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为研究卡氏肺孢子虫肺炎 ( PCP)大鼠炎症反应及肺损伤 ,通过皮下注射 8～ 1 2周醋酸可的松免疫抑制诱导建立 Sprague-Dawley大鼠 PCP模型。将大鼠分为四组 , 组 :正常对照 ( n=6) ,为未用药的健康大鼠 ; 组 :阴性对照 ( n=6) ,为无肺部感染的大鼠 ; 组 :细菌性肺炎 ( n=1 1 ) ; 组 :PCP( n=1 4)。计数支气管肺泡灌洗液 ( BAL F)中的细胞数并行分类 ,测定总蛋白 ( TP)、白蛋白 ( AL B)含量及碱性磷酸酶 ( AL P)、乳酸脱氢酶 ( L DH)及 型胶原酶 ( MMP-2、MMP-9)活性。比较 PCP及细菌性肺炎其炎症反应及肺损伤的差别。PCP其 BAL F中细胞总数较阴性对照组增加 ( P<0 .0 1 ) ,但低于细菌性肺炎组。PCP其 BAL F中白蛋白 ( 62 2 .5± 484.0 μg/ ml)较阴性对照组增加 ( 3 5.8± 1 6.2 μg/ ml,P<0 .0 1 )。PCP其 BAL F中 AL P及 L DH活性 (分别为 2 1 7.0± 81 .4U/ L,2 0 .8± 8.2 U/ dl)也高于阴性对照组 ( P<0 .0 1 )。 PCP大鼠 BAL F中 型胶原酶活性增加 ( P<0 .0 0 1 )。PCP炎症发应不同于细菌性肺炎。在 PCP,肺泡毛细血管膜通透性明显增加 ,存在明显肺损伤
To investigate the inflammatory response and lung injury in Pneumocystis carinii pneumonia (PCP) rats, a PCP model of Sprague-Dawley rats was induced by immunosuppression with cortisone 8-12 weeks subcutaneously. The rats were divided into four groups: normal control (n = 6), healthy rats without medication; group: negative control (n = 6) rats without lung infection; group: bacterial pneumonia (n = 1 1); Group: PCP (n = 1 4). The numbers of total protein (TP), albumin (AL B) and ALP, L DH and Type collagenase (MMP-2, MMP-9) activity. Comparison of PCP and bacterial pneumonia, inflammatory response and lung injury differences. The total number of cells in BALF of PCP increased compared with the negative control group (P <0.01), but lower than that of bacterial pneumonia group. Albumin (62.25 ± 484.0 μg / ml) in BALF of PCP increased compared with the negative control group (5.8 ± 6.22 μg / ml, P <0.01). The ALP and L DH activities in BALF of PCP were also higher than those of the negative control group (21.07 ± 81.4U / L and 208.8.2U / dl, respectively) (P <0.01). BALP intermediate collagenase activity increased in PCP rats (P <0.01). PCP inflammation should be different from bacterial pneumonia. In PCP, alveolar capillary membrane permeability increased significantly, there was significant lung injury