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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

Damage to the gastrointestinal mucosa caused by ischemia - reperfusion is a significant clinical problem associated with various physiopathological conditions. Our group has conducted various studies in patients in critical conditions and in animal models to identify early damage to the gastric mucosa under ischemia using impedance spectroscopy. It is important to perform a quantitative histopathological analysis which can be linked to changes in impedance of the gastric mucosa under conditions of ischemia and I/R. Aim. To propose a tissue lesion index which considers pathological alterations inherent to the inflammatory process and cell damage which may be directly related to changes in impedance under conditions of ischemia and I/R. Methods. The animals were randomly distributed into 4 groups: control, ischemia (30 min), and I/R (30 and 60 min). Qualitative histopathological analysis was performed; the vascular area, glandular lumen area, the number of damaged cells, and the depth of the erosion were also quantified to obtain a scale to propose a tissue lesion index (TLI). Results. Under ischemic conditions, histopathological analysis showed edema and necrosis in epithelial cells, and vascular congestion. In I/R (30 and 60 min) conditions, areas of epithelial erosion were generated. Damage was classified based on the TLI. A TLI threshold of 3 showed a predictive value of tissue lesion. Conclusion. The proposed gastric lesion index allows us to objectively quantify and classify damage to the gastric mucosa produced by I/R.

Gastrointestinal ischemia/reperfusion (I/R) generates pathological alterations that could lead to death. Early ischemic damage markers could be used to guide therapy and improve outcomes. Aim. To relate hypoxia-inducible factor 1α (HIF-1α) activation and inducible nitric oxide synthase (iNOS) expression to gastric impedance changes due to I/R damage. Methods. Experimental animals were randomly distributed into 3 groups: control, ischemia (30 min) and I/R (60 min). Gastric ischemia was generated by celiac artery clamping for 30 min, and then blood flow was restored for 60 min. Impedance spectra and biopsies of the glandular portion were obtained for histological and immunohistochemical analyses. Immunodetection of both HIF-1α and iNOS was performed. Results. Under ischemia and I/R conditions, there was an increase (p