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Am J Physiol Heart Circ Physiol 273: H2721-H2725, 1997;
0363-6135/97 $5.00
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Vol. 273, Issue 6, H2721-H2725, December 1997

Postischemic endothelium-dependent vascular reactivity is preserved in adhesion molecule-deficient mice

Michael A. Banda, David J. Lefer, and D. Neil Granger

Department of Molecular and Cellular Physiology, Louisiana State University Medical Center, Shreveport, Louisiana 71130

Previous studies utilizing monoclonal antibodies directed against specific leukocyte-endothelial cell adhesion proteins have suggested that neutrophils mediate endothelial cell injury in a number of vascular beds after ischemia-reperfusion (I/R). In the present study, we investigated superior mesenteric artery (SMA) vascular reactivity to acetylcholine (ACh) and sodium nitroprusside (SNP) after occlusion and reperfusion in wild-type (C57BL/6) mice and in gene-targeted mice that are deficient in either CD11/CD18, intercellular adhesion molecule 1 (ICAM-1), or P-selectin. All mice were 4 wk of age, and the SMA was occluded for 45 min and then reperfused for 45 min. Segments of SMA were isolated and suspended in organ chambers and contracted with phenylephrine (10-5 M), and the maximal vasorelaxation to ACh (10-6 M) and SNP (10-6 M) was measured. SMA from sham-operated C57BL/6 mice relaxed 83.5 ± 3.3% to ACh and 91.7 ± 3.4% to SNP. In contrast, segments of SMA from C57BL/6 mice subjected to I/R demonstrated a marked impairment in vasorelaxation to ACh (51.3 ± 4.7%, P < 0.01 vs. sham) without any impairment in the vasoreactivity to SNP (86.1 ± 5.5%). In CD11/CD18-deficient mice, SMA reactivity to ACh (84.7 ± 2.3%) and SNP (91.2 ± 2.8%) was unaffected by I/R. Similarly, SMA rings from ICAM-1-deficient mice exhibited normal vasorelaxation to ACh and SNP with maximal vasorelaxation of 83.1 ± 2.9 and 87.4 ± 3.0%, respectively. We also observed profound preservation of endothelium-dependent vasorelaxation after I/R in P-selectin-deficient mice. These findings indicate that leukocyte-endothelial cell adhesion molecule deficiency is associated with the preservation of endothelium-dependent vascular responses after I/R.

P-selectin; intercellular adhesion molecule 1; CD11/CD18; neutrophils


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