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迷走神经在失血性休克犬高渗复苏中的作用。

The role of the vagus nerve in hypertonic resuscitation of hemorrhagic shocked dogs.

作者信息

Velasco I T, Baena R C

机构信息

Laboratorio de Emergências Clínicas (LIM 51), Faculdade de Medicina, Universidade de São Paulo, São Paulo, SP, Brasil.

出版信息

Braz J Med Biol Res. 2004 Mar;37(3):419-25. doi: 10.1590/s0100-879x2004000300020. Epub 2004 Mar 3.

DOI:10.1590/s0100-879x2004000300020
PMID:15060712
Abstract

Previous studies have suggested a critical role for the vagi during the hypertonic resuscitation of hemorrhagic shocked dogs. Vagal blockade prevented the full hemodynamic and metabolic recovery and increased mortality. This interpretation, however, was challenged on the grounds that the blockade also abolished critical compensatory mechanisms and therefore the animals would die regardless of treatment. To test this hypothesis, 29 dogs were bled (46.0 +/- 6.2 ml/kg, enough to reduce the mean arterial pressure to 40 mmHg) and held hypotensive for 45 min. After 40 min, vagal activity was blocked in a reversible manner (0 masculine C/15 min) and animals were resuscitated with 7.5% NaCl (4 ml/kg), 0.9% NaCl (32 ml/kg), or the total volume of shed blood. In the vagal blocked isotonic saline group, 9 of 9 dogs, and in the vagal blocked replaced blood group, 11 of 11 dogs survived, with full hemodynamic and metabolic recovery. However, in the hypertonic vagal blocked group, 8 of 9 dogs died within 96 h. Survival of shocked dogs which received hypertonic saline solution was dependent on vagal integrity, while animals which received isotonic solution or blood did not need this neural component. Therefore, we conclude that hypertonic resuscitation is dependent on a neural component and not only on the transient plasma volume expansion or direct effects of hyperosmolarity on vascular reactivity or changes in myocardial contraction observed immediately after the beginning of infusion.

摘要

先前的研究表明,迷走神经在失血性休克犬的高渗复苏过程中起关键作用。迷走神经阻断会妨碍血流动力学和代谢的完全恢复,并增加死亡率。然而,这种解释受到了质疑,理由是阻断迷走神经也会消除关键的代偿机制,因此无论治疗如何,动物都会死亡。为了验证这一假设,对29只犬进行放血(46.0±6.2毫升/千克,足以将平均动脉压降至40毫米汞柱)并使其低血压状态维持45分钟。40分钟后,以可逆方式阻断迷走神经活动(0个男性C/15分钟),然后用7.5%氯化钠(4毫升/千克)、0.9%氯化钠(32毫升/千克)或等量失血对动物进行复苏。在迷走神经阻断的等渗盐水组中,9只犬中有9只存活,在迷走神经阻断的回输血液组中,11只犬中有11只存活,血流动力学和代谢完全恢复。然而,在高渗迷走神经阻断组中,9只犬中有8只在96小时内死亡。接受高渗盐溶液的休克犬的存活取决于迷走神经的完整性,而接受等渗溶液或血液的动物则不需要这种神经成分。因此,我们得出结论,高渗复苏依赖于一种神经成分,而不仅仅依赖于短暂的血浆容量扩充,或高渗性对血管反应性的直接影响,或输注开始后立即观察到的心肌收缩变化。

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