Hypertension Unit, Heart Institute (InCor), School of Medicine, University of São Paulo (FMUSP), Avenida Dr Eneas de Carvalho Aguiar 44, São Paulo/SP, Brazil 05403-000.
Department of Post-graduation in Medicine, Nove de Julho University (UNINOVE), Rua Vergueiro 235/249, São Paulo/SP, Brazil 01504-001.
Exp Biol Med (Maywood). 2020 Feb;245(3):245-253. doi: 10.1177/1535370219897883. Epub 2020 Jan 27.
Hypertensive status induces modifications in the respiratory profile. Previous studies have indicated that hypertensive rats show increased respiratory-sympathetic coupling compared to normotensive rats. However, these effects and especially the mechanisms underlying such effects are not well known. Thus, we evaluated the influence of high blood pressure and autonomic dysfunction on a ventilatory pattern associated with lung injury and on the ubiquitin-proteasome system of the diaphragm muscle. Autonomic cardiovascular modulation (systolic BP variance and low-frequency band and pulse interval variance) and arterial blood gases patterns (pH, pO, HCO, SpO), can be changed by hypertension, as well exacerbated chemoreflex pressor response. We observed that the diaphragm muscle of SHR showed increase in type I cross-sectional fiber (16%) and reduction in type II cross-sectional fiber area (41%), increased activity of the ubiquitin-proteasome system and lipid peroxidation, with no differences between groups in the analysis of ubiquitinated proteins and misfolded proteins. Our results showed that hypertension induced functional compensatory/adverse alterations associated with diaphragm fiber type changes and protein degradation as well as changed autonomic control of circulation. In conclusion, we believe there is an adaptation in ventilatory pattern in regarding to prevent the development of fatigue and muscle weakness and improve ventilatory endurance.
It was well known that hypertension can be driven by increased sympathetic activity and has been documented as a central link between autonomic dysfunction and alterations in the respiratory pattern. Our study demonstrated the impact of hypertension in ventilatory mechanics and their relationship with diaphragm muscle protein degradation. These findings may assist us in future alternative treatments to prevent diaphragm fatigue and weakness in hypertensive patients.
高血压状态会引起呼吸模式的改变。先前的研究表明，与正常血压大鼠相比，高血压大鼠的呼吸-交感耦联增加。然而，这些影响，尤其是这些影响的机制，尚不清楚。因此，我们评估了高血压和自主神经功能障碍对与肺损伤相关的通气模式以及膈肌肌肉的泛素-蛋白酶体系统的影响。自主心血管调节（收缩压方差和低频带和脉搏间隔方差）和动脉血气模式（pH、pO、HCO、SpO）可能因高血压而改变，并且化学感受器反射性升压反应也会加剧。我们观察到，SHR 的膈肌表现出 I 型横截面纤维增加（16%）和 II 型横截面纤维面积减少（41%），泛素-蛋白酶体系统和脂质过氧化活性增加，而在泛素化蛋白和错误折叠蛋白的分析中两组之间没有差异。我们的结果表明，高血压引起与膈肌纤维类型变化和蛋白质降解相关的功能性代偿/不利改变，以及循环自主控制的改变。总之，我们认为在通气模式方面存在适应，以防止疲劳和肌肉无力的发展，并提高通气耐力。
众所周知，高血压可能是由于交感神经活动增加引起的，并且已经被证明是自主神经功能障碍和呼吸模式改变之间的一个中心联系。我们的研究表明了高血压对通气力学的影响及其与膈肌肌肉蛋白降解的关系。这些发现可能有助于我们在未来寻找预防高血压患者膈肌疲劳和无力的替代治疗方法。
