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异丙酚预防肠缺血再灌注后肺损伤。

Propofol prevents lung injury following intestinal ischemia-reperfusion.

机构信息

Experimental Surgery Laboratory, Laikon Hospital, Athens, Greece.

出版信息

J Surg Res. 2012 Jan;172(1):146-52. doi: 10.1016/j.jss.2010.07.034. Epub 2010 Aug 6.

DOI:10.1016/j.jss.2010.07.034
PMID:20855084
Abstract

BACKGROUND

The antioxidant properties of propofol have been shown to improve ischemia/reperfusion injury. We investigated whether anesthesia with propofol can ameliorate remote lung injury induced by intestinal ischemia-reperfusion (IIR).

MATERIALS AND METHODS

Thirty male Wistar rats were randomly allocated in three groups (n = 10 each): animals in group Sham were anesthetized with ketamine and xylazine and then laparotomy and sham IIR followed. Animals in group IIR received ketamine and xylazine and were then subjected to clamping of the superior mesenteric artery for 45 min and reperfusion for 4 h. Group IIR+P received anesthesia with propofol and then IIR was induced, as in group IIR. Blood samples for blood gases and malondialdehyde measurements were drawn at the end of reperfusion. Bronchoalveolar lavage fluid (BALF) was obtained to measure cell counts, total protein, and phospholipids levels.

RESULTS

Induction of IIR resulted in deteriorated oxygenation, acidemia, and inflammatory cells sequestration, along with increased BALF protein content and increased proportions of small surfactant aggregates. Anesthesia with propofol alleviated intestinal injury and efficiently prevented lipid oxidation. In group IIR+P inflammatory cell infiltration and pulmonary histologic changes were significantly limited. The increase in BALF total protein and the changes in surfactant aggregates were prevented, leading to normal systemic oxygenation.

CONCLUSION

Using propofol to induce and maintain anesthesia efficiently prevented IIR-induced lung injury. Systemic antioxidant protection, improvement of intestinal injury, inhibition of the inflammatory response, and preservation of the alveolar-capillary permeability seem to be crucial mediating mechanisms for this simple and clinically relevant intervention.

摘要

背景

丙泊酚的抗氧化特性已被证明可以改善缺血/再灌注损伤。我们研究了丙泊酚麻醉是否可以改善肠缺血/再灌注(IIR)引起的远隔肺损伤。

材料和方法

30 只雄性 Wistar 大鼠随机分为 3 组(每组 10 只):Sham 组动物用氯胺酮和甲苯噻嗪麻醉,然后进行剖腹手术和假 IIR;IIR 组接受氯胺酮和甲苯噻嗪麻醉,然后夹闭肠系膜上动脉 45 分钟,再灌注 4 小时;IIR+P 组用丙泊酚麻醉,然后诱导 IIR。再灌注结束时抽取血液样本测量血气和丙二醛水平。获取支气管肺泡灌洗液(BALF)以测量细胞计数、总蛋白和磷脂水平。

结果

IIR 的诱导导致氧合恶化、酸中毒和炎症细胞的捕获,同时 BALF 蛋白含量增加,小表面活性剂聚集物的比例增加。丙泊酚麻醉减轻了肠道损伤,并有效地预防了脂质氧化。在 IIR+P 组中,炎症细胞浸润和肺组织学变化明显受限。BALF 总蛋白的增加和表面活性剂聚集物的变化得到了预防,从而实现了全身氧合的正常化。

结论

使用丙泊酚诱导和维持麻醉可以有效地预防 IIR 引起的肺损伤。全身抗氧化保护、改善肠道损伤、抑制炎症反应和维持肺泡毛细血管通透性似乎是这种简单且具有临床相关性的干预措施的关键介导机制。

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