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大鼠高口咽气道阻力诱导的代偿机制。

Compensatory mechanisms induced by high oropharyngeal airway resistance in rats.

作者信息

Kalogjera L, Pegan B, Petric V

机构信息

Department of Otorhinolaryngology/Head and Neck Surgery, University Hospital Dr Mladen Stojanovic, Zagreb, Yugoslavia.

出版信息

Acta Otolaryngol. 1991;111(2):384-8. doi: 10.3109/00016489109137406.

Abstract

Acid base balance changes were observed during 72 h following bilateral nasal obstruction in rats. Mouth breathing caused acute respiratory acidosis and marked aerophagia, leading to spontaneous death of the experimental animal 80 to 90 h postoperatively. Stenotic oropharyngeal airway, due to palatal-epiglottic approximation, is supposed to be responsible for respiratory insufficiency in the nose obstructed rats. The compensatory changes in respiratory mechanics caused by high oropharyngeal airway resistance, together with some possible reflex changes, may have caused either air swallowing or aspiration. As changes in acid base balance parameters did not show breakdown of the compensatory mechanisms during the first 72 h postoperatively, it is supposed that the increased air volume in stomach and guts, causing elevation of the diaphragm and paralytic ileus, contributed to the experimental animals' death.

摘要

在大鼠双侧鼻阻塞后的72小时内观察到酸碱平衡变化。张口呼吸导致急性呼吸性酸中毒和明显的吞气症,导致实验动物在术后80至90小时自发死亡。由于腭-会厌接近导致口咽气道狭窄,被认为是鼻阻塞大鼠呼吸功能不全的原因。高口咽气道阻力引起的呼吸力学代偿性变化,以及一些可能的反射性变化,可能导致了吞气或误吸。由于酸碱平衡参数的变化在术后最初72小时内未显示代偿机制的崩溃,因此推测胃和肠道内气量增加导致膈肌抬高和麻痹性肠梗阻,是实验动物死亡的原因。

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