O3-induced mucosa-linked airway muscle hyperresponsiveness in the guinea pig
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1990/07/01
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Description:The effect of ozone (10028156) on airway muscle hyperresponsiveness was studied in guinea-pigs. Specific airway resistance (sRaw) to increasing concentrations of aerosolized acetylcholine-chloride (ACh) was measured in unanesthetized spontaneously breathing male Hartley-guinea-pigs before and 30 minutes after they were exposed to 0 or 3.0 parts per million ozone for 2 hours. The animals were then killed and the tracheas were removed. Ring segments of the tracheal tissue were prepared from each animal and mounted in muscle chambers. The contractile responses of the tracheal rings to increasing concentrations of substance-P, ACh, or potassium-chloride were measured in the presence of 10 micromolar (microM) indomethacin. Indomethacin was added to inhibit possible effects of any cyclooxygenase products generated during the experiments. In some experiments, the tracheal rings were pretreated with 1microM phosphoramidon or the mucosa had been removed before adding substance-P, ACh, or potassium-chloride. Ozone did not significantly affect sRaw. Ozone enhanced the bronchial hyperreactivity induced by ACh. Substance-P and ACh induced hyperresponsiveness (increased contractile activity) in-vitro in the tracheal rings. The effects were significantly more pronounced in tracheal rings from ozone exposed animals. Potassium-chloride did not affect contractile activity in any preparation. Phosphoramidon pretreatment abolished the effect of substance-P, but not ACh, on tracheal ring hyperreactivity. Removal of the mucosa had no effect on tracheal ring hyperresponsiveness to substance-P, but abolished the responses to ACh. The authors conclude that these data indicate that airway muscle responsiveness to acute ozone induced bronchial hyperreactivity may be linked to some noncyclooxygenase mucosa derived factor in the guinea-pig. [Description provided by NIOSH]
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ISSN:8750-7587
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Pages in Document:7-13
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Volume:69
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Issue:1
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NIOSHTIC Number:nn:00232418
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Citation:J Appl Physiol 1990 Jul; 69(1):7-13
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Contact Point Address:Internal Medicine Univ of Tennessee, Memphis 956 Court Avenue Memphis, TN 38163
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Federal Fiscal Year:1990
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Performing Organization:University of Cincinnati, Cincinnati, Ohio
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Peer Reviewed:True
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Start Date:19880301
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Source Full Name:Journal of Applied Physiology
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End Date:19920229
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Main Document Checksum:urn:sha-512:0612155bbac7a4a6c9f567fff035cb41c2304a9753eb5ab87284ffc1027e687469a662c8c22b6a4e2e8d0c783f82004e48aae9d0a71c5b4e7f6fcb2ce3e71b03
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