Mihai Oltean, Jasmine Bagge, Anna Casselbrant, Andreas Lundgren, Lucas Ferreira da Anunciação, Lucia de Miguel Gomez, Tomas Lorant, Mats Hellström, Michael Olausson
{"title":"Intestinal mucosal perfusion and integrity are maintained in hypotensive brain dead mice.","authors":"Mihai Oltean, Jasmine Bagge, Anna Casselbrant, Andreas Lundgren, Lucas Ferreira da Anunciação, Lucia de Miguel Gomez, Tomas Lorant, Mats Hellström, Michael Olausson","doi":"10.1159/000540020","DOIUrl":null,"url":null,"abstract":"<p><p>Brain death (BD) leads to complex hemodynamic and inflammatory alterations which may compromise organ perfusion and induce morphologic and functional damage in various organs. The intestine is particularly sensitive to hypoperfusion and donor hypotension usually precludes intestinal donation. Previous studies reported inflammatory intestinal changes following BD but information on mucosal integrity and perfusion are lacking. BD was induced in mice by inflating an epidural balloon catheter. Controls underwent only anesthesia and tracheostomy. Intestinal perfusion was assessed using laser Doppler flowmetry (LDF). Intestinal injury was assessed after 2h of BD by the Chiu-Park score and morphometry. Intestinal tight junction (TJ) proteins (claudin-1, claudin-3, occludin, tricellulin) as well as inflammatory activation (intercellular adhesion molecule-1, vascular cell adhesion molecule-1, and interleukin-6) were also analysed and compared with a sham group. Although blood pressure decreased in BD mice, intestinal perfusion remained similar between BD and sham mice. Histologically, mucosal injury was absent/minimal and TJs appeared well maintained in both groups. BD may trigger intrinsic, autoregulatory mechanisms to preserve microvascular tissue perfusion and mucosal integrity in spite of mild hypotension.</p>","PeriodicalId":12222,"journal":{"name":"European Surgical Research","volume":" ","pages":""},"PeriodicalIF":1.7000,"publicationDate":"2024-06-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"European Surgical Research","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1159/000540020","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"SURGERY","Score":null,"Total":0}
引用次数: 0
Abstract
Brain death (BD) leads to complex hemodynamic and inflammatory alterations which may compromise organ perfusion and induce morphologic and functional damage in various organs. The intestine is particularly sensitive to hypoperfusion and donor hypotension usually precludes intestinal donation. Previous studies reported inflammatory intestinal changes following BD but information on mucosal integrity and perfusion are lacking. BD was induced in mice by inflating an epidural balloon catheter. Controls underwent only anesthesia and tracheostomy. Intestinal perfusion was assessed using laser Doppler flowmetry (LDF). Intestinal injury was assessed after 2h of BD by the Chiu-Park score and morphometry. Intestinal tight junction (TJ) proteins (claudin-1, claudin-3, occludin, tricellulin) as well as inflammatory activation (intercellular adhesion molecule-1, vascular cell adhesion molecule-1, and interleukin-6) were also analysed and compared with a sham group. Although blood pressure decreased in BD mice, intestinal perfusion remained similar between BD and sham mice. Histologically, mucosal injury was absent/minimal and TJs appeared well maintained in both groups. BD may trigger intrinsic, autoregulatory mechanisms to preserve microvascular tissue perfusion and mucosal integrity in spite of mild hypotension.
期刊介绍:
''European Surgical Research'' features original clinical and experimental papers, condensed reviews of new knowledge relevant to surgical research, and short technical notes serving the information needs of investigators in various fields of operative medicine. Coverage includes surgery, surgical pathophysiology, drug usage, and new surgical techniques. Special consideration is given to information on the use of animal models, physiological and biological methods as well as biophysical measuring and recording systems. The journal is of particular value for workers interested in pathophysiologic concepts, new techniques and in how these can be introduced into clinical work or applied when critical decisions are made concerning the use of new procedures or drugs.