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Ultrastructural Alteration of Pulmonary Capillary Endothelial Glycocalyx During Endotoxemia
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A1843 - Ultrastructural Alteration of Pulmonary Capillary Endothelial Glycocalyx During Endotoxemia
Author Block: R. Zaikokuji1, H. Okada2, G. Takemura3, K. Suzuki2, R. Inagawa2, C. Takada2, H. Yano2, I. Muraki2, Y. Kakino2, T. Yoshida2, S. Yoshida2, H. Ushikoshi2, S. Ogura2; 1Biofunctional Analysis, Gifu Pharmaceutical University, Gifu, Japan, 2Emergency and Disaster Medicine, Gifu University Graduate School of Medicine, Gifu, Japan, 3Internal Medicine, Asahi University School of Dentistry, Gifu, Japan.
Rationale: The most recent diagnostic criteria for sepsis includes organ failure. Microvascular endothelial injury is thought to lead to the multiple organ failure seen in sepsis, although the precise mechanism is still controversial. Acute respiratory distress syndrome (ARDS) is the primary complication during the sequential development of multiple organ dysfunction in sepsis, and endothelial injury is deeply involved. Sugar-protein glycocalyx coats all healthy vascular endothelium, and its disruption is one factor thought to contribute to microvascular endothelial dysfunction during sepsis. Objectives: To observe the three-dimensional ultrastructural alterations in the pulmonary capillary endothelium, including the glycocalyx, during sepsis-induced pulmonary vasculitis. Methods: We investigated the three-dimensional ultrastructure of pulmonary vascular endothelial glycocalyx in a mouse lipopolysaccharide-induced endotoxemia model. Lungs were fixed with lanthanum-containing alkaline fixative to preserve the glycocalyx. Measurements and Main Results: On both scanning and transmission electron microscopy, the capillary endothelial glycocalyx appeared as a moss-like structure entirely covering the endothelial cell surface in normal mice. In the septic lung after liposaccharide injection, however, this structure was severely disrupted, appearing to be peeling away and coagulated. In addition, syndecan-1 levels were significantly reduced in the septic lung, and numerous spherical structures containing glycocalyx were observed on the endothelial surface. Conclusions: It appears endothelial glycocalyx in the lung is markedly disrupted under experimental endotoxemia conditions. This supports the notion that disruption of the glycocalyx is causally related to the microvascular endothelial dysfunction characteristic of sepsis-induced ARDS.
Author Block: R. Zaikokuji1, H. Okada2, G. Takemura3, K. Suzuki2, R. Inagawa2, C. Takada2, H. Yano2, I. Muraki2, Y. Kakino2, T. Yoshida2, S. Yoshida2, H. Ushikoshi2, S. Ogura2; 1Biofunctional Analysis, Gifu Pharmaceutical University, Gifu, Japan, 2Emergency and Disaster Medicine, Gifu University Graduate School of Medicine, Gifu, Japan, 3Internal Medicine, Asahi University School of Dentistry, Gifu, Japan.
Rationale: The most recent diagnostic criteria for sepsis includes organ failure. Microvascular endothelial injury is thought to lead to the multiple organ failure seen in sepsis, although the precise mechanism is still controversial. Acute respiratory distress syndrome (ARDS) is the primary complication during the sequential development of multiple organ dysfunction in sepsis, and endothelial injury is deeply involved. Sugar-protein glycocalyx coats all healthy vascular endothelium, and its disruption is one factor thought to contribute to microvascular endothelial dysfunction during sepsis. Objectives: To observe the three-dimensional ultrastructural alterations in the pulmonary capillary endothelium, including the glycocalyx, during sepsis-induced pulmonary vasculitis. Methods: We investigated the three-dimensional ultrastructure of pulmonary vascular endothelial glycocalyx in a mouse lipopolysaccharide-induced endotoxemia model. Lungs were fixed with lanthanum-containing alkaline fixative to preserve the glycocalyx. Measurements and Main Results: On both scanning and transmission electron microscopy, the capillary endothelial glycocalyx appeared as a moss-like structure entirely covering the endothelial cell surface in normal mice. In the septic lung after liposaccharide injection, however, this structure was severely disrupted, appearing to be peeling away and coagulated. In addition, syndecan-1 levels were significantly reduced in the septic lung, and numerous spherical structures containing glycocalyx were observed on the endothelial surface. Conclusions: It appears endothelial glycocalyx in the lung is markedly disrupted under experimental endotoxemia conditions. This supports the notion that disruption of the glycocalyx is causally related to the microvascular endothelial dysfunction characteristic of sepsis-induced ARDS.
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