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 .