Abstract
ObjectiveWe aimed to review and discuss some of the latest research results related to post-burn pathophysiological changes and provide some clues for future study.BackgroundBurns are one of the most common and serious traumas and consist of a series of pathophysiological changes of thermal injury. Accompanied by thermal damage to skin and soft tissues, inflammatory mediators are released in large quantities. Changes in histamine, bradykinin, and cytokines such as vascular endothelial growth factor (VEGF), metabolic factors such as adenosine triphosphate (ATP), and activated neutrophils all affect the body’s vascular permeability.MethodsWe searched articles with subject words “microvascular permeability”, “burn” “endothelium”, and “endothelial barrier” in PubMed in English published from the beginning of database to Dec, 2020.ConclusionsThe essence of burn shock is the rapid and extensive fluid transfer in burn and non-burn tissue. After severe burns, the local and systemic vascular permeability increase, causing intravascular fluid extravasation, leading to a progressive decrease in effective circulation volume, an increase in systemic vascular resistance, a decrease in cardiac output, peripheral tissue edema, multiple organ failure, and even death. There are many cells, tissues, mediators and structures involved in the pathophysiological process of the damage to vascular permeability. Ulinastatin is a promising agent for this problem.
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