当前位置: X-MOL 学术J. Cardiovasc. Pharmacol. › 论文详情
Our official English website, www.x-mol.net, welcomes your feedback! (Note: you will need to create a separate account there.)
Ovariectomy reduces vasocontractile responses of rat middle cerebral arteries after focal cerebral ischemia.
Journal of Cardiovascular Pharmacology ( IF 3 ) Pub Date : 2021-10-13 , DOI: 10.1097/fjc.0000000000001158
Mimmi Rehnström 1 , Hilda Ahnstedt 1 , Diana N Krause 2 , Marie Louise Edvinsson 3 , Kristian Agmund Haanes 4 , Lars Edvinsson 1, 4
Affiliation  

Effects of sex hormones on stroke outcome is not fully understood. A deleterious consequence of cerebral ischemia is upregulation of vasoconstrictor receptors in cerebral arteries that exacerbate stroke injury. Here, we tested the hypothesis that female sex hormones alter vasocontractile responses after experimental stroke in vivo or following organ culture in vitro, a model of vasocontractile receptor upregulation. Female rats with intact ovaries and ovariectomized females treated with 17β-estradiol, progesterone or placebo were subjected to transient, unilateral middle cerebral artery occlusion followed reperfusion (I/R). The maximum contractile response, measured my wire myography, in response to the endothelin B (ETB) receptor agonist sarafotoxin 6c was increased in female arteries after I/R, but the maximum response was significantly lower in arteries from ovariectomized females. Maximum contraction mediated by the serotonin agonist 5-carboxamidotryptamine (5-CT) was diminished after I/R, with arteries from ovariectomized females showing a greater decrease in maximum contractile response. Contraction elicited by angiotensin II was similar in all arteries. Neither estrogen nor progesterone treatment of ovariectomized females affected I/R-induced changes in ETB and 5-CT induced vasocontraction. These findings suggest sex hormones do not directly influence vasocontractile alterations that occur after ischemic stroke; however, loss of ovarian function does impact this process.

中文翻译:

卵巢切除术可降低局灶性脑缺血后大鼠大脑中动脉的血管收缩反应。

性激素对中风结果的影响尚不完全清楚。脑缺血的一个有害后果是脑动脉中血管收缩受体的上调,这加剧了中风损伤。在这里,我们测试了女性性激素在体内实验性中风或体外器官培养后改变血管收缩反应的假设,这是一种血管收缩受体上调的模型。用 17β-雌二醇、孕酮或安慰剂治疗的具有完整卵巢的雌性大鼠和切除卵巢的雌性大鼠经受短暂的单侧大脑中动脉闭塞后再灌注 (I/R)。在 I/R 后,女性动脉对内皮素 B (ETB) 受体激动剂 sarafotoxin 6c 的反应是最大收缩反应,测量我的线肌图,但卵巢切除女性的动脉中的最大反应明显较低。由 5-羟色胺激动剂 5-羧胺基色胺 (5-CT) 介导的最大收缩在 I/R 后减弱,来自去卵巢的女性的动脉显示最大收缩反应的下降幅度更大。血管紧张素 II 引起的收缩在所有动脉中相似。去卵巢女性的雌激素和孕激素治疗均不影响 I/R 诱导的 ETB 变化和 5-CT 诱导的血管收缩。这些发现表明,性激素不会直接影响缺血性中风后发生的血管收缩变化。然而,卵巢功能的丧失确实会影响这一过程。卵巢切除女性的动脉显示最大收缩反应的下降幅度更大。血管紧张素 II 引起的收缩在所有动脉中相似。去卵巢女性的雌激素和孕激素治疗均不影响 I/R 诱导的 ETB 变化和 5-CT 诱导的血管收缩。这些发现表明,性激素不会直接影响缺血性中风后发生的血管收缩变化。然而,卵巢功能的丧失确实会影响这一过程。卵巢切除女性的动脉显示最大收缩反应的下降幅度更大。血管紧张素 II 引起的收缩在所有动脉中相似。去卵巢女性的雌激素和孕激素治疗均不影响 I/R 诱导的 ETB 变化和 5-CT 诱导的血管收缩。这些发现表明,性激素不会直接影响缺血性中风后发生的血管收缩变化。然而,卵巢功能的丧失确实会影响这一过程。这些发现表明,性激素不会直接影响缺血性中风后发生的血管收缩变化。然而,卵巢功能的丧失确实会影响这一过程。这些发现表明,性激素不会直接影响缺血性中风后发生的血管收缩变化。然而,卵巢功能的丧失确实会影响这一过程。
更新日期:2021-10-13
down
wechat
bug