Orthopedic trauma-induced pulmonary injury in the obese Zucker rat.

Orthopedic trauma-induced pulmonary injury in the obese Zucker rat.
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DOI:
10.1111/j.1549-8719.2010.00061.x
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发表时间:
2010-11
期刊:
Microcirculation (New York, N.Y. : 1994)
影响因子:
--
通讯作者:
Russell GV
Russell GV
中科院分区:
其他
文献类型:
--
作者:
Xiang L;Hester RL;Fuller WL;Sebai ME;Mittwede PN;Jones EK;Aneja A;Russell GV

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患有骨科创伤的肥胖受试者表现出炎症增加和肺水肿风险增加。 PGE2 的产生在炎症期间升高并与血管通透性增加相关。我们假设骨科创伤后肥胖患者的肺水肿是由于 PGE2 升高以及由此导致的肺通透性增加所致。在瘦(LZ)和肥胖 Zucker 大鼠(OZ)的双后肢中诱发骨科创伤。第二天,比较 LZ、OZ、有创伤的 LZ(LZT)和有创伤的 OZ(OZT)组之间的血浆 IL-6 和 PGE2 水平、肺水肿和肺气体交换能力。在应用 PGE2 之前和之后测量 LZ 和 OZ 中离体肺的血管通透性。与其他组相比,OZT 表现出血浆 IL-6 和 PGE2 水平升高、肺湿/干重比和支气管肺泡蛋白浓度增加以及肺气体交换受损。吲哚美辛治疗使血浆 PGE2 水平和肺水肿正常化。 OZ 中离体肺的基础肺通透性高于 LZ,并且在用 PGE2 治疗后通透性进一步增加。这些结果表明,骨科创伤后 OZ 中的肺水肿是由于 PGE2 升高以及由此导致的肺通透性增加所致。
Obese subjects with orthopedic trauma exhibit increased inflammation and an increased risk of pulmonary edema. PGE2 production is elevated during inflammation and associated with increased vascular permeability. We hypothesize that pulmonary edema in obesity following orthopedic trauma is due to elevated PGE2 and resultant increases in pulmonary permeability. Orthopedic trauma was induced in both hindlimbs in lean (LZ) and obese Zucker rats (OZ). On the following day, plasma IL-6 and PGE2 levels, pulmonary edema, and pulmonary gas exchange capability were compared between groups: LZ, OZ, LZ with trauma (LZT), and OZ with trauma (OZT). Vascular permeability in isolated lungs was measured in LZ and OZ before and after application of PGE2. As compared with the other groups, the OZT exhibited elevated plasma IL-6 and PGE2 levels, increased lung wet/dry weight ratio and bronchoalveolar protein concentration, and an impaired pulmonary gas exchange. Indomethacin treatment normalized plasma PGE2 levels and pulmonary edema. Basal pulmonary permeability in isolated lungs was higher in OZ than LZ, with a further increase in permeability following treatment with PGE2. These results suggest that pulmonary edema in OZ following orthopedic trauma is due to an elevated PGE2 and resultant increases in pulmonary permeability.
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