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迷走神经刺激调节创伤性失血性休克中的肠道损伤和肺通透性。

Vagal nerve stimulation modulates gut injury and lung permeability in trauma-hemorrhagic shock.

机构信息

Department of Surgery, New Jersey Medical School, University of Medicine and Dentistry of New Jersey, Newark, New Jersey, USA.

出版信息

J Trauma Acute Care Surg. 2012 Aug;73(2):338-42; discussion 342. doi: 10.1097/TA.0b013e31825debd3.

Abstract

BACKGROUND

Hemorrhagic shock is known to disrupt the gut barrier leading to end-organ dysfunction. The vagus nerve can inhibit detrimental immune responses that contribute to organ damage in hemorrhagic shock. Therefore, we explored whether stimulation of the vagus nerve can protect the gut and recover lung permeability in trauma-hemorrhagic shock (THS).

METHODS

Male Sprague-Dawley rats were subjected to left cervical vagus nerve stimulation at 5 V for 10 minutes. The right internal jugular and femoral artery were cannulated for blood withdrawal and blood pressure monitoring, respectively. Animals were then subjected to hemorrhagic shock to a mean arterial pressure between 30 mm Hg and 35 mm Hg for 90 minutes then reperfused with their own whole blood. After observation for 3 hours, gut permeability was assessed with fluorescein dextran 4 in vivo injections in a ligated portion of distal ileum followed by Evans blue dye injection to assess lung permeability. Pulmonary myeloperoxidase levels were measured and compared.

RESULTS

Vagal nerve stimulation abrogated THS-induced lung injury (mean [SD], 8.46 [0.36] vs. 4.87 [0.78]; p < 0.05) and neutrophil sequestration (19.39 [1.01] vs. 12.83 [1.16]; p < 0.05). Likewise, THS gut permeability was reduced to sham levels.

CONCLUSION

Neuromodulation decreases injury in the THS model as evidenced by decreased gut permeability as well as decreased lung permeability and pulmonary neutrophil sequestration in a rat model.

摘要

背景

已知失血性休克会破坏肠道屏障,导致终末器官功能障碍。迷走神经可以抑制有害的免疫反应,从而减少失血性休克引起的器官损伤。因此,我们探讨了刺激迷走神经是否可以保护肠道并恢复创伤性失血性休克(THS)中的肺通透性。

方法

雄性 Sprague-Dawley 大鼠接受左侧颈迷走神经 5V 刺激 10 分钟。右侧颈内静脉和股动脉分别用于采血和血压监测。然后,动物将经历失血性休克,平均动脉压维持在 30mmHg 至 35mmHg 之间 90 分钟,然后用自身全血再灌注。观察 3 小时后,通过结扎回肠远端的荧光素右旋糖酐 4 体内注射评估肠道通透性,然后注射 Evans 蓝染料评估肺通透性。测量并比较肺髓过氧化物酶水平。

结果

迷走神经刺激消除了 THS 诱导的肺损伤(平均值[标准差],8.46[0.36]比 4.87[0.78];p<0.05)和中性粒细胞聚集(19.39[1.01]比 12.83[1.16];p<0.05)。同样,THS 肠道通透性降低至假手术水平。

结论

神经调节可减少 THS 模型中的损伤,这表现为肠道通透性降低,以及肺通透性和肺中性粒细胞聚集减少,这在大鼠模型中得到了证实。

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