatment with capsaicin and whether viral respiratory infections could potentiate ovalbumin‐aerosol‐induced tracheal hyperresponsiveness.
Animals were inoculated intratracheally with bovine parainfluenza‐3 virus or control medium 7 days after treatment with capsaicin (50 mg kg−1, s.c). Four days after inoculation, tracheal contractions were measured to increasing concentrations of substance P, histamine and the cholinoceptor agonist, arecoline.
In tracheae from virus‐infected guinea‐pigs, contractions in response to substance P, histamine and arecoline were significantly enhanced (P<0.01) by 144%, 46% and 77%, respectively. Capsaicin pretreatment inhibited the hyperresponsiveness to substance P partly (62%) and to histamine and arecoline completely.
In another series of experiments animals were first sensitized with ovalbumin (20 mg kg−1, i.p.). After 14 days animals were exposed to either saline or ovalbumin aerosols for 8 days. After 4 aerosol exposures (4 days) animals were inoculated with either parainfluenza‐3 virus or control medium. One day after the last ovalbumin aerosol, tracheal contraction in response to increasing concentrations of substance P, histamine and arecoline was measured.
Tracheae from ovalbumin‐aerosol‐exposed control inoculated animals showed a similar degree of airway hyperresponsiveness to saline‐aerosol‐exposed virus‐treated guinea‐pigs. Virus inoculation of ovalbumin‐treated animals significantly potentiated the tracheal contractions to substance P compared to either of the treatments alone. The contractions in response to histamine and arecoline were only slightly enhanced.
In conclusion, sensory nerves and/or tachykinins are involved in virus‐induced airway hyperresponsiveness in guinea‐pigs and viral respiratory infections can potentiate the increase in tracheal responsiveness to bronchoconstrictor agonists after ovalbumin exposure.
We investigated whether virus‐induced airway hyperresponsiveness in guinea‐pigs could be modulated by pretreatment with capsaicin and whether viral respiratory infections could potentiate ovalbumin‐aerosol‐induced tracheal hyperresponsiveness.
Animals were inoculated intratracheally with bovine parainfluenza‐3 virus or control medium 7 days after treatment with capsaicin (50 mg kg−1, s.c). Four days after inoculation, tracheal contractions were measured to increasing concentrations of substance P, histamine and the cholinoceptor agonist, arecoline.
In tracheae from virus‐infected guinea‐pigs, contractions in response to substance P, histamine and arecoline were significantly enhanced (P<0.01) by 144%, 46% and 77%, respectively. Capsaicin pretreatment inhibited the hyperresponsiveness to substance P partly (62%) and to histamine and arecoline completely.
In another series of experiments animals were first sensitized with ovalbumin (20 mg kg−1, i.p.). After 14 days animals were exposed to either saline or ovalbumin aerosols for 8 days. After 4 aerosol exposures (4 days) animals were inoculated with either parainfluenza‐3 virus or control medium. One day after the last ovalbumin aerosol, tracheal contraction in response to increasing concentrations of substance P, histamine and arecoline was measured.
Tracheae from ovalbumin‐aerosol‐exposed control inoculated animals showed a similar degree of airway hyperresponsiveness to saline‐aerosol‐exposed virus‐treated guinea‐pigs. Virus inoculation of ovalbumin‐treated animals significantly potentiated the tracheal contractions to substance P compared to either of the treatments alone. The contractions in response to histamine and arecoline were only slightly enhanced.
In conclusion, sensory nerves and/or tachykinins are involved in virus‐induced airway hyperresponsiveness in guinea‐pigs and viral respiratory infections can potentiate the increase in tracheal responsiveness to bronchoconstrictor agonists after ovalbumin exposure.
DOI: 10.1111/j.1476-5381.1995.tb15917.x
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