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3D Cine Magnetic Resonance Imaging of Respiratory Motion in Mechanically Ventilated Mice and Rats

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Published on: September 19, 2025

Titin and diaphragm dysfunction in mechanically ventilated rats.

Hieronymus W H van Hees¹, Willem-Jan M Schellekens, Gilberto L Andrade Acuña

¹Department of Pulmonary Diseases, Radboud University Nijmegen Medical Centre, Nijmegen, The Netherlands.

Intensive Care Medicine

|February 14, 2012

Summary

Mechanical ventilation weakens diaphragm muscle fibers, reducing their force generation. This is linked to myosin loss and altered titin phosphorylation, impacting ventilator weaning.

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Area of Science:

Physiology
Muscle Biology

Background:

Mechanical ventilation can induce diaphragm weakness, complicating ventilator weaning.
Myosin and titin are crucial for muscle force generation.

Purpose of the Study:

To investigate if myosin and titin loss or dysfunction contribute to mechanical ventilation-induced diaphragm weakness.

Main Methods:

Male Wistar rats were subjected to 18 hours of mechanical ventilation (MV) or served as controls.
Diaphragm and soleus muscles were analyzed for functional and biochemical properties.

Main Results:

MV reduced diaphragm fiber active force and myosin concentration.
Passive force generation in diaphragm fibers decreased by ~35% in MV rats.
Titin content remained unchanged, but its phosphorylation status likely altered passive force.

Conclusions:

Mechanical ventilation impairs diaphragm fiber force-generating capacity and passive properties.
Myosin loss contributes to reduced active force, while altered titin phosphorylation affects passive force.
These effects were specific to the diaphragm, not observed in the soleus muscle.