轻度高压氧暴露可在缺血/再灌注期间保护心脏,并影响血管松弛。

IF 2.9 4区 医学 Q2 PHYSIOLOGY Pflugers Archiv : European journal of physiology Pub Date : 2024-10-01 Epub Date: 2024-07-25 DOI:10.1007/s00424-024-02992-3
Christopher Gutierrez, Magdalena Peirone, Andrea Carranza, Guillermo Di Girolamo, Patricia Bonazzola, Rocío Castilla
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引用次数: 0

摘要

轻度高压氧疗法(mHBOT)是一种辅助疗法,用于组织氧合降低的情况,使用低于 1.5 ATA 的压力和 100% 的氧气(而不是 1.9-3 ATA 的传统高压氧),因此成本更低、更容易实施,而且同样有效。因此,我们研究了 mHBOT 对心血管系统的影响。我们评估了受到缺血/再灌注损伤的离体心脏的机械和能量参数,以及暴露于 mHBOT 的大鼠的动脉收缩反应。在心脏中,mHBOT 提高了缺血前的收缩速度和缺血时的舒张末压,并在再灌注期间提高了压力和收缩经济性。mHBOT 可在缺血/再灌注期间保护心脏,并影响血管松弛。
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Mild hyperbaric oxygen exposure protects heart during ischemia/reperfusion and affects vascular relaxation.

Mild hyperbaric oxygen therapy (mHBOT) is an adjuvant therapy used in conditions where tissue oxygenation is reduced and is implemented using pressures less than 1.5 ATA and 100% O2 (instead of the classical HBOT at 1.9-3 ATA) which results in cheaper, easier to implement, and equally effective. mHBOT is offered for wellness and beauty and as an anti-aging strategy, in spite of the absence of studies on the cardiovascular system. Consequently, we investigated the impact of mHBOT on the cardiovascular system. Mechanical and energetic parameters of isolated heart submitted to ischemia/reperfusion injury and arterial contractile response from mHBOT-exposed rats were evaluated. In the heart, mHBOT increased pre-ischemic velocity of contraction and ischemic end-diastolic pressure and developed pressure and contractile economy during reperfusion. mHBOT decreased infarct size and increased the plasma nitrite levels. In the artery, mHBOT increased acetylcholine sensitivity. mHBOT protects the heart during ischemia/reperfusion and affects vascular relaxation.

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来源期刊
CiteScore
8.80
自引率
2.20%
发文量
121
审稿时长
4-8 weeks
期刊介绍: Pflügers Archiv European Journal of Physiology publishes those results of original research that are seen as advancing the physiological sciences, especially those providing mechanistic insights into physiological functions at the molecular and cellular level, and clearly conveying a physiological message. Submissions are encouraged that deal with the evaluation of molecular and cellular mechanisms of disease, ideally resulting in translational research. Purely descriptive papers covering applied physiology or clinical papers will be excluded. Papers on methodological topics will be considered if they contribute to the development of novel tools for further investigation of (patho)physiological mechanisms.
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