Hersch M I, McLeod J G, Satchell P M, Early R G, Sullivan C E
Department of Medicine, University of Sydney, NSW, Australia.
Respir Physiol. 1989 May;76(2):257-76. doi: 10.1016/0034-5687(89)90102-3.
Slowly adapting pulmonary stretch receptors (SARs) participate in numerous respiratory reflexes, including the Hering-Breuer lung inflation reflex (HBR), and reflex control of respiratory rate and depth. In addition, SAR discharge may modulate airway tone. We studied the effect of acrylamide neuropathy, which causes reversible dysfunction of SARs and their myelinated vagal afferents, on the breathing pattern, HBR and airway tone in conscious dogs. As neuropathy evolved, breathing became slow and deep, and both the apnoeic and bronchodilatory responses to lung inflation were markedly reduced, findings consistent with SAR dysfunction. Recovery of clinical neuropathy and respiratory reflexes followed acrylamide withdrawal. Despite the obvious abnormalities of SAR-mediated reflexes in acrylamide-affected dogs, airway tone remained normal and sinus arrhythmia prominent in the presence of neuropathy, suggesting that small diameter vagomotor efferents are relatively resistant to acrylamide. Acrylamide neuropathy provides a useful preparation for the study of vagomotor function in animals in which feedback from myelinated pulmonary afferents is attenuated.
慢适应性肺牵张感受器(SARs)参与多种呼吸反射,包括黑林-布雷尔肺充气反射(HBR)以及呼吸频率和深度的反射性控制。此外,SAR放电可能调节气道张力。我们研究了丙烯酰胺神经病变对清醒犬呼吸模式、HBR和气道张力的影响,该病变会导致SAR及其有髓迷走传入神经出现可逆性功能障碍。随着神经病变的发展,呼吸变得缓慢而深沉,对肺充气的呼吸暂停和支气管舒张反应均明显减弱,这些发现与SAR功能障碍一致。丙烯酰胺停用后,临床神经病变和呼吸反射得以恢复。尽管受丙烯酰胺影响的犬中SAR介导的反射存在明显异常,但在神经病变存在的情况下,气道张力仍保持正常,窦性心律失常明显,这表明小直径迷走运动传出神经对丙烯酰胺相对具有抗性。丙烯酰胺神经病变为研究有髓肺传入神经反馈减弱的动物的迷走运动功能提供了一种有用的模型。