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首页> 外文期刊>Journal of Cerebral Blood Flow and Metabolism: Official Journal of the International Society of Cerebral Blood Flow and Metabolism >Estrogen restores postischemic sensitivity to the thromboxane mimetic U46619 in rat pial artery.
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Estrogen restores postischemic sensitivity to the thromboxane mimetic U46619 in rat pial artery.

机译：雌激素可恢复大鼠胸动脉对血栓烷模拟物U46619的缺血后敏感性。

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摘要

The objectives of the study were to (1) characterize the dose-response relationship to the TXA2 analog, U46619 (0.01, 0.1, and 1 micromol/L) after global cerebral ischemia, (2) determine whether chronic 17beta-estradiol (E2) replacement alters this relationship, and (3) determine if E2's mechanisms are transduced through cognate estrogen receptors. Rats were assigned to five groups (n=6): placebo-implanted ovariectomized (OVX) females, OVX plus chronic E2 (CE), OVX plus acute E2 (AE), OVX plus chronic E2 plus the estrogen receptor inhibitor ICI 182,780 (CEI), and OVX plus acute E2 plus ICI 182,780 (AEI). Rats were anesthetized, intubated, cannulated (femoral artery and vein), fitted with a closed cranial window, and subjected to 15-min reversible forebrain ischemia (4-vessel occlusion, 4-VO) and 60 mins of reperfusion. Arterial blood gases, intrawindow pressure, and temperature were controlled. Vessel diameter was measured before and 5 mins after superfusion of each concentration of U46619. Compared with preischemic responses, contractile response to U46619 was depressed at all concentrations after ischemia in the OVX group. In the chronic E2 and acute E2 groups, contractile response to 1 micromol/L of U46619 was normalized to near baseline values. However, in the CEI and the AEI groups, postischemic vasoconstriction was similar to that observed in the OVX rats. We conclude that E2 targets the cerebral microvasculature to preserve postischemic pial artery reactivity and that the effect is receptor mediated. Restoration of normal constriction to vascular agonists may be an important mechanism by which E2 protects the vasculature and diminishes tissue damage after ischemia.
机译：该研究的目的是（1）表征全脑缺血后与TXA2类似物U46619（0.01、0.1和1 micromol / L）的剂量反应关系，（2）确定是否慢性17β-雌二醇（E2）替代改变这种关系，并且（3）确定E2的机制是否通过同源雌激素受体转导。将大鼠分为五组（n = 6）：安慰剂植入的卵巢切除（OVX）雌性，OVX加慢性E2（CE），OVX加急性E2（AE），OVX加慢性E2加雌激素受体抑制剂ICI 182,780（CEI ），以及OVX加急性E2加ICI 182,780（AEI）。对大鼠进行麻醉，插管，插管（股动脉和静脉），安装闭合的颅窗，并进行15分钟可逆性前脑缺血（4血管闭塞，4-VO）和60分钟的再灌注。控制动脉血气，窗内压力和温度。在每种浓度的U46619重叠之前和之后5分钟测量容器直径。与缺血前反应相比，OVX组缺血后所有浓度对U46619的收缩反应均降低。在慢性E2和急性E2组中，对1 micromol / L U46619的收缩反应被标准化为接近基线值。但是，在CEI和AEI组中，缺血后的血管收缩与在OVX大鼠中观察到的相似。我们得出的结论是，E2靶向大脑微脉管系统以保留缺血后的颈动脉反应性，并且其作用是受体介导的。恢复血管激动剂的正常收缩可能是重要的机制，通过这种机制E2可以保护血管并减少缺血后的组织损伤。

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