Thrombosis and Altered expression of Intercellular Adhesion Molecule-1 (Icam-1) after Avulsion Injury in Rat Vessels

Abstract

This study was undertaken to characterize the relative degrees of arterial and venous trauma after graded avulsion injuries. Rat femoral arteries and veins were subjected to reproducible avulsion injuries using forces of between 60 and 220g. Thrombotic occlusion occurred at lower avulsion forces in veins than in arteries. Histologic and scanning electron microscopic analysis indicated increased endothelial disruption and exposed elastic lamina with increasing avulsion force in both vessels, but more prominently in arteries. Intercellular adhesion molecule-1 (ICAM-1) mRNA expression was evident at 3 and 6 hours after avulsion injury in veins, but only with higher avulsion-force injuries in arteries. ICAM-1 mRNA expression was not found in either vessel before or after this 3 to 6 hour post-injury interval. These results indicate that the amount of avulsion force to which traumatized extremity vessels are subjected has a direct effect on the degree of intimal injury and subsequent thrombosis.

Alterations in blood-brain barrier ICAM-1 expression and brain microglial activation after λ-carrageenan-induced inflammatory pain

“…Once stimulated, the endothelial cell undergoes a number of morphological changes, including increased surface expression of adhesion molecules, cytoskeletal reorganization, and activation of signaling pathways (5,17,37). A strong and repeatable correlation between induction of ICAM-1 and increased BBB permeability has been shown in a number of pathologies characterized by acute inflammation, including atherosclerosis, ischemia, human immunodeficiency virus encephalitis, and autoimmune disorders (4,19,38,47). Furthermore, loss of endothelial cell, tight junction proteins, occludin, and zonula occludens-1 was observed in cerebral vascular endothelium during neutrophil-induced BBB breakdown (1).…”

Stimulation of Nitric Oxide Production Contributes to the Antithrombotic Effect of Stromal Cell–Derived Factor-1α in Preventing Microsurgical Anastomotic Thrombosis

“…Vessels treated with SDF-1α showed less thrombosis adhering to the denuded vascular intima (►Fig. 5).…”

“…[1][2][3][4] Although there are multiple causes for failure of microsurgical anastomosis, intimal injury plays a critical role. 5 It has been demonstrated that end-to-end anastomosis results in widespread loss of intima. 6 Loss of intima following microsurgical anastomosis leads to exposure of subendothelial tissue and release of tissue factor, which initiates the process of thrombosis formation.…”

Association between Soluble Intercellular Adhesion Molecule-1 and Soluble Vascular Cell Adhesion Molecule-1 Levels and Left Atrial Thrombosis Gradation in Mitral Stenosis

“…Molekul adhesi yang bersirkulasi, seperti soluble intercellular adhesion molecule-1 (sVCAM-1) dan soluble vascular cell adhesion molecule-1 (sVCAM-1), telah terbukti meningkat pada pasien dengan SM. 7 Beberapa penelitian telah memaparkan asosiasi ICAM-1 dan VCAM-1 dengan proses dan kejadian trombosis [8][9][10] , namun belum pernah diteliti hubungan ICAM-1 dan VCAM-1 dengan trombosis atrium kiri pada SM. Pada perempuan.…”