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失血性休克时功能残气量增加的机制

Mechanism of functional residual capacity increase in haemorrhagic shock.

作者信息

Nagy S, Hantos Z, Deavers S I, Tóth I, Klebniczki J, Adamicza A

出版信息

Acta Chir Hung. 1983;24(4):295-306.

PMID:6230849
Abstract

Shock was elicited in anaesthetized dogs by maintaining a haemorrhagic hypotension of 4 kPa until 30 per cent spontaneous refusion, followed by total reinfusion. Functional residual capacity (FRC) and minute ventilation increased considerably similarly to our previous experiments. Lactate content in both the external intercostal and the biceps femoris muscles increased significantly in advanced shock. The expiratory external abdominal oblique muscle showed electromyographic signs of fatigue. At the height of the FRC changes tonic contraction of the external intercostal muscle could be demonstrated electron microscopically. This tonic contraction is the main factor in the large FRC rise in late shock forming the basis of a hitherto unknown vicious circle.

摘要

通过维持4 kPa的出血性低血压直至30%的自体再灌注,随后进行完全再灌注,在麻醉犬中引发休克。功能残气量(FRC)和分钟通气量的增加幅度与我们之前的实验相似。在重度休克时,肋间外肌和股二头肌中的乳酸含量均显著增加。呼气时腹外斜肌出现肌电图疲劳迹象。在FRC变化达到峰值时,可通过电子显微镜观察到肋间外肌的强直性收缩。这种强直性收缩是晚期休克时FRC大幅升高的主要因素,构成了一个迄今未知的恶性循环的基础。

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