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首页> 外文期刊>American Journal of Physiology >Early gestation dexamethasone programs enhanced postnatal ovine coronary artery vascular reactivity.
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Early gestation dexamethasone programs enhanced postnatal ovine coronary artery vascular reactivity.

机译：早期妊娠地塞米松方案可提高产后绵羊冠状动脉的血管反应性。

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Excessive exposure of the fetus to maternally derived corticosteroids has been linked to the development of adult-onset diseases. To determine if early gestation corticosteroid exposure alters subsequent coronary artery reactivity, we administered dexamethasone (0.28 mg.kg(-1).day(-1)) to pregnant ewes at 27-28 days gestation (term being 145 days). Vascular responsiveness was assessed in endothelium-intact coronary and mesenteric arteries isolated from steroid-exposed and age-matched control fetal sheep at 123-126 days gestation and lambs at 4 mo of age. Lambs exposed to maternal dexamethasone had higher mean arterial blood pressures than the age-matched controls (93 +/- 3 vs. 83 +/- 5 mmHg, P < 0.05). Mesenteric arteries from the steroid-exposed fetuses displayed diminished responses to ANG II, relative to controls. In 4-mo-old lambs, prenatal dexamethasone exposure significantly increased coronary artery vasoconstriction to ANG II, ACh, and U-46619, but not KCl. In contrast, postnatal mesenteric artery reactivity was unaltered by steroid exposure. Compared with fetal mesenteric reactivity, postnatal mesenteric reactivity to ANG II, phenylephrine, and U-46619 was diminished, whereas the response to 120 mmol/l KCl was heightened. Coronary artery ANG II receptor protein expression was not significantly altered by steroid exposure in either age group. These findings demonstrate that early-gestation glucocorticoid exposure programs postnatal elevations in blood pressure and selectively enhances coronary artery responsiveness to second messenger-dependent vasoconstrictors. Glucocorticoid-induced alterations in coronary vascular smooth muscle structure or function may provide a mechanistic link between an adverse intrauterine environment and later cardiovascular disease.
机译：胎儿过度暴露于母体来源的皮质类固醇与成人疾病的发展有关。为了确定妊娠早期皮质类固醇暴露是否会改变随后的冠状动脉反应性，我们在妊娠27-28天（术语为145天）对怀孕的母羊服用了地塞米松（0.28 mg.kg（-1）.day（-1））。在妊娠123-126天时从类固醇暴露和与年龄匹配的对照胎羊中分离的内皮完整的冠状动脉和肠系膜动脉评估血管反应，在4 mo龄时评估羔羊的血管反应性。暴露于母体地塞米松的羔羊的平均动脉血压高于年龄匹配的对照组（93 +/- 3 vs. 83 +/- 5 mmHg，P <0.05）。相对于对照组，暴露于类固醇的胎儿的肠系膜动脉对ANG II的反应减弱。在4个月大的羔羊中，产前地塞米松暴露显着增加了对ANG II，ACh和U-46619的冠状动脉血管收缩，但对KCl却没有。相反，类固醇暴露不会改变产后肠系膜动脉的反应性。与胎儿肠系膜反应性相比，产后对ANG II，去氧肾上腺素和U-46619的肠系膜反应性降低，而对120 mmol / l KCl的反应增强。在任一年龄组中，类固醇暴露均未显着改变冠状动脉ANG II受体蛋白的表达。这些发现表明，妊娠早期糖皮质激素暴露可控制出生后血压升高，并选择性增强冠状动脉对第二信使依赖性血管收缩剂的反应性。糖皮质激素引起的冠状血管平滑肌结构或功能的改变可能在子宫内不良环境与后来的心血管疾病之间提供机械联系。

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