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The Interaction of Leukocytes and Adhesion Molecules in Mesenteric Microvessel Endothelial Cells after Internal Capsule Hemorrhage
Author(s) -
JIN XUELONG,
LI XIAOHUI,
ZHANG LIMIN,
ZHAO JIE
Publication year - 2012
Publication title -
microcirculation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.793
H-Index - 83
eISSN - 1549-8719
pISSN - 1073-9688
DOI - 10.1111/j.1549-8719.2012.00185.x
Subject(s) - microvessel , capsule , cell adhesion molecule , adhesion , mesentery , pathology , chemistry , medicine , microbiology and biotechnology , immunology , biology , immunohistochemistry , organic chemistry , botany
Please cite this paper as : Jin X‐L, Li X‐H, Zhang L‐M, Zhao J. The interaction of leukocytes and adhesion molecules in mesenteric microvessel endothelial cells after internal capsule hemorrhage. Microcirculation   19 : 539–546, 2012. Abstract Objective:  To explore the correlation between hemorheological variations and the expression of cell adhesion molecules in mesenteric microvessel endothelial cells after internal capsule hemorrhage. Methods:  We established an internal capsule hemorrhage model. Then leukocyte–endothelium interaction was observed and hemorheological variations in mesenteric microvessels were evaluated in the following aspects: blood flow volume, diameter of microvessels, blood flow rate, and shear rate. We also measured the expression of vascular cell adhesion molecule‐l and intercellular adhesion molecule‐1 (ICAM‐1) in mesenteric microvessel endothelial cells with immunohistochemistry stain. Results:  Leukocyte–endothelium interaction intensified after internal capsule hemorrhage. Besides, blood flow volume and velocity decreased, diameter narrowed, and shear rate reduced. Immunohistochemical staining of vascular cell adhesion molecule‐l and ICAM‐1in mesenteric microvessel endothelial cells was stronger. Conclusions:  VCAM‐1 and ICAM‐1 expression in mesenteric microvessels increased as a result of decreased wall shear stress in stress state following internal capsule hemorrhage, and then further shear stress change from interaction of enhanced production of CAMs and leukocytes created a vicious cycle of leukocytes margination, adhesion, and transmigration that could ultimately result in stress gastrointestinal ulcer.

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