抽象的
急性哮喘的恶性通货膨胀与吸气肌肉活动有关,在到期期间持续存在。本研究的主要目的是评估快速适应受体(RARS),缓慢适应受体(SARS)和C-纤维结束在产生终末潮气吸气活性(ETIA)中的作用。通过静脉内施用组胺和连续阴道(CNAP)在麻醉,自发的呼吸猫中诱导etia。为了区分从三种类型的肺受体之间的反射活动,迷走神经都被冷却至4个不同的温度(TVG)4至37℃。众所周知,CNAP刺激rars并抑制SARS。组胺用于刺激rars,这与连续正气道压力(CPAP)组合以进一步刺激SARS。在18只猫中,刺激(组胺和CNAP)中的刺激和胸骨内肋间肌肉中唤起了eTia。迷进术后,任何组胺也不是CNAP再诱发ETIA。在TVG = 37摄氏度下,CPAP抑制组胺诱导的etia;然而,这种抑制在TVG之间在14至8摄氏度之间减少了.Tyia在8度和4摄氏度之间的TVG之间急剧下降,并且在TVG = 4度CETIA几乎消失了。在TVG = 37度和22摄氏度在CNAP期间的etia值大于响应组胺的eATIA; whereas, at Tvg = 10 degrees C comparable ETIA values were obtained. It was shown that ETIA is a vagal reflex activity in which C-fibre endings are not involved. Histamine-induced ETIA originates from stimulation of RARs, and is inhibited by stimulation of SARs. Mechanical stimulation of RARs is a forceful stimulus to induce ETIA. This suggests that hyperinflation in acute asthma might be due, at least in part, to ETIA resulting from an imbalance between SAR and RAR activity.