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J Appl Physiol (February 1, 2002). doi:10.1152/japplphysiol.01213.2001
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Articles in PresS, published online ahead of print February 1, 2002
J Appl Physiol, 10.1152/jap.01213.2001
Submitted on December 10, 2001
Accepted on January 24, 2002

Altered Diaphragm Contractile Properties with Controlled Mechanical Ventilation

Catherine S Sassoon1*, Vincent J Caiozzo2, Albana Manka1, and Gary C Sieck3

1 Department of Medicine, VA Long Beach Health Care System, Long Beach, CA, USA; Department of Medicine, University of California, Irvine, Irvine, CA, USA
2 Department of Orthopaedic Surgery, Physiology and Biophysics, Univeristy of California, Irvine, Irvine, CA, USA
3 Department of Anesthesiology, Physiology and Biophysics, Mayo Clinic, Rochester, MN, USA

* To whom correspondence should be addressed. E-mail: csassoon{at}uci.edu.

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: receiving 1 day or 3 days of CMV, 1 day or 3 days of continuous positive airway pressure (CPAP) of 0 cm H2O, and a control group. The CMV rate was set sufficient to suppress diaphragm electrical activity. Compared to the controls, phrenic-stimulated maximum transdiaphragmatic pressure did not decrease with CPAP, but decreased to 63% after 1 day, and 49% after 3 days of CMV. The in-vitro tetanic force (Po) decreased to 86% after 1 day, and 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 Po correlated with the volume density of abnormal myofibrils. We conclude that CMV had a detrimental effect on diaphragm contractile properties.




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