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本文介绍家兔实验性呼吸窘迫综合征时呼吸功能的变化。静脉注射油酸后呼吸频率迅速增加,肺通气量则经历三个时相的变化,依次为最初通气增大期、延迟通气增大期和通气不足期。胸廓呼吸运动的幅度随着时间的延长逐渐加大而潮气量则逐渐减少。O_2吸收率及 CO_2排出率在通气不足期显著减少。血气分析提示,在通气增大期有呼吸性碱中毒,至通气不足期出现酸中毒。动脉血 PO_2在注射油酸后20min 时尚能维持在80mmHg 左右,以后则明显下降。切断双侧迷走神经后再注射油酸,呼吸不再增快,最初通气增大期显著减弱,而延迟通气增大期和通气不足期照常发生。切断双侧窦神经后再注射油酸,仍见呼吸加快和最初通气增大期,但延迟通气增大期消失。上述结果表明:动物注射油酸后,呼吸加快和最初通气增大期是通过迷走神经实现的,而延迟通气增大期则是由于缺 O_2,刺激外周化学感受器所致。
This article describes the changes in respiratory function in rabbits with experimental respiratory distress syndrome. After the intravenous injection of oleic acid, the respiratory rate increased rapidly. The pulmonary ventilation experienced three phases of phase change, followed by the initial period of increased ventilation, the delayed phase of delayed ventilation and the period of hypoventilation. The amplitude of thoracic respiratory movement gradually increased with time and the tidal volume decreased gradually. O 2 absorption rate and CO 2 emission rate decreased significantly during hypoventilation. Blood gas analysis suggests that there is respiratory alkalosis during the period of increased ventilation and acidosis until the period of hypoventilation. Arterial blood PO_2 20min after injection of oleic acid can still be maintained at about 80mmHg, then significantly decreased. After cutting off bilateral vagal nerve injection of oleic acid, respiration no longer increased, the initial period of increased airway significantly weakened, while delayed ventilation and hypopnea period as usual. Bilateral sinusoidal nerve cut off after injection of oleic acid, still see accelerated breathing and initial ventilation increased period, but delayed disappearance of increased airway. The above results show that: after the animals injected oleic acid, the respiration is accelerated and the initial period of increased aeration is achieved by the vagus nerve, while the delay of delayed aeration is due to the lack of O2, which stimulates the peripheral chemoreceptors.