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首页> 外文期刊>American Journal of Physiology >Age-associated impairment in vasorelaxation to fluid shear stress in the female vasculature is improved by TNF-alpha antagonism.
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Age-associated impairment in vasorelaxation to fluid shear stress in the female vasculature is improved by TNF-alpha antagonism.

机译：TNF-α拮抗作用可改善女性血管中与弹性松弛相关的年龄相关性血管舒张损伤。

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摘要

Aging is associated with alterations in vascular homeostasis, including a reduction in flow-mediated vasodilation, which in women is related to the onset of menopause. We previously found that in female animals, aging is associated with an increase in TNF-alpha. Thus we investigated the role of in vivo TNF-alpha inhibition on vascular responses to shear stress in aging female rats. Mesenteric arteries (approximately 150 microm) were isolated from young (3 mo) and ovariectomized Sprague-Dawley female rats approaching reproductive senescence (12 mo) treated with either placebo or a TNF-alpha inhibitor (etanercept; 0.3 mg/kg) and were mounted on a pressure myograph system. Vessels were equilibrated at an intraluminal pressure of 60 mmHg and then preconstricted with phenylephrine at approximately 70% of their initial diameter. Perfusate flow was increased in steps from 0 to 150 microl/min. Compared with young vessels, aged vessels have a decrease in flow-mediated dilation [maximal dilation (means +/- SE): 52 +/- 4 vs. 24 +/- 15%; P < 0.05], which was improved by TNF-alpha inhibition. Moreover, in aged vessels maximal dilation to flow was achieved at higher levels of shear stress compared with young vessels. In all groups, flow-mediated dilation was abolished by either endothelial removal or nitric oxide synthase inhibition with N(G)-nitro-L-arginine methyl ester. However, the modulation by N(G)-nitro-L-arginine methyl ester was reduced in vessels from aged animals compared with young animals but was improved in the etanercept-treated aged animals. In vivo chronic TNF-alpha inhibition improves flow-mediated arterial dilation in resistance arteries of aged female animals.
机译：衰老与血管动态平衡的改变有关，包括血流介导的血管舒张的减少，在女性中这与更年期的发作有关。我们先前发现在雌性动物中，衰老与TNF-α的增加有关。因此，我们调查了体内TNF-α抑制在衰老雌性大鼠对切应力的血管反应中的作用。从安慰剂或TNF-α抑制剂（etanercept; 0.3 mg / kg）处理的幼年（3 mo）和去卵巢的Sprague-Dawley雌性大鼠接近生殖衰老（12 mo）分离肠系膜动脉（约150微米）并固定在压力肌电图仪系统上。在60 mmHg的腔内压力下平衡血管，然后在约其初始直径的70％处用去氧肾上腺素预收缩。灌注液流量从0到150微升/分钟逐步增加。与年轻的血管相比，老龄血管的血流介导的扩张减少[最大扩张（平均值+/- SE）：52 +/- 4 vs. 24 +/- 15％; P ＜0.05]，其通过TNF-α抑制得到改善。此外，在老化的血管中，与年轻的血管相比，在较高的剪应力水平下可实现最大的流量扩张。在所有组中，通过内皮去除或用N（G）-硝基-L-精氨酸甲酯抑制一氧化氮合酶，消除了流量介导的扩张。然而，与年幼动物相比，老年动物血管中N（G）-硝基-L-精氨酸甲酯的调节作用降低，但依那西普处理的老年动物中其调节作用得到改善。体内慢性TNF-α抑制作用可改善老年雌性动物抗性动脉的血流介导性动脉扩张。

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