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作者采用清醒绵羊内毒素急性肺损伤模型,观察了大剂量地塞米松(Dex)对肺损伤的保护作用.结果发现,预先给予Dex后,肺损伤反应明显减轻,肺动脉压显著降低(5.4±0.6～4.2±0.2 kPa,P<0.05),肺淋巴流量(23.5±7.4～11.0±6.7 ml/30 min,P<0.05)、血浆血栓素B_2(TXB_2,2.6±0.7～0.6±0.2ng/ml,P<0.01)和肺组织磷脂酶A_2(PLA_2,354±78～142±52U,P<0.01)活性均受到明显抑制;组织病理学显示,肺泡和肺间质水肿减轻,白细胞、红细胞渗出减少.表明Dex能抑制PLA_2活性,阻止TXB_2的升高,从而降低肺动脉高压和毛细血管通透性,减少细胞渗出,对内毒素急性肺损伤有保护作用.
In this study, we observed the protective effect of high-dose dexamethasone on acute lung injury induced by endotoxin in sheep and found that Dex had a markedly decreased lung injury response and decreased pulmonary arterial pressure (5.4 ± 0.6 ~ 4.2 ± 0.2 kPa, P <0.05), pulmonary lymph flow (23.5 ± 7.4-11.0 ± 6.7 ml / 30 min, P <0.05) and plasma thromboxane B 2 (TXB_2, 2.6 ± 0.7-0.6 ± 0.2 ng / P <0.01), and phospholipase A2 (PLA2, 354 ± 78 ~ 142 ± 52 U, P <0.01) in lung tissue were significantly inhibited. Histopathology showed that alveolar and interstitial edema were alleviated and leucocyte and erythrocyte exudation were decreased Dex could inhibit the activity of PLA 2 and prevent the increase of TXB 2, thereby reducing the pulmonary hypertension and capillary permeability, decreasing the exudation of cells and protecting against endotoxin acute lung injury.