Bioelectric, tissue, and molecular characteristics of the gastric mucosa at different times of ischemia

Abstract

Gastrointestinal ischemia may be presented as a complication associated with late shock detection in patients in critical condition. Prolonged ischemia can cause mucosal integrity to lose its barrier function, triggering alterations that can induce organ dysfunction and lead to death. Electrical impedance spectroscopy has been proposed to identify early alteration in ischemia-induced gastric mucosa in this type of patients. This work analyzed changes in impedance parameters, and tissue and molecular alterations that allow us to identify the time of ischemia in which the gastric mucosa still maintains its barrier function. The animals were randomly distributed in four groups: Control, Ischemia 60, 90, and 120 min. Impedance parameters were measured and predictive values were determined to categorize the degree of injury using a receiver operating characteristic curve. Markers of inflammatory process and apoptosis (iNOS, TNFα, COX-2, and Caspase-3) were analyzed. The largest increase in impedance parameters occurred in the ischemia 90 and 120 min groups, with resistance at low frequencies (RL) and reactance at high frequencies (XH) being the most related to damage, allowing prediction of the occurrence of reversible and irreversible tissue damage. Histological analysis and apoptosis assay showed progressive mucosal deterioration with irreversible damage ( p < 0.001) starting from 90 min of ischemia. Furthermore, a significant increase in the expression of iNOS, TNFα, and COX-2 was identified in addition to apoptosis in the gastric mucosa starting from 90 min of ischemia. Tissue damage generated by an ischemia time greater than 60 min induces loss of barrier function in the gastric mucosa.

Pharmacological targeting of gastric mucosal barrier with traditional Chinese medications for repairing gastric mucosal injury

“…Subsequently, most focal injuries tend to occur within the interior of the epithelium, where broken blood vessels are more prevalent due to the dysregulation of vascular endothelial cells (ECs), resulting in reduced GMBF, ischaemia, hypoxia and tissue necrosis. Relevant studies have indicated that tissue damage caused by ischemia lasting for more than 60 min induces the loss of barrier function in the GM ( Eduardo, et al, 2021 ). And the damaging agents that accompany with GMBF can reach the lamina propria, causing gastric hydrochloric acid-related disorders mediated by parietal cells that penetrate into the interior of the lamina propria.…”