[Research advances in mechanisms and detection methods of vascular endothelial barrier dysfunction in sepsis-induced organ injury].

Sepsis-induced multiple organ dysfunction syndrome (MODS) is the leading cause of mortality in critically ill patients, and widespread disruption of the vascular endothelial barrier represents the central pathological event. The integrity of the endothelial barrier is crucial for maintaining microcirculatory homeostasis. In sepsis, the dysregulated inflammatory response leads to a dramatic increase in microvascular permeability through multiple mechanisms, including endothelial cell activation, oxidative stress, disruption of intercellular junctions, degradation of the glycocalyx, and the promotion of immunothrombosis, ultimately driving organ failure. This review systematically elaborates on the mechanisms underlying vascular endothelial barrier injury across different organs (e.g., the lung, heart, intestine, kidney, and brain) in sepsis, with a particular focus on methodological advances in assessing barrier function, aiming to provide optimal detection strategies for various organs. By detailing universal techniques such as transendothelial electrical resistance (TEER) measurement, fluorescent tracer permeability assays, Evans Blue leakage, and intravital microscopy imaging, it further summarizes specific assessments for key target organs, including the lung, intestine, kidney, and brain. The importance of employing a multi-technique approach and multi-level validation for the comprehensive evaluation of barrier function is emphasized. Finally, this review synthesizes the methods for detecting the vascular endothelial barrier from different perspectives and discusses future directions for technological innovation and clinical translation. The overall goal of this review is to provide a systematic methodological reference and conceptual framework for in-depth research into the pathological mechanisms and therapeutic strategies targeting vascular endothelial dysfunction in sepsis-induced organ injury.