Delmore G, Koller E A
Pflugers Arch. 1977 Nov 25;372(1):1-6. doi: 10.1007/BF00582199.
The study is based on plethysmographic, neurophysiological and respiratory mass-spectrographic records established during anaphylactic or histamine-induced bronchial asthma attacks in guinea-pigs. The frequency of occurrence of the augmented breaths (sighs) is correlated with the intensity of the lung deflation reflex (tachypnoea) which arises during the attack. In the acute phase of the asthma attack, the sighs increase in number and reinforce the uneven ventilation which underlies stimulation of the pulmonary deflation receptors. The sigh becomes an essential component of the vicious circle of uneven ventilation and vagal lung deflation reflex induced. This circle is broken in the recovery phase of the asthma attack, during which the sighs decrease in number, as the conditions underlying their occurrence subside; they now lessen the uneven ventilation and by reopening closed lung units promote a return to normal conditions in lung mechanics. It is concluded that augmented breaths, like the asthmatic tachypnoea, are caused by uneven ventilation resulting in pulmonary self-compression and in turn stimulation of the pulmonary deflation (irritant) endings. Some factors which possibly contribute to the elicitation of augmented breaths are discussed.
该研究基于豚鼠在过敏性或组胺诱导的支气管哮喘发作期间建立的体积描记、神经生理学和呼吸质谱记录。深呼吸(叹息)的发生频率与发作期间出现的肺萎陷反射(呼吸急促)的强度相关。在哮喘发作的急性期,叹息次数增加并加剧了不均匀通气,而不均匀通气是刺激肺萎陷感受器的基础。叹息成为不均匀通气和迷走神经肺萎陷反射所诱发恶性循环的一个重要组成部分。在哮喘发作的恢复期,这个循环被打破,在此期间,随着叹息发生的基础条件消退,叹息次数减少;它们现在减少了不均匀通气,并通过重新开放关闭的肺单位促进肺力学恢复到正常状态。得出的结论是,深呼吸与哮喘性呼吸急促一样,是由不均匀通气导致肺自我压缩,进而刺激肺萎陷(刺激)末梢引起的。讨论了一些可能导致深呼吸诱发的因素。