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Endothelial Cell Injury in Cardiovascular Surgery: Ischemia-Reperfusion
Edward M. Boyle, Timothy H. Pohlman, Carol J. Cornejo, Edward D. Verrier The Annals of Thoracic Surgery Volume 62, Issue 6, Pages (December 1996) DOI: /S (96)
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Fig. 1 Hypoxic endothelial cell activation. Hypoxia stimulates Weibel-Palade bodies to release P-selectin and activates NF-κB. NF-κB is translocated to the nucleus, where it promotes the transcription of E-selectin, intracellular adhesion molecule (ICAM), Tissue factor, interleukin-8 (IL-8) and interleukin-1 (IL-1). Interleukin-1 feeds back to promote more endothelial cell activation through the activation of NF-κB. The Annals of Thoracic Surgery , DOI: ( /S (96) )
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Fig. 2 Neutrophil adhesion is a multistep process that involves initial contact between the neutrophil and members of the selectin family of adhesion molecules (P-selectin, E-selectin) expressed on the activated endothelium. These low-affinity bonds result in rolling and slowing of the leukocytes. As this occurs the neutrophil becomes activated and a firm bond occurs between integrins on the leukocyte surface (ie, CD 1118) and adhesion molecules on the endothelium (ie, intracellular adhesion molecule-1, vascular cell adhesion molecule, platelet-endothelial cell adhesion molecule). (LPS = lipopolysaccharide.) The Annals of Thoracic Surgery , DOI: ( /S (96) )
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Fig. 3 The no-reflow phenomenon. Hypoxia results in activation of the endothelial cell layer that promotes leukocyte adhesion and degranulation, endothelial swelling, platelet activation, micothrombosis, and increased vasomotor tone. This contributes to impaired microcirculatory flow, despite what appears to be adequate perfusion through the large epicardial arteries. Adherent neutrophils infiltrate the underlying myocardium and promote lipid peroxidation, enzymatic degradation of membranes, calcium overload, and excitation contraction uncoupling. Collectively these events result in impaired myocardial function. The Annals of Thoracic Surgery , DOI: ( /S (96) )
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