Effects of estrogen on leukocyte adhesion after transient forebrain ischemia.
Effects of estrogen on leukocyte adhesion after transient forebrain ischemia.
复制标题
雌激素对短暂前脑缺血后白细胞粘附的影响。
DOI:
10.1161/01.str.31.9.2231
复制
发表时间:
2000
期刊:
影响因子:
8.3
通讯作者:
Pelligrino,DA
中科院分区:
文献类型:
--
作者:
Santizo,RA;Anderson,S;Ye,S;Koenig,HM;Pelligrino,DA
Background and Purpose—Recent findings indicate that estrogen (ie, 17β-estradiol [E2]) provides neuroprotection in models of transient global and focal ischemia. Enhanced postischemic leukocyte adhesion and infiltration have been linked to neuropathology in the brain as well as other tissues. We recently showed that estrogen reduces leukocyte adhesion in the cerebral circulation of female rats during resting conditions.Methods—We compared leukocyte adhesion in pial venules in vivo in intact, ovariectomized (OVX), and E2-treated OVX female rats subjected to transient forebrain ischemia (30-minute right common carotid artery occlusion and hemorrhagic hypotension) and reperfusion. Adherent rhodamine-6G–labeled leukocytes were viewed through a closed cranial window with the use of intravital microscopy. Leukocyte adhesion was measured before ischemia and at different times after reperfusion.Results—Before ischemia, leukocyte adhesion (measured as a percentage of venular area occupied by adherent leukocytes) was 2 to 3 times greater in OVX versus intact or E2-treated OVX rats (7.0%, 3.4%, and 2.2%, respectively). This difference disappeared at 120 minutes of reperfusion, when comparable levels of enhanced leukocyte adhesion were observed in all groups. In OVX rats, leukocyte adhesion remained elevated after 4 and 6 hours of reperfusion (11.6% and 12.9%, respectively), while the other 2 groups showed significantly lower levels (5.0% and 5.8% for intact rats and 7.0% and 7.2% for E2-treated OVX rats).Conclusions—Present results demonstrate that estrogen modulates leukocyte adhesion in the cerebral circulation after transient forebrain ischemia. This effect suggests that decreased leukocyte adhesion may be an important mechanism in estrogen-mediated neuroprotection.