| | | | | 尾加压素受体拮抗剂对急性肺损伤的干预效应 | | | 梁子敬;赖荣德 | | | 目的探讨尾加压素受体拮抗剂(urotensin receptor antagonist,URA)对损伤肺的影响。方法健康SPF级Sprague Dawley(SD)大鼠49只,随机分为A、B、C三组:抽取7只注射生理盐水作为正常对照(A组);B、C两组各21只,二组所有大鼠用油酸复制急性肺损伤(acute lung injury,ALI)模型,B组为模型对照组,C组在模型基础上加用URA为干预组。三组均于注射后3h各抽动脉血作血气分析测定血氧分压,A组抽动脉血后全部活杀取肺,B、C两组分别于3(抽动脉血后)及12、24h三个时间段各取7只活杀取肺,右肺称湿重后烘干,左肺立即以中性福尔马林固定作病理切片。结果A组大鼠注射生理盐水后无异常表现,B、C两组注射油酸后均出现呼吸急促、活动减少或不合群、紫绀等表现,与A组相比,B、C两组动脉血氧分压(PaO2)明显下降(P<0.05),肺湿/干(W/D)比值明显升高(P<0.05),但A、B两组间差异无统计学意义(P>0.05)。C组活动能力改善较B组更快,肺组织病理符合急性肺损伤变化,随时间延长,炎症细胞、红细胞、肺水肿进行性加重,但C组红细胞渗出较B组有所减少。结论尾加压素受体拮抗剂可能对急性肺损伤动物肺损害有保护作用。 【作者单位】:广州医学院附属第一医院急诊科;广州医学院附属第一医院急诊科 【关键词】:急性肺损伤;尾加压素受体拮抗剂;肺湿/干重比;肺组织病理学变化 【基金】:广东省广州市教育局基金资助项目(1053) 【分类号】:R563.8 【DOI】:CNKI:SUN:JJYZ.0.2007-08-010 【正文快照】: ALI是临床上常见的急症,也是急性呼吸窘迫综合征(ARDS)的早期阶段,病情进展快,死亡率高,是目前研究热点之一。虽其确切发病机制不甚明确,多种细胞、细胞因子、炎症介质形成的效应网络相互作用导致ALI/ARDS发病,是目前广为认可的机制[1]。研究发现,血管活性物质在ALI发病过程中也起着一定的作用,血管活性物质尾加压素Ⅱ(urotensinⅡ,UⅡ)在ALI血浆及支气管肺泡灌洗液中明显升高[2-3]。本研究使用尾加压素受体拮抗剂对油酸型ALI模型进行干预,探讨其在ALI中的作用。1材料与方法1.1实验动物及器材1.1.1实验动物SPF级健康SD大鼠49只… | | | 推荐 CAJ下载 PDF下载 | | | CAJViewer7.0阅读器支持所有CNKI文件格式,AdobeReader仅支持PDF格式 | | | | Effect of urotensin receptor antagonist om acute lung injury | | | LIANG Zi-jing;LAI Rong-de.Emergency Medicine Department;The First Affiliated Hospital of Guangzhou Medical College;Guangzhou 510120;China | | | Objective To investigate the effect of urotensin receptor antagonist(URA) to the damaged lung of acute lung injury(ALI). Method Forty-nine specified-pathogens free(SPF) grade Sprague Dawley(SD)rats were randomly divided into three groups:seven for group A,as normal group;the other forty two rats were divided into group B and C,twenty one rats in each group.Rats of group A were injected with normal saline as control group.Group B and C were injected with oleic acid as model group,and group C injected with URA.Three hours after injection,artery blood were drawn for blood gas analysis in all rats.All rats of group A were killed,and seven in group B and group C were killed after artery blood were taken,then another seven at twelve hours in both group B and C were killed.The rest rats of group B and group C at twenty four hours were killed.Lung tissue was taken for pathology analyse in all rats. Result Rats in group A was normal after injection.Breathless,activity reducing,misfit, cyanosis appeared in both group B and group C.Compared with group A,oxygen pressure of artery blood(PaO2) was reduced significantly(P<0.05),wet/dry ratio(W/D) was increased(P<0.05),but there was no significant difference in group B and group C(P>0.05).With time prolonged,inflammation cell and red blood cell(RBC) exudated out of alveolar,lung edema aggravated progressively,exudation of RBC was less in alveolar and lung interstitial group C than group B. Conclusions Urotensin receptor antagonist maybe have some protective function on the damaged lung of ALI. 【Keyword】:Acute lung injury;Urotensin receptor antagonist;Wet/dry ratio;Morphologic changes of lung |
| | | | | | 1 | Q i J,Du J,Tang X,et al; The upregu lation of endotheli-al n itric oxide synthase and urotensin-Ⅱis assoc iatedw ith pu lmonary hypertension and vascu lar d iseases in ratsproduced by aortocaval shunting[J] [M];Heart Vessels; 2004年 | | 2 | Gendron G,Simard B,Gobeil FJ,et al; Human urotensin-Πenhances plasma extravasationinspecific vascular districtsin Wistar rats[J] [M];Can J Physiol Pharmacol; 2004年 | | 3 | Vergura R,Camarda V,Rizzi A,et al; UrotensinⅡstimulates plasma extravasationin mice via UTreceptor activation[J] [M];Naunyn Schmiedebergs Arch Pharmacol; 2004年 | | 4 | Johns DG,Ao Z,Naselsky D,et al; Urotensin-II-mediated cardiomyocyte hypertrophy:effect of receptor antagonism and role of inflammatory mediators[J] [M];Naunyn Schmiedebergs Arch Pharmacol; 2004年 | | 5 | Levy BD,Shapiro SD; Acute respiratory distress syndrome[M] [M];Harrison‘s Principles of Internal Medicine; 2005年 | | 6 | Ames RS,Sarau HM,Chambers JK,et al; Human uro-tensin-Ⅱis a potent vasoconstrictor and agonist for the orphan receptor GPR14[J] [M];Nature; 1999年 | | 7 | Le Mevel JC,Olson KR,Conklin D,et al; Cardiovescular actions of trout urotensinΠinthe conscious trout,Oncorhychus mykiss[J] [M];Am J Physiol; 1996年 | | 8 | Itoh H, Itoh Y, Rivier J, et al; Contraction of major artery segments of rat by fish neuropeptide urotensin II [M];American Journal of Physiology; 1987年 | | 9 | Russell FD; Emergingroles of urotensin-Ⅱincardiovascular disease[J] [M];Pharmacol Ther; 2004年 | | 10 | Birker-Robaczewska M,Boukhadra C,Studer R,et al; The expression of urotensinΠreceptor[U2R]is up-regulated byinterferon-gamma[J] [M];J Recept Signal Transduct Res; 2003年 |
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| | | | | | 1 | 邱海波,蒋雄斌,周韶霞,郑杰,窦国祥; TH1/TH2平衡变化在急性肺损伤中的意义 [A];2001年全国中西医结合急救医学学术会议论文集 [C]; 2001年 | | 2 | 张畔,刘剑虹,王兵; 一氧化碳中毒并发急性肺损伤的临床研究 [A];2001年全国中西医结合急救医学学术会议论文集 [C]; 2001年 | | 3 | 刘斌剑; LPS所致急性肺损伤时小鼠肺组织病理变化及其与KGFR表达水平的关系 [A];2004第二届世界华人临床生化和检验医学大会第六届全国检验医学学术会议论文汇编 [C]; 2004年 | | 4 | 于化鹏,王继承,邓火金,樊慧珍,杜江; 急性肺损伤大鼠肺组织结构及Cx26表达的变化 [A];中华医学会第七次全国呼吸病学术会议暨学习班论文汇编 [C]; 2006年 | | 5 | 杨丽丽,刘志,戢新平,刘刚,关福兰; 急性肺损伤动物模型在高CO_2通气时病理生理指标变化的研究 [A];2003全国SARS防治学术交流会论文集 [C]; 2003年 | | 6 | 孙海晨,聂时南,邵旦兵,钱晓明,唐文杰,许宝华,吴学豪; 内毒素诱导小鼠急性肺损伤早期基因表达谱的研究 [A];第十一次全国急诊医学学术会议暨中华医学会急诊医学分会成立二十周年庆典论文汇编 [C]; 2006年 | | 7 | 蔡培泉; 毒性气体致急性肺损伤8例报导 [A];2000年全国危重病急救医学学术会议论文集 [C]; 2000年 | | 8 | 于化鹏,王继承,邓火金,陈新,樊慧珍; 急性肺损伤大鼠紧密连接的改变及Claudin-3表达的变化 [A];中华医学会第七次全国呼吸病学术会议暨学习班论文汇编 [C]; 2006年 | | 9 | 祝胜美,张红刚; 输血相关性急性肺损伤 [A];2004年浙江省麻醉学学术年会论文汇编 [C]; 2004年 | | 10 | 赵金垣; 活性氧是化学性急性肺损伤(ALI)的启动因子 [A];中华预防医学会第二届学术年会暨全球华人公共卫生协会第二届年会论文集 [C]; 2006年 |
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