重温后的β-上腺刺激不能减轻大鼠心肌细胞中低温引起的收缩功能障碍
Torstein Schanche1, Young Soo Han2, Cole W Jensen2
1Department of Physiology & Biomedical Engineering, Mayo Clinic Rochester, MN, USA; Anesthesia and Critical Care Research Group, Department of Clinical Medicine, UiT, The Arctic University of Norway, 9037, Tromsø, Norway.
Cryobiology
|June 10, 2024
概括
上腺素治疗在低温和再升温 (H/R) 后不会改善心肌功能. 这项研究发现,虽然上腺素通常会增加心脏收缩能力,但它无法恢复心肌细胞受H/R损坏的功能.
科学领域:
- 心脏病学 心脏病学
- 生理学 生理学 生理学
- 生物化学 生物化学
背景情况:
- 由于心脏收缩功能障碍,严重的意外低温会导致血液动力学不稳定.
- 像上腺素这样的catecholamines被用来治疗这种不稳定性.
- 之前的研究表明,在低温和再升温 (H/R) 后,上腺素效应减弱.
研究的目的:
- 为了研究上腺素对激发 - 收缩合在H / R之后孤立的老鼠心肌细胞的影响.
- 为了确定上腺素是否可以减轻H/R诱导的心脏收缩功能障碍.
主要方法:
- 隔离的成年雄性大鼠心肌细胞被电刺激.
- 细胞质 ([Ca2+]) 和收缩反应 (sarcomere 长度缩短) 被测量.
- 细胞经过H/R协议 (冷却到15°C2h,然后再加热到37°C) 在上腺素治疗评估之前.
主要成果:
- 在37°C时,上腺素增加了心肌细胞[Ca2+]和收缩能力,这取决于度.
- 在H/R之后,收缩反应减少,[Ca2+]稍微升高.
- 上腺素 (25nM) 没有改善H/R后的收缩反应减弱,也没有增加[Ca2+].
结论:
- 上腺素治疗不会减轻心肌细胞中低温和重新升温引起的收缩功能障碍.
- 这项研究突出显示了H/R后心脏功能障碍背后的受损细胞机制.
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