Key result
Balloon injury in rabbit subclavian arteries abolished leukocyte-induced contraction and enhanced leukocyte adhesiveness (1.7 and 1.8 fold at 24 and 48 h), correlating with upregulated adhesion molecules.
Why the study?
Does balloon injury alter leukocyte adhesion and contraction in rabbit subclavian arteries?
Does balloon injury alter leukocyte adhesion and contraction in rabbit subclavian arteries?
Balloon angioplasty induces upregulation of adhesion molecules and enhances leukocyte adhesion and migration into the injured vessel wall in a rabbit model.
No immediate clinical implications for angioplasty; extends rabbit model data on adhesion molecules but leaves open human translation.
The aim of this study was to examine the changes in leukocyte adhesion and leukocyte-induced contraction in balloon-injured rabbit subclavian artery and to correlate these changes with vessel morphology and expression of adhesion molecules on the injured arteries. 2. Rabbits were anaesthetized and their left subclavian arteries were injured by balloon inflation and withdrawal followed by sacrifice at 2, 24, 48 h or 8 days after injury. The left and right subclavian arteries were removed and leukocytes were isolated from autologous rabbit blood. Leukocyte-induced contraction was measured in 5-HT precontracted artery rings and leukocyte adhesion was measured using (51)Cr-labelled leukocytes. Immunocytochemistry using paraffin-embedded tissue was employed to detect changes in the expression of adhesion molecules on injured arteries. 3. Autologous leukocytes caused a contraction of rabbit subclavian artery rings, which was prevented by L-NAME (10(-3) M). Balloon-induced injury abolished the contractile response to leukocytes, which correlated with loss of carbachol-induced relaxation 4. Balloon injury markedly enhanced the adhesiveness of the subclavian artery for leukocytes, most notably at 24 and 48 h after injury (1.7 and 1.8 fold respectively). Increased leukocyte adhesion at these two time points correlated with an upregulation of E-selectin, P-selectin and VCAM-1 expression on the remaining endothelium of the injured artery. 5. Vessel morphology revealed that balloon inflation had induced an infiltration of inflammatory cells into the vessel wall, the greatest increase being seen at 24 h after injury. 6. It is concluded that an increase in the expression of E-selectin, P-selectin and VCAM-1 following balloon-induced injury leads to enhanced leukocyte adhesion and migration into the injured vessel.
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Kennedy et al. (2000) studied Balloon-injured rabbit subclavian artery. Balloon injury (inflation and withdrawal) vs. Uninjured arteries was evaluated on Leukocyte adhesion and leukocyte-induced contraction. Balloon injury in rabbit subclavian arteries abolished leukocyte-induced contraction and enhanced leukocyte adhesiveness (1.7 and 1.8 fold at 24 and 48 h), correlating with upregulated adhesion molecules.
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