Reply to Horn et al.

Reply to Horn et al.
复制标题

回复霍恩等人。

DOI:
10.1152/japplphysiol.00339.2022
复制
发表时间:
2022
期刊:
Journal of applied physiology (Bethesda, Md. : 1985)
影响因子:
--
通讯作者:
Richardson,RussellS
Richardson,RussellS
中科院分区:
--
文献类型:
--
作者:
Trinity,JoelD;Drummond,MicahJ;Fermoyle,Caitlin;McKenzie,AlecI;Supiano,MarkA;Richardson,RussellS

文献摘要

相似文献

TO THE EDITOR: We thank Mr. Horn and Drs. Benhke and Poole for their interest in our review on the novel topic of “Cardiovasomobility,” which highlights the integration of cardiovascular and skeletal muscle health to mobility and activity (1). Despite our best attempt to make our review as comprehensive as possible, the vascular consequences of mechanical ventilation did not receive adequate discussion. Indeed, as described by Horn et al.(2) in their Letter to the Editor, and detailed in a series of studies from their group, mechanical ventilation is associated with rapid and robust diaphragm resistance vessel dysfunction characterized by significant losses in shear rate, blood flow, and concomitant impairments in endothelial-dependent and-independent vasodilation (3, 4). Of note, diaphragm resistance vessel structure and mechanical properties are rapidly altered after mechanical ventilation (5). For these reasons, the integrated vascular and respiratory muscle dysfunction associated with mechanical ventilation is noteworthy and certainly falls within the context of cardiovasomobility. Forcing the constantly active diaphragm to be quiescent with mechanical ventilation may provide an ideal scenario to evaluate the link between vascular and skeletal muscle health and function.The clinical importance of mechanical ventilation and the deleterious complications associated with this procedure underscores the need for additional research evaluating mechanisms and treatments to protect diaphragm resistance vessel function. Oxidative stress has been directly linked to mechanical ventilation-induced diaphragm weakness and contractile dysfunction (6). Our cardiovasomobility review posits that oxidative stress and mitochondrial dysfunction are likely critical initiators of cardiovascular and skeletal muscle dysfunction during disuse. Certainly, further investigation targeting oxidative stress and redox balance to preserve diaphragm resistance vessel function is warranted. Although our cardiovasomobility review focused primarily on the integration of vascular and locomotor skeletal muscle function in the context of disuse and physical activity, critical links between vascular function and respiratory muscle function certainly fall under the cardiovasomobility umbrella. In fact, we contend that the cardiovasomobility