Related Experiment Video
Updated: May 24, 2026
05:51
Measuring Diaphragm Thickness and Function Using Point-of-Care Ultrasound
Published on: November 3, 2023
Both high level pressure support ventilation and controlled mechanical ventilation induce diaphragm dysfunction and
Matthew B Hudson1, Ashley J Smuder, W Bradley Nelson
1Department of Applied Physiology and Kinesiology, Center for Exercise Science, University of Florida, Gainesville, FL, USA.
Critical Care Medicine
|March 20, 2012
Summary
High levels of pressure support ventilation cause diaphragm weakness and atrophy, similar to controlled mechanical ventilation. This weakness is linked to oxidative stress and protease activation in diaphragm muscles.
Area of Science:
- Respiratory physiology
- Muscle biology
- Critical care medicine
Background:
- Controlled mechanical ventilation (CMV) causes diaphragm inactivity, leading to rapid weakness and atrophy.
- Pressure support ventilation (PSV) allows partial diaphragm activity, but its effects on diaphragm structure and function are less understood.
Purpose of the Study:
- To investigate the impact of high-level pressure support ventilation (PSV) on diaphragm pathology.
- To test the hypothesis that PSV decreases diaphragm pathology compared to CMV.
Main Methods:
- Sprague-Dawley rats were exposed to control, 12-hour CMV, 18-hour CMV, 12-hour PSV, or 18-hour PSV.
- Diaphragm specimens were analyzed for oxidative stress (4-hydroxynonenal), proteolytic activity (caspase-3, calpain-1), fiber cross-sectional area, and specific force.
Main Results:
- Both 12PSV and 18PSV significantly reduced diaphragmatic specific force compared to controls, but less than CMV.
- Prolonged PSV (18PSV) and CMV (12CMV, 18CMV) induced significant diaphragm fiber atrophy.
- Oxidative stress and protease activation increased in diaphragms exposed to prolonged PSV and CMV.
Conclusions:
- High-level, prolonged PSV leads to diaphragm atrophy and contractile dysfunction.
- PSV-induced diaphragm weakness and atrophy are associated with oxidative stress and protease activation, similar to CMV.
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