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衰老而非与年龄相关的炎症,决定了血压以及内皮对急性炎症的反应。

Aging, not age-associated inflammation, determines blood pressure and endothelial responses to acute inflammation.

作者信息

Lane-Cordova Abbi D, Ranadive Sushant M, Kappus Rebecca M, Cook Marc D, Phillips Shane A, Woods Jeffrey A, Wilund Kenneth R, Baynard Tracy, Fernhall Bo

机构信息

aDepartment of Preventive Medicine, Feinberg School of Medicine, Northwestern University, Chicago, Illinois bDepartment of Anesthesiology, Mayo Clinic, Rochester, Minnesota cDepartment of Health and Exercise Science, Appalachian State University, Boone, North Carolina dDepartment of Kinesiology and Nutrition ePhysical Therapy, University of Illinois at Chicago, Chicago fDepartment of Kinesiology and Community Health, University of Illinois at Urbana-Champaign, Urbana, Illinois, USA.

出版信息

J Hypertens. 2016 Dec;34(12):2402-2409. doi: 10.1097/HJH.0000000000001103.

Abstract

BACKGROUND

Aging is characterized by a state of chronic, low-grade inflammation that impairs vascular function. Acute inflammation causes additional decrements in vascular function, but these responses are not uniform in older compared with younger adults. We sought to determine if older adults with low levels of baseline inflammation respond to acute inflammation in a manner similar to younger adults. We hypothesized age-related differences in the vascular responses to acute inflammation, but that older adults with low baseline inflammation would respond similarly to younger adults.

METHOD

Inflammation was induced with an influenza vaccine in 96 participants [older = 67 total, 38 with baseline C-reactive protein (CRP) > 1.5 mg/l and 29 with CRP < 1.5 mg/l; younger = 29]; serum inflammatory markers IL-6 and CRP, blood pressure and flow-mediated dilation (FMD) were measured 24 and 48 h later.

RESULTS

Younger adults increased IL-6 and CRP more than the collective older adult group and increased pulse pressure, whereas older adults decreased SBP and reduced pulse pressure. The entire cohort decreased FMD from 11.3 ± 0.8 to 8.3 ± 0.7 to 8.7 ± 0.7% in younger and from 5.8 ± 0.3 to 5.0 ± 0.4 to 4.7 ± 0.4% in older adults, P less than 0.05 for main effect. Older adult groups with differing baseline CRP had the same IL-6, blood pressure, and FMD response to acute inflammation, P less than 0.05 for all interactions, but the low-CRP group increased CRP at 24 and 48 h (from 0.5 ± 0.1 to 1.4 ± 0.2 to 1.7 ± 0.3 mg/l), whereas the high-CRP group did not (from 4.8 ± 0.5 to 5.4 ± 0.5 to 5.4 ± 0.6 mg/l), P less than 0.001 for interaction.

CONCLUSION

Aging, not age-related chronic, low-grade inflammation, determines the vascular responses to acute inflammation.

摘要

背景

衰老的特征是处于一种损害血管功能的慢性低度炎症状态。急性炎症会导致血管功能进一步下降,但与年轻人相比,老年人的这些反应并不一致。我们试图确定基线炎症水平较低的老年人对急性炎症的反应方式是否与年轻人相似。我们假设在对急性炎症的血管反应中存在与年龄相关的差异,但基线炎症水平较低的老年人的反应将与年轻人相似。

方法

对96名参与者接种流感疫苗以诱发炎症反应[老年人共67名,其中38名基线C反应蛋白(CRP)>1.5mg/l,29名CRP<1.5mg/l;年轻人29名];在24小时和48小时后测量血清炎症标志物白细胞介素-6(IL-6)和CRP、血压以及血流介导的血管舒张功能(FMD)。

结果

年轻人IL-6和CRP的升高幅度大于老年人群体的总体升高幅度,且脉压升高,而老年人收缩压降低、脉压减小。整个队列中,年轻人的FMD从11.3±0.8%降至8.3±0.7%再降至8.7±0.7%,老年人从5.8±0.3%降至5.0±0.4%再降至4.7±0.4%,主效应P<0.05。基线CRP不同的老年人群体对急性炎症的IL-6、血压和FMD反应相同,所有交互作用P<0.05,但低CRP组在24小时和48小时时CRP升高(从0.5±0.1mg/l升至1.4±0.2mg/l再升至1.7±0.3mg/l),而高CRP组未升高(从4.8±0.5mg/l升至5.4±0.5mg/l再升至5.4±0.6mg/l),交互作用P<0.001。

结论

决定对急性炎症血管反应的是衰老,而非与年龄相关的慢性低度炎症。

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