<原著>実験喘息モルモット気道反応性亢進における気道炎症とchemical mediatorsの役割

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The mechanism of airway hyperreactivity (AHR) was studied using ovalbumin (OA) sensitized guinea pigs as asthmatic models. Sensitivity of nonpeculiar airwayreactivity to histamine was accelerated by administering more OA than is usual for guinea pigs. In peculiar airway reactivity to OA, guinea pigs that were intraperitoneally injected with 2,000 μg of OA the first time, had stronger airway reactivity than guinea pigs that were intraperitoneally injected with 1,000 μg of OA the first time. Airway reactivity to histamine was accelerated in the sensitized guinea pigs 12hrs. after OA inhalation. No airway inflammation was demonstrated in the BALF and lung tissue of sensitized guinea pigs, although airway inflammation with central eosinophils infiltration and neutrophils was demonstrated 12hrs. after OA inhalation. Prostaglandin E2 (PGE_2), thromboxane B_2 (TXB_2), leukotriene C_4 (LTC_4), and leukotriene B_4 (LTB_4) levels in BALF did not differ between sensitized guinea pigs and nonsensitized guinea pigs. Whether AHR to histamine was inhibited by administering leukotriene (LTs) antagonist (ONO-1078), cyclooxygenase synthetase inhibitor (indomethacin), thoromboxane A_2 (TXA_2) antagonist (S-1452), and platelet activating factor (PAF) antagonist (Y-24180) was studied. ONO-1078 30 mg/kg and indomethacin 5 mg/kg did not inhibit AHR to histamine, but S-1452 3 mg/kg and Y-24180 1 mg/kg did inhibit AHR to histamine. These results suggest that airway inflammation is not a prerequisite for AHR, but TXA_2 and PAF are related to AHR in OA sensitized guinea pigs.
近畿大学の論文
1993-06-25

<原著>実験喘息モルモット気道反応性亢進における気道炎症とchemical mediatorsの役割

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