Gut ischemia-reperfusion affects gut mucosal immunity: A possible mechanism for infectious complications after severe surgical insults*

Abstract

Despite the maintained mucosal immunoglobulin A level, gut I/R markedly reduces GALT cell numbers, with changes in lymphocyte phenotypes. These alterations may be associated with increased morbidity due to infectious complications after severe surgical insults.

Gut oxygenation and oxidative damage during and after laparoscopic and open left-sided colon resection: a prospective, randomized, controlled clinical trial

“…Increased release of reactive oxygen species also is responsible for impaired gut function, which might translate into clinical relevant delayed recovery of intestinal motility, decreased function of antimicrobial mechanisms, and increased microbial translocation, which may be responsible for infections after surgery [45][46][47][48][49]. Again, in large clinical trials LPS, colorectal resection has been constantly associated with a quicker recovery of bowel movement, a better barrier function, a more efficient humoral and cellular immune response, and a significant reduction of infectious complications than open operations, as partially confirmed by the present data [5][6][7][8][9].…”

Intestinal Ischemia-Reperfusion Injury Alters Purinergic Receptor Expression in Clinically Relevant Extraintestinal Organs

“…Many associated pathophysiologic phenomena have been studied, some of which have been implicated as possible mediators of the extra-intestinal organ dysfunction seen during progression of SIRS to multiple organ failure (MOF) (5,6). Areas currently under investigation include the activation of local immune cells (7), alteration of intestinal permeability with subsequent bacterial translocation (8), changes in the local-regional production of inflammatory mediators (9), production of reactive oxygen species (10), changes in coagulation (11), and alteration in the expression of cellular adhesion molecules (12). Despite the extensive efforts in this field of study, the proximal cause of MOF secondary to IIR-induced SIRS has yet to be clearly elucidated.…”

Effect of Glutamine on Intestinal Function in Critically Ill Patients

“…Однако большинством исследователей признается тот факт, что ки шечная флора и эндотоксины могут быть пусковым механиз мом и поддерживающим фактором развития синдрома систем ного воспалительного ответа, органной дисфункции у больных с нарушенной проницаемостью кишечной стенки. [10,41,42]. Нарушение кишечного барьера можно ожидать у всех больных, находящихся в критическом состоя нии [7,43], с массивными ожогами [3,5], после проведения ис кусственного кровообращения [14], с тяжелой политравмой [6], после трансплантации костного мозга [44] и у больных с циррозом печени на фоне хронического алкоголизма [19].…”