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Articles in PresS, published online ahead of print September 5, 2002
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00957.2001
Submitted on November 2, 2001
Accepted on August 16, 2002
1 Biomedical Engineering and Cardiovascular Research Center and Surgery, University of Virginia, Charlottesville, VA, USA
2 Medicine and Center for Blood Research, Harvard Medical School, Boston, MA, USA
* To whom correspondence should be addressed. E-mail: klausley{at}virginia.edu.
Estrogen increases nitric oxide (NO) production by inducing the activity of endothelial nitric oxide synthase (eNOS) (Simoncini et al, Nature 407:538, 2000). Ischemia (30 min) and reperfusion (I/R) increased the number of adherent leukocytes and decreased their rolling velocities in mouse cremaster muscle venules with a strong dependence on wall shear rate. Minimum rolling velocity at approximately 5 minutes after the onset of reperfusion was accompanied by increased P-selectin expression. This preceded the peak in leukocyte adhesion (at 10-15 minutes). In untreated WT mice, I/R caused a decrease of leukocyte rolling velocity from 37 to 26 µm/s and a 2.0-fold increase in leukocyte adhesion. Both were completely abolished by 0.25 mg estrogen i.p. 1 hour before surgery. In eNOS-/- mice, the decrease of leukocyte rolling velocity and increase in adhesion were similar, but were only marginally improved by estrogen. We conclude that the protective effect of estrogen, as measured by leukocyte rolling and adhesion, is significantly reduced in eNOS-/- mice, suggesting that induction of eNOS activity is the major mechanism of vasoprotection by estrogen in this model.
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