糖尿病酮症酸中毒家兔肺泡超微结构和细胞化学的研究-东南大学学报医学版

糖尿病酮症酸中毒家兔肺泡超微结构和细胞化学的研究

单位：东南大学医学院,附属南京第二医院,江苏,南京,210003

分类号：R378.21, R363.1

出版年·卷·期（页码）：2006·25·第四期（251-254）

摘要：

目的:研究糖尿病酮症酸中毒肺损伤的发病机制.方法: 实验组(DK组,n=6)给予四氧嘧啶(alloxen)150mg·kg-1和链脲佐菌素(STZ)150mg·kg-1,对照组(NS组,n=6)使用生理盐水,72h后行动脉血气分析,处死动物,取肺组织标本,做病理学检查,采用铅离子捕获法做常规超微结构、酸性磷酸酶(ACPase)细胞化学检查.结果:NS组血气分析正常;肺泡上皮细胞组织结构完整;溶酶体内ACPase活性表达,溶酶体结构完整.DK组体质量下降,动脉血气分析显示达到糖尿病酮症酸中毒标准;光镜可见肺泡内出血和肺泡隔的增厚、断裂;超微结构可见有肺泡上皮损伤、血管内有炎症细胞贴壁、肺泡内见炎症细胞等改变;肺泡上皮细胞内溶酶体形态不规则,细胞浆内有散在黑色酶颗粒,溶酶体数量增多.结论:糖尿病酮症酸中毒能引起肺上皮细胞组织结构损坏和细胞内溶酶体的破坏.

Objective To research the pathogenesis of type Ⅰ alveolar cells in rabbits with diabetic ketoacidosis(DKA).Methods Twelve male New Zealand rabbits were divided into experimental group(DK group,n=6) and control group(NS group,n=6).A combination of streptozocin(STZ,150()mg·kg^{-1}) and alloxan monohydroate(150()mg·kg^{-1}) was intravenously administered into the animals of the DK group;and the NS group was given the same dose of normal sodium chloride.The rabbits with DKA were survived at 72 hours after agent challenging.Blood gas and urine acetone were detected,then all the animals were killed.Ultrastructure detection by ionized lead capture method and cytohistochemical staining with acid phosphates(ACPase) in lungs were performed.Results Glucose concentration in the DKA rabbits was rising to 17()mmol·L^{-1},and urine acetone body was appeared.Haemorrhage in the alveolus,emphysema,thickening of alveolus walls,and exudation of inflammatory cells were shown in the DK group.The damages of alveolar epithelium and capillary endothelium were observed.The ACPase activity was localized in lysosome,and the increases of lysosomes in the DK group was shown compared with that in the NS group.Conclusion The damages of type Ⅰ alveolar cells and lososome illness and injuries of membrane organelles in alveolar epithelium are involved in the pathogenesis of DKA.

参考文献：

[1] ENGLISH P, WILLIAMS G. Hyperglycaemic crises and lactic acidosis in diabetes mellitus. 2004. doi:10.1136/pgmj.2002.004291
[2] HARRIS G D, FIORDALISI I, YU C. Maintaining normal intracranial pressure in a rabbit model during treatment of severe diabetic ketoacidemia. 1996(20). doi:10.1016/S0024-3205(96)00505-X
[3] LEWIS P R, KNIGHT D P. Cytochemical staining methods for electron microscopy, 1992
[4] 刘松平. 糖尿病肺损害. 国外医学(内分泌学分册)2004(5). doi:10.3760/cma.j.issn.1673-4157.2004.05.025
[5] RAYANI H H, GEWOLB I H. Glucose decreases steady state mRNA content of hydrophobic surfactant proteins B and C in fetal rat lung explants. 1999
[6] MOUSA K, ONADEKO B O, MUSTAFA H T. Technetium 99mTcDTPA clearance in the evaluation of pulmonary involvement in patients with diabetes mellitus. 2000(11). doi:10.1053/rmed.2000.0887
[7] 张宏, 白景文, 于振涛. 2型糖尿病患者慢性肺损伤的超微病理改变及临床意义. 解剖学报2005(6)
[8] LAFFEY J G, ENGELBERTS D, KAVANAGH B P. Buffering hypercapnic acidosis worsens acute lung injury. 2000(1)
[9] 顾小军, 常家宝, 朱晓云. 选择素在糖尿病酮症酸中毒肺损伤中的作用. 中国病理生理杂志2002(12)
[10] 殷国庆, 张运生, 钟备. 不同剂量5%苏打对脑膜炎双球菌感染性休克家兔心功能的影响. 南京铁道医学院学报1999(3)
[11] YIN G Q, QIU H B, DU K H. Endotoxic shock model with fluid resuscitation in Macaca mulatta, 2005

服务与反馈：

【文章下载】【发表评论】【查看评论】【加入收藏】

提示：您还未登录，请登录！点此登录