衰老对苯肾上腺素诱导的小鼠膀胱松弛的影响

Ci ji yi xue za zhi = Tzu-chi medical journal Pub Date : 2019-02-18 eCollection Date: 2020-01-01 DOI:10.4103/tcmj.tcmj_178_18
Chun-Kai Hsu, Hsi-Hsien Chang, Stephen Shei-Dei Yang
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摘要

目的:我们已经证明,苯肾上腺素(PE)能激活辣椒素敏感神经,然后激活辣椒素敏感神经释放一种未知物质,促进肾上腺素能神经释放去甲肾上腺素(NE)。随后,NE 刺激小鼠逼尿肌中的β-ARs,导致膀胱(UB)神经源性松弛:我们研究了衰老小鼠的膀胱是否存在感觉-运动功能障碍。为了研究老龄雄性-C57BL/6小鼠(12个月与24个月龄小鼠)PE诱导的逼尿肌松弛的变化,我们分离了小鼠的膀胱UB条,将其切成条状并安装在器官浴中:结果:使用组织槽线肌电图估测了UTB条对各种药物的收缩力。乙酰胆碱(ACh)和KCl诱导的UTB条收缩在24个月和12个月的小鼠之间没有显著差异。24个月小鼠NE诱导的膀胱条松弛明显低于12个月小鼠。去势膀胱条对 NE 的松弛反应也有类似的降低。西洛多辛和利多卡因可抑制 NE 引起的松弛。PE 不能诱导老龄小鼠膀胱带收缩。相比之下,24 个月小鼠的 PE 诱导松弛反应弱于 12 个月小鼠:我们的研究结果表明,PE 诱导的松弛与年龄有关。结论:我们的研究结果表明,PE 诱导的松弛与年龄有关,衰老似乎会导致感觉运动功能障碍。未来需要更多的动物和人体研究来证明这一概念及其临床实用性。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

The aging effects on phenylephrine-induced relaxation of bladder in mice.

The aging effects on phenylephrine-induced relaxation of bladder in mice.

The aging effects on phenylephrine-induced relaxation of bladder in mice.

The aging effects on phenylephrine-induced relaxation of bladder in mice.

Objective: We have demonstrated that phenylephrine (PE) activates the capsaicin-sensitive nerves, and then activates capsaicin-sensitive nerves to release an unknown substance that facilitates the release of norepinephrine (NE) from adrenergic nerves. Subsequently, NE stimulates β-ARs in the detrusor muscle in mice, leading to neurogenic relaxation of the urinary bladder (UB).

Materials and methods: We examined if there existed sensory-motor dysfunction in UB of aging mice. To investigate the change of PE-induced detrusor relaxation in aging male-C57BL/6 mice (12- vs. 24-month-old mice), UB strips from mice were isolated, cut into strips, and mounted in the organ bath.

Results: The UB strip contractility responding to various agents was estimated using tissue bath wire myography. Acetylcholine (ACh) and KCl-induced UB strips contraction was not significantly different between 24- and 12-month mice. NE-induced UB strips relaxation was significantly lower in 24-month than 12-month mice. Denuded bladder strips showed similar decreased relaxation response to NE. This NE-induced relaxation was inhibited by silodosin and lidocaine. PE did not induce contraction in UB strips of aging mice. In contrast, PE-induced relaxation was weaker in 24-month than 12-month mice.

Conclusion: Our results suggested that the PE-induced relaxation was age related. Aging seemed to lead the sensory-motor dysfunction. More animal and human studies are required to prove this concept and its clinical usefulness in the future.

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