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1 Department of Medicine, Veterans Affairs Long Beach Health Care System and University of California, Irvine; 2 Department of Orthopaedic Surgery, Physiology, and Biophysics, University of California, Irvine, California 90822; and 3 Department of Anesthesiology and Physiology and Biophysics, Mayo Clinic, Rochester, Minnesota 55905
This study shows that, over time, diaphragm inactivity with controlled mechanical ventilation (CMV) decreases diaphragm force and produces myofibril damage contributing to the reduced force. We measured in vivo and in vitro diaphragm contractile and morphological properties in 30 sedated rabbits grouped (n = 6) as follows: 1 or 3 days of CMV, 1 or 3 days of 0 cmH2O continuous positive airway pressure, and control. The CMV rate was set sufficient to suppress diaphragm electrical activity. Compared with the control group, phrenic-stimulated maximum transdiaphragmatic pressure did not decrease with continuous positive airway pressure but decreased to 63% after 1 day of CMV and to 49% after 3 days of CMV. The in vitro tetanic force decreased to 86% after 1 day of CMV and to 44% after 3 days of CMV. After 3 days of CMV, significant myofibril damage occurred in the diaphragm but not in the soleus. The decrease in tetanic force correlated with the volume density of abnormal myofibrils. We conclude that CMV had a detrimental effect on diaphragm contractile properties.
passive ventilation; diaphragm inactivity; diaphragm muscle force; force-frequency relationship; myosin heavy chain isoform expression
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