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衰老是大鼠血管舒张反应受损的原因。

Aging impairs vasodilatory responses in rats.

机构信息

Department of Anesthesiology and Pain Medicine, Wonju College of Medicine, Yonsei University, Wonju, Korea.

出版信息

Korean J Anesthesiol. 2011 Dec;61(6):506-10. doi: 10.4097/kjae.2011.61.6.506. Epub 2011 Dec 20.

DOI:10.4097/kjae.2011.61.6.506
PMID:22220229
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC3249574/
Abstract

BACKGROUND

Aging causes profound changes of stiffness and compliance in the cardiovascular system, which contributes to decreased cardiovascular reserve. Mechanisms of the underlying endothelial vasodilator dysfunction in vasodilator signaling pathways may occur at multiple sites within any of these pathways.

METHODS

Age-related changes in the vasculature were investigated in adult young (3-6 months, Y) and old (26-29 month, O) Wistar rats (n = 6). The aortas were carefully dissected from the rat and cut into rings 1.5-2.0 mm in length to measure in vitro isometric tension. Vasorelaxant responses of aortic rings to acetylcholine (ACh), sodium nitroprusside (SNP) and P1075 were examined using Dose Response software (AD Instruments, Mountain View, CA).

RESULTS

Endothelium-dependent vasodilator function was impaired. The endothelium of aging rats impaired endothelial NO dependent vasodilation, but the machinery for vasodilation was not impaired.

CONCLUSIONS

Age-related NO-mediated vasorelaxation in the aging endothelium was inhibited and appears to be major mechanism of vascular change and impaired vascular regulation.

摘要

背景

衰老导致心血管系统的僵硬和顺应性发生深刻变化，这导致心血管储备能力下降。在血管舒张信号通路中的任何一个途径中，内皮血管舒张功能障碍的潜在机制可能发生在多个部位。

方法

本研究在成年幼鼠（3-6 个月，Y）和老年鼠（26-29 个月，O）中研究了血管的衰老相关变化（n=6）。小心地从大鼠中分离出主动脉，并切成 1.5-2.0mm 长的环，以测量体外等长张力。使用剂量反应软件（AD 仪器，山景城，CA）检查主动脉环对乙酰胆碱（ACh）、硝普钠（SNP）和 P1075 的血管舒张反应。

结果

内皮依赖性血管舒张功能受损。衰老大鼠的内皮损害了内皮 NO 依赖性血管舒张，但血管舒张的机制没有受损。

结论

衰老内皮中与年龄相关的 NO 介导的血管舒张受到抑制，这似乎是血管变化和血管调节受损的主要机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cef6/3249574/2b128400b779/kjae-61-506-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cef6/3249574/b436d1a8f30f/kjae-61-506-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cef6/3249574/10f41e40bf74/kjae-61-506-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cef6/3249574/2911bea1fb5a/kjae-61-506-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cef6/3249574/914251bf671f/kjae-61-506-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cef6/3249574/2b128400b779/kjae-61-506-g005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cef6/3249574/b436d1a8f30f/kjae-61-506-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cef6/3249574/10f41e40bf74/kjae-61-506-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cef6/3249574/2911bea1fb5a/kjae-61-506-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cef6/3249574/914251bf671f/kjae-61-506-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/cef6/3249574/2b128400b779/kjae-61-506-g005.jpg

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