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氧化应激导致雌激素缺乏的绝经后女性出现慢性腿部血管收缩。

Oxidative stress contributes to chronic leg vasoconstriction in estrogen-deficient postmenopausal women.

作者信息

Moreau Kerrie L, DePaulis Ashley R, Gavin Kathleen M, Seals Douglas R

机构信息

Dept. of Integrative Physiology, University of Colorado, Boulder, CO, USA.

出版信息

J Appl Physiol (1985). 2007 Mar;102(3):890-5. doi: 10.1152/japplphysiol.00877.2006. Epub 2006 Nov 16.

DOI:10.1152/japplphysiol.00877.2006
PMID:17110511
Abstract

Basal whole leg blood flow and vascular conductance are reduced in estrogen-deficient postmenopausal compared with premenopausal women. The underlying mechanisms are unknown, but oxidative stress could be involved. We studied 9 premenopausal [23 +/- 1 yr (mean +/- SE)] and 20 estrogen-deficient postmenopausal (55 +/- 1 yr) healthy women. During baseline control, oxidized low-density lipoprotein (LDL), a marker of oxidative stress, was 50% greater in the postmenopausal women (P < 0.001). Basal whole leg blood flow (duplex ultrasound of femoral artery) was 34% lower in the postmenopausal women because of a 38% lower leg vascular conductance (P < 0.0001); mean arterial pressure was not different. Intravenous administration of a supraphysiological dose of the antioxidant ascorbic acid increased leg blood flow by 15% in the postmenopausal women as a result of an increase in leg vascular conductance (both P < 0.001), but it did not affect leg blood flow in premenopausal controls or mean arterial pressure in either group. In the pooled subjects, the changes in leg blood flow and leg vascular conductance with ascorbic acid were related to baseline plasma oxidized LDL (r = 0.46 and 0.53, P < 0.01) and waist-to-hip ratio and total body fat (r = 0.41-0.44, all P < 0.05). Our results are consistent with the hypothesis that oxidative stress contributes to chronic leg vasoconstriction and reduced basal whole leg blood flow in estrogen-deficient postmenopausal women. This oxidative stress-related suppression of leg vascular conductance and blood flow may be linked in part to increased total and abdominal adiposity.

摘要

与绝经前女性相比,雌激素缺乏的绝经后女性全腿基础血流量和血管传导率降低。其潜在机制尚不清楚,但可能涉及氧化应激。我们研究了9名绝经前健康女性[23±1岁(均值±标准误)]和20名雌激素缺乏的绝经后健康女性(55±1岁)。在基础对照期间,氧化应激标志物氧化型低密度脂蛋白(LDL)在绝经后女性中高出50%(P<0.001)。绝经后女性的全腿基础血流量(股动脉双功超声)降低了34%,原因是腿部血管传导率降低了38%(P<0.0001);平均动脉压无差异。静脉注射超生理剂量的抗氧化剂抗坏血酸使绝经后女性的腿部血流量增加了15%,这是由于腿部血管传导率增加所致(两者P<0.001),但对绝经前对照者的腿部血流量或两组的平均动脉压均无影响。在汇总的受试者中,抗坏血酸引起的腿部血流量和腿部血管传导率变化与基线血浆氧化型LDL相关(r=0.46和0.53,P<0.01),与腰臀比和全身脂肪相关(r=0.41 - 0.44,均P<0.05)。我们的结果与以下假设一致,即氧化应激导致雌激素缺乏的绝经后女性慢性腿部血管收缩和全腿基础血流量降低。这种与氧化应激相关的腿部血管传导率和血流量抑制可能部分与全身和腹部肥胖增加有关。

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