Cheng Shi, He Sanguang, Zhang Jialin
Department of General Surgery, First Affiliated Hospital, China Medical University, Shenyang 110001, China.
Zhonghua Wai Ke Za Zhi. 2002 Aug;40(8):609-12.
To discuss the role of alveolar macrophage activation in rats with acute necrotizing pancreatitis (ANP) associated with lung injury.
30 adult Sprague-Dawley rats were randomly divided into five groups (n = 6): normal control group, one-hour group, three-hour group, six-hour group and twelve-hour group after ANP induction. ANP was induced by intraductal administration of 3% sodium taurocholate, while the normal control received an infusion of physiological saline. Alveolar macrophages were harvested by bronchoalveolar lavage. The protein content of lavage fluids, the myeloperoxidase of lung tissue (MPO), and tumor necrosis factor alpha (TNFalpha) and nitric oxide (NO) secreted by alveolar macrophages were examined. The expression of TNFalpha mRNA and inducible nitric oxide synthase (iNOS) mRNA was measured with reverse transcription-polymerase chain reaction technique. Histology of the lung and pancreas was scored in a blinded fashion.
Lung injury was gradually aggravated with disease progression. The level of myeloperoxidase of lung tissue and protein content of bronchoalveolar lavage fluids increased progressively and reached the peak at 12 hour [(10.78 +/- 0.58) U/g for MPO and (2 011.0 +/- 105.5) micro g/ml for protein respectively]. TNFalpha and NO secreted by alveolar macrophages were gradually elevated and peaked on the sixth hour, the maximums were (1 624.2 +/- 149.2) pg/ml and (88.8 +/- 6.5) micro mol/L respectively, but decreased on the twelfth hour. The expression of TNFalpha mRNA and iNOS mRNA was similar with the changes of TNFalpha and NO, upregulated after induction of acute necrotizing pancreatitis and reached their peaks on the sixth hour, then downregulated on the twelfth hour. All the parameters of ANP groups compared to control group were statistical significant (P < 0.05). The histology scores demonstrated an increasing damage of the lung. The expression of TNFalpha mRNA and iNOS mRNA is closely related to lung injury (r = 0.67 for TNFalpha mRNA and r = 0.64 for iNOS mRNA respectively, P < 0.01).
The activation of alveolar macrophage may play an important role in lung injury associated with acute necrotizing pancreatitis.
探讨肺泡巨噬细胞激活在急性坏死性胰腺炎（ANP）大鼠伴发肺损伤中的作用。
将30只成年Sprague-Dawley大鼠随机分为五组（n = 6）：正常对照组、ANP诱导后1小时组、3小时组、6小时组和12小时组。通过胰胆管内注射3%牛磺胆酸钠诱导ANP，而正常对照组输注生理盐水。通过支气管肺泡灌洗收集肺泡巨噬细胞。检测灌洗液的蛋白质含量、肺组织髓过氧化物酶（MPO）以及肺泡巨噬细胞分泌肿瘤坏死因子α（TNFα）和一氧化氮（NO）。采用逆转录-聚合酶链反应技术检测TNFα mRNA和诱导型一氧化氮合酶（iNOS）mRNA的表达。对肺和胰腺的组织学进行盲法评分。
随着疾病进展，肺损伤逐渐加重。肺组织髓过氧化物酶水平和支气管肺泡灌洗液蛋白质含量逐渐升高，并在12小时达到峰值[MPO为（10.78±0.58）U/g；蛋白质为（2011.0±105.5）μg/ml] 。肺泡巨噬细胞分泌的TNFα和NO逐渐升高，并在第6小时达到峰值，最大值分别为（1624.2±149.2）pg/ml和（88.8±6.5）μmol/L，但在第12小时下降 20 。TNFα mRNA和iNOS mRNA的表达与TNFα和NO的变化相似，在急性坏死性胰腺炎诱导后上调，并在第6小时达到峰值然后在第12小时下调。与对照组相比，ANP组的所有参数均具有统计学意义（P < 0.05）。组织学评分显示肺损伤加重。TNFα mRNA和iNOS mRNA的表达与肺损伤密切相关（TNFα mRNA的r = 0.67，iNOS mRNA的r = 0.64，P < 0.01）。
肺泡巨噬细胞的激活可能在急性坏死性胰腺炎相关的肺损伤中起重要作用。
