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Platonin mitigates acute lung injury in haemorrhagic shock rats.

机译:铂蛋白可减轻失血性休克大鼠的急性肺损伤。

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AIM OF THE STUDY: Enhanced oxidative stress and inflammatory response are crucial in mediating the development of acute lung injury induced by haemorrhagic shock with resuscitation. Platonin, a potent antioxidant, possesses potent anti-inflammation capacity. We sought to elucidate whether platonin could mitigate acute lung injury in haemorrhagic shock/resuscitation rats. METHODS: Seventy-two adult male rats were randomized to receive haemorrhagic shock/resuscitation (HS), HS plus platonin (10, 50, or 100mug/kg intravenous injection immediately after resuscitation), sham instrumentation (Sham), or Sham plus platonin (100mug/kg) (n=12 in each group). Haemorrhagic shock was induced by blood drawing and mean blood pressure was maintained at 40-45mmHg for 120min. Then, resuscitation was achieved by shed blood/saline mixtures re-infusion. After monitoring for another 8h, rats were sacrificed. RESULTS: Arterial blood gas and histological findings, in concert with assays of leukocyte infiltration (polymorphonuclear leukocytes/alveoli ratio and myeloperoxidase activity) and lung water content (wet/dry weight ratio), confirmed that haemorrhagic shock/resuscitation caused significant lung injury. Significant increases in concentrations of inflammatory molecules (chemokine, cytokine, and prostaglandin E(2)) as well as nitric oxide and malondialdehyde in lung tissues confirmed that haemorrhagic shock/resuscitation elicited inflammatory response and imposed oxidative stress in rats. Platonin at the dosages of 50 and 100mug/kg, but not 10mug/kg, significantly attenuated the inflammatory response and oxidative stress induced by haemorrhagic shock/resuscitation. Most important, platonin at the dosages of 50 and 100mug/kg, but not 10mug/kg, significantly mitigated the lung injury induced by haemorrhagic shock/resuscitation. CONCLUSIONS: Platonin mitigates acute lung injury in haemorrhagic shock/resuscitation rats.
机译:研究目的:氧化应激和炎症反应的增强在介导出血性休克复苏引起的急性肺损伤的发展中至关重要。铂是有效的抗氧化剂,具有有效的抗发炎能力。我们试图阐明白蛋白是否可以减轻失血性休克/复苏大鼠的急性肺损伤。方法:72只成年雄性大鼠随机接受出血性休克/复苏(HS),HS加白蛋白(复苏后立即静脉注射10、50或100mug / kg),假手术器械(Sham)或Sham加白蛋白( 100杯/千克)(每组n = 12)。抽血引起失血性休克,平均血压维持40-45mmHg 120分钟。然后,通过流血/盐水混合物的重新输注实现复苏。监测另外8小时后,处死大鼠。结果:动脉血气和组织学检查结果与白细胞浸润(多形核白细胞/肺泡比和髓过氧化物酶活性)和肺水含量(湿重/干重比)的测定相吻合,证实出血性休克/复苏引起了严重的肺损伤。肺组织中炎症分子(趋化因子,细胞因子和前列腺素E(2))以及一氧化氮和丙二醛浓度显着增加,证实出血性休克/复苏引起大鼠炎症反应并施加氧化应激。剂量为50和100 ug / kg,而不是10 ug / kg的白蛋白显着减轻了由出血性休克/复苏引起的炎症反应和氧化应激。最重要的是,以50和100μg/ kg而不是10μg/ kg的剂量使用铂宁,可以显着减轻出血性休克/复苏引起的肺损伤。结论:白蛋白减轻了失血性休克/复苏大鼠的急性肺损伤。

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