1 Introduction
Heat stroke is identified as multi-organ dysfunction syndrome (MODS) secondary to systemic inflammatory response (SIRS) triggered by hyperthermia,1, 2 with mortality reached 63.2% under intensive care. 3 Recent studies indicate that the host inflammatory response and coagulatory disorder secondary to heat stroke are associated with MODS. 4 A large number of proinflammatory factors and cytokines are released as a result of the excessive activation of leukocytes and endothelial cells, which led to continuous and intense inflammatory injury. 5, 6 On the other hand, microcirculation of tissues and organs secondary to vascular endothelial injury contributed to ischemia, hypoxia and metabolic disorders of tissues and organs, and further worsen and exacerbated inflammatory response. 7, 8 Taken together, it is suggested that vascular endothelial injury, circulatory dysfunction and SIRS are closely related, which drives severe heat stroke to MODS development.
Endothelial glycocalyx, an important structure of vascular endothelial surface, maintained the structural and functional stability of endothelium effectively and prevented the adhesion of inflammatory cells. 9 Imbalance between synthesis and degradation of glycocalyx caused structural and functional damages, and further aggravated vascular endothelial and tissue injury via mediating adhesion between inflammatory and endothelial cells. Shreds of evidence have demonstrated that vascular endothelium dysfunction induced by glycocalyx injury was the key factor that magnified the inflammatory response in sepsis and promoted SIRS to MODS. 10, 11 Additionally, glycocalyx is known to induce acute lung injury (ALI) or adult respiratory distress syndrome via accelerating leukocyte adhesion.12, 13
Hyperthermia may facilitate the leakage of lipopolysaccharide (LPS) from the intestine to the systemic circulation early, which excessively activates endothelial cells to exaggerate the inflammatory and coagulation responses. 1 Our previous studies suggested that mesenteric lymph played critical roles in the pathogenesis of endothelium injury in heats stroke rats.7 Several evidence indicated that high LPS levels were investigated in the portal vein and systemic circulation in patients with heat stroke and animal models. 14 Collectively, in the present study, Human pulmonary microvascular endothelial cell (HPMEC) was explored to observe the injury characteristic of vascular endothelial glycocalyx under heat stress combined with LPS double hitsin vitro .