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首页> 外文期刊>American Journal of Physiology >Low-dose carbon monoxide reduces airway hyperresponsiveness in mice.
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Low-dose carbon monoxide reduces airway hyperresponsiveness in mice.

机译：低剂量一氧化碳减少小鼠气道高反应性。

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Carbon monoxide (CO) in expired gas has been shown to be elevated with asthma; however, its function is not known, and there is some potential that it may serve a bronchoprotective role to decrease airway hyperresponsiveness (AHR). Thus the ability of CO to reverse methacholine (MCh)-induced bronchoconstriction was evaluated in C57BL/6 (C57) and A/J mice with and without airway inflammation produced by ovalbumin (OVA). Acutely administered CO (1% in air, 10 min) reduced MCh-driven increases in lung resistance in OVA-challenged C57 mice by an average of 50% (from 14.5 to 7.1 cmH2O.ml-1.s-1), whereas no effect was observed in naive C57 mice or OVA-challenged C57 mice inhaling air alone. Acutely inhaled CO (500 ppm = 0.05%, for 10 min) reduced MCh-induced airway reactivity (AR) by 20-60% in airway hyperresponsive naive A/J mice, whereas repeated 10-min administrations of 500 ppm CO over a 5-day period decreased AR by 50%. Repeated administration of low-dose CO [250 (0.025%) and (0.05%) 500 ppm, 1 h/day, 5days] to A/J mice with airway inflammation likewise resulted in a drop of AR by 50%, compared with those not receiving CO. Inhibition of guanylyl cyclase/guanosine 3',5'-cyclic monophosphothioate (cGMP) using 1H-[1,2,4] oxydiazolo[4,3-a]quinoxalin-1-one or a competitive inhibitor, Rp diastereomers of 8-bromo-cGMP, resulted in inhibition of the effect of CO on AHR, suggesting that the effects of CO were mediated through this mechanism. These results indicate that low-dose CO can effectively reverse AHR in the presence and absence of airway inflammation in mice and suggest a potential role for CO in the modulation of AHR.
机译：已显示呼出气中的一氧化碳（CO）会因哮喘而升高;然而，其功能尚不清楚，并且可能具有支气管保护作用，以降低气道高反应性（AHR）。因此，在具有和不具有由卵白蛋白（OVA）产生的气道炎症的C57BL / 6（C57）和A / J小鼠中评估了CO逆转乙酰甲胆碱（MCh）诱导的支气管收缩的能力。急性给予的CO（在空气中1％，10分钟）可降低OCh攻击的C57小鼠的MCh驱动的肺阻力平均增加50％（从14.5到7.1 cmH2O.ml-1.s-1），而没有在仅吸入空气的幼稚C57小鼠或OVA攻击的C57小鼠中观察到这种作用。急性吸入一氧化碳（500 ppm = 0.05％，持续10分钟）可使气道高反应性纯净A / J小鼠的MCh诱导的气道反应性（AR）降低20-60％，而在5分钟内重复10分钟给予500 ppm CO天期间，AR减少了50％。与患有气道炎症的A / J小鼠重复给予低剂量CO [250（0.025％）和（0.05％）500 ppm，1 h /天，5天]同样导致AR下降50％不接受CO。使用1H- [1,2,4]氧二唑并[4,3-a]喹喔啉-1-酮或竞争性抑制剂Rp抑制鸟苷酸环化酶/鸟苷3'，5'-环一硫代磷酸酯（cGMP） 8-溴-cGMP的非对映异构体导致CO对AHR的抑制作用，表明CO的影响是通过这种机制介导的。这些结果表明，在有或没有小鼠气道炎症的情况下，低剂量CO均可有效逆转AHR，并暗示CO在AHR调节中的潜在作用。

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