Life and death at the mucosal-luminal interface: New perspectives on human intestinal ischemia-reperfusion

Abstract

Intestinal ischemia is a frequently observed phenomenon. Morbidity and mortality rates are extraordinarily high and did not improve over the past decades. This is in part attributable to limited knowledge on the pathophysiology of intestinal ischemia-reperfusion (IR) in man, the paucity in preventive and/or therapeutic options and the lack of early diagnostic markers for intestinal ischemia. To improve our knowledge and solve clinically important questions regarding intestinal IR, we developed a human experimental intestinal IR model. With this model, we were able to gain insight into the mechanisms that allow the human gut to withstand short periods of IR without the development of severe inflammatory responses. The purpose of this review is to overview the most relevant recent advances in our understanding of the pathophysiology of human intestinal IR, as well as the (potential) future clinical implications.

Gut-training: the impact of two weeks repetitive gut-challenge during exercise on gastrointestinal status, glucose availability, fuel kinetics, and running performance

“…Epithelial injury is a key feature of exercise-induced gastrointestinal syndrome, which appears to originate from splanchnic hypoperfusion and subsequent gastrointestinal ischaemia (Evennett et al 2009;Grootjans et al 2016;ter Steege and Kolkman 2012;van Wijck et al 2011;van Wijck et al 2012). Despite evidence of increased epithelial injury after GC1 (144%) and GC2…”

“…The cause/s of gastrointestinal symptoms during running appear to be multifactorial in origin and stem from 'exercise-induced gastrointestinal syndrome', in which the primary driving D r a f t 5 factors are: 1) splanchnic hypoperfusion and subsequent intestinal epithelial injury, increased intestinal permeability, systemic responses (i.e., endotoxaemia and cytokinaemia), and impaired intestinal nutrient absorption; and 2) stress induced increases in sympathetic drive and subsequent reductions in enteric nervous system activity, which alters intestinal motility and absorption capacity (Gill et al 2015a;Gill et al 2015b;Grootjans et al 2016;Leipers 2015;ter Steege and Kolkman 2012;van Wijck et al 2012). …”

Type Three Secretion System-Dependent Microvascular Thrombosis and Ischemic Enteritis in Human Gut Xenografts Infected with Enteropathogenic Escherichia coli

“…3C to E, black arrows). The detachment of sheets of epithelial cells together from the villi is a known characteristic of acute gut ischemia (10). None of the xenografts infected with the ΔescV mutant organisms demonstrated the abovedescribed pathological lesions, as indicated by the histological score (Fig.…”

The Unpredictably Deadly Twist: A Case of Acute Mesenteric Ischaemia after Successful Gastrectomy

“…The subsequent loss of fluids into the intestinal lumen causes hypotension until real shock. Moreover, the same intestinal necrosis will push intestinal bacteria to translocate from bowel lumen to systemic blood flow, giving origin, in the end, to a septic shock [3][4][5].…”

“…Untreated, AMI will trigger the sequence of events that passes through mesenteric infarction, intestinal necrosis, sepsis and, eventually, death. An early recognition and a prompt intervention may halt and reverse this process optimizing recovery, whereas a late diagnosis, done after intestinal necrosis has developed, is the main responsible for the high mortality of the disease [1,3,4].…”