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Early effects of mechanical ventilation on isotonic contractile properties and MAF-box gene expression in the diaphragm

¹Department of Medicine, Veterans Affairs Long Beach Healthcare System, Long Beach; Departments of ²Medicine, ³Orthopedic Surgery, and ⁴Physiology and Biophysics, University of California, Irvine, California

Submitted 1 February 2005 ; accepted in final form 10 April 2005

This study aimed to determine the time-dependent effects of diaphragmatic inactivity on its maximum shortening velocity (V_max) and the muscle atrophy F-box (MAF-box, atrogin-1) gene expression during controlled mechanical ventilation (CMV). Twenty-four New Zealand White rabbits were grouped into 1 day, 2 days, and 3 days of CMV and controls in equal numbers. The in vitro isotonic contractile properties of the diaphragm were determined. In addition, myosin heavy chain protein and mRNA, myosin light chain, MAF-box mRNA, and volume density of abnormal myofibrils were measured. Tetanic force decreased, and V_max increased from control of 6.4 to 6.6, 7.7, and 8.1 muscle lengths per second after 1, 2, and 3 days of CMV, respectively (P < 0.02). The increased V_max compensated for the decreased tetanic force; consequently, compared with the controls, maximum power output was unchanged after 3 days of CMV. V_max correlated with the volume density of abnormal myofibrils [y = 0.1x + 5.7 (r = 0.87, P < 0.01)]. In the diaphragm, MAF-box was overexpressed (355% of control) after 1 day of CMV, before the evidence of structural myofibril disarray. In conclusion, CMV produced a time-dependent increase in V_max that was associated with the degree of myofibrillar disarray and independent of changes in myosin isoform expression. Furthermore, CMV produced an increase in MAF-box mRNA levels that may be partially or completely responsible for the degree of myofibrillar disarray resulting from CMV.

positive pressure; maximum shortening velocity; myosin heavy chain; myofibril injury; muscle atrophy F-box; atrogin-1

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