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Laboratory and Animal Investigations |

Reloading the Diaphragm Following Mechanical Ventilation Does Not Promote Injury*

Darin Van Gammeren, MAEd; Darin J. Falk, MAEd; Keith C. DeRuisseau, PhD; Jeff E. Sellman, BS; Marc Decramer, MD; Scott K. Powers, PhD, EdD
Author and Funding Information

*From the Department of Applied Physiology and Kinesiology (Mr. Van Gammeren, Mr. Falk, Drs. DeRuisseau and Powers, and Mr. Sellman), Center for Exercise Science, University of Florida, Gainesville, FL; and the Respiratory Muscle Research Unit (Dr. Decramer), Laboratory of Pneumology, Katholieke Universiteit Leuven, Leuven, Belgium.

Correspondence to: Scott K. Powers, PhD, EdD, Center for Exercise Science, University of Florida, Room 25 FLG, Gainesville, FL 32611; e-mail: spowers@hhp.ufl.edu



Chest. 2005;127(6):2204-2210. doi:10.1378/chest.127.6.2204
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Study objective: Mechanical ventilation (MV) is used clinically to treat patients who are incapable of maintaining adequate alveolar ventilation. Prolonged MV is associated with diaphragmatic atrophy and a decrement in maximal specific force production (Po). Collectively, these alterations may predispose the diaphragm to injury on the return to spontaneous breathing (ie, reloading). Therefore, these experiments tested the hypothesis that reloading the diaphragm following MV exacerbates MV-induced diaphragmatic contractile dysfunction, while causing muscle fiber membrane damage and inflammation.

Methods: To test this postulate, Sprague-Dawley rats were randomly assigned to the following groups: (1) control; (2) 24 h of controlled MV; and (3) 24 h of controlled MV followed by 2 h of anesthetized spontaneous breathing. Controls were anesthetized in the short term but were not exposed to MV, whereas MV animals were anesthetized, tracheostomized, and ventilated. Reloaded animals remained under anesthesia, but were removed from MV and returned to spontaneous breathing for 2 h.

Results: Compared to the situation with control animals, MV resulted in a 26% decrement in diaphragmatic specific Po without muscle fiber membrane damage, as measured by an increase in membrane permeability (using the procion orange technique). Further, there were no increases in neutrophil or macrophage influx. Two hours of reloading did not exacerbate MV-induced diaphragmatic contractile dysfunction or cause fiber membrane damage, but increased neutrophil infiltration, myeloperoxidase activity, and muscle edema.

Conclusion: We conclude that the return to spontaneous breathing following 24 h of controlled MV does not exacerbate MV-induced diaphragm contractile dysfunction or result in fiber membrane damage, but increases neutrophil infiltration.

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