摘要
目的:探讨实验性急性胰腺炎(acute pancreatitis,AP)合并肺损伤的发生机制及前列腺素E1(PGE1)的保护作用．方法:健康成年SD大鼠78只,随机平均分为假手术组(SO组)、AP组和PGE1组,采用十二指肠闭袢法建立大鼠AP模型．PGE1组制模后即刻经颈静脉持续每分钟输入PGE160 ng／kg．观察胰腺和肺组织的病理组织学改变,测定血清淀粉酶、肺组织中性粒细胞髓过氧化物酶 (MPO)活性、脂质过氧化产物(LPO)水平及肺毛细血管通透性(LCP),免疫组织化学ABC法检测肺组织细胞黏附分子-1(ICAM-1)的表达．结果:制模后12和24 h,AP组大鼠胰腺和肺组织病理损伤持续加重,肺组织MPO(12 h: 5．65±0．80 vs 1．22±0．71 kat／g,P<0．01;24 h: 7．22±1．05 vs 1．48±0．57 kat／g,P<0．01)和 LPO(12 h:1．44±0．63 vs 0.38±0．07μmol／g． P<0．01;24 h:3．64±0．83 vs 0．44±0．15 μmol／ g,P<0．01)水平以及LCP(12 h:145．4±23．0 vs 47．3±5．5 μg／g组织湿重,P<0．01)明显高于SO组,AP组大鼠肺组织ICAM-1表达呈阳性或强阳性,而SO组呈阴性;与AP组比较, PGE1组的胰腺病理损伤虽未减轻,但肺组织 MPO(12 h:2．96±1．04 vs 5．65±0．80 kat／g, P<0．05;24 h:3．68±1．15 vs 7．22±1．05 kat／g, P<0．05)和LPO (12 h:0．86±0.34 vs 1．44± 0．63 μmol／g,P<0．05;24 h:1．69±0．45 vs 3．64 ±0．83 μmol／g,P<0．05)水平以及LCP(12 h: 105．9±23．9 vs 145．4±23．0 μg／g组织湿重, P<0．05)明显降低,ICAM-1表达下调．肺间质出血、水肿和中性粒细胞(PMN)浸润明显减轻．结论:肺组织ICAM-1过度表达、PMN浸润和氧自由基大量释放与AP早期肺损伤的发生关系密切．PGE1通过降低肺组织ICAM-1表达, 抑制PMN活化和氧自由基释放,从而减轻AP 早期肺损伤．
AIM： To explore the mechanism of lung injury in experimental acute pancreatitis （AP） and the protective effect of prostaglandin E1 （PGE1）.
METHODS： Seventy-eight rats were averagely and randomly divided into sham operation, AP, and PGE1 group. AP model was induced by creating a closed duod enal loop in rats. The rats in PGE1 group were intravenously injected with PGE1 （60 ng/kg）. The histopathological changes of pancreatic and pulmonary tissues were examined by microscopy. The serum level of amylase, the activity of myeloperoxidase （MPO）, the pulmonary level of lipid peroxidation （LPO）, and lung capillary permeability （LCP） were measured. The expression of pulmonary intercellular adhesion molecule-1 （ICAM-1） was determined by immunohistochemical technique （ABC）.
RESULTS： In AP group, the progressive pathological damages in the pancreas and lung tissues were clearly observed. The activity of pulmonary MPO （12 h： 5.65 ± 0.80 vs 1.22 ± 0.71 kat/g, P 〈 0.01; 24 h： 7.22 ± 1.05 vs 1.48 ± 0.57 kat/g, P 〈 0.01）, the level of LPO （12 h： 1.44 ± 0.63 vs 0.38 ± 0.07μmol/g, P 〈 0.01; 24 h： 3.64 ± 0.83 vs 0.44 ± 0.15 μmol/g, P 〈 0.01） and LCP （12 h： 145.4 ± 23.0 vs 47.3 ± 5.5 μg/g wet weight, P 〈 0.01）, as well as pulmonary ICAM-1 expression were markedly increased as compared with those in sham operation group. In comparison with those in AP group, the activity of MPO （12 h： 2.96 ± 1.04 vs 5.65 ± 0.80 kat/g, P 〈 0.05; 24 h： 3.68 ± 1.15 vs 7.22 ± 1.05 kat/g, P 〈 0.05） and the level of LPO （12 h： 0.86 ± 0.34 vs 1.44 ± 0.63 μmol/g, P 〈 0.05; 24 h： 1.69 ± 0.45 vs 3.64 ± 0.83 μmol/g, P 〈 0.05） in the lung tissues were significantly decreased, and the level of LCP （12 h： 105.9 ± 23.9 vs 145.4 ± 23.0 μg/g wet weight, P 〈 0.05）, as well as pulmonary ICAM-1 expression was down-regulated （12 h： P 〈 0.05; 24 h： P 〈 0.01） in PGE1 group. Pathological examination revealed that intra-alveolar hemorrh
出处
《世界华人消化杂志》
CAS
北大核心
2006年第17期1688-1692,共5页
World Chinese Journal of Digestology
关键词
急性胰腺炎
肺损伤
前列腺素E1
细胞间
黏附分子-1
中性粒细胞
氧自由基
Acute pancreatitis
Lung injury
Prosotaglandin E1
Intercellular adhesion molecule-I
Polymorphonuclear leukocytes
Free oxygen radicals
