Lengthening contractions (CL) are known to cause injury in limb skeletal muscle. It is unknown whether the diaphragm (DPM), the primary muscle of inspiration, could be induced to undergo CL in vivo and whether DPM injury occurs as a result. We hypothesized that the DPM could be stimulated to undergo lengthening contractions at physiologic frequencies in vivo and that DPM muscle would decrease following CL, indicating injury. We studied 4 anesthetized (Ketamine/Xylazine), supine, intubated, and mechanically ventilated female New Zealand White rabbits (3.15 ± 0.99 kg). Pressure of the airway opening (Pao) was measured as an indicator of force generating capacity of the DPM. Changes in midcostal diaphragm fiber length were measured via surgical implantation of sonomicrometer crystals (1mm diam). CL were induced by superimposing bilateral transvenous phrenic stimulations of the DPM at 20 Hz (duty cycle: 30 sec on/30 sec off) on mechanical ventilation(tidal volume = 20 ml, frequency = 25/min) for ten minutes. Changes in force production were evaluated by measuring frequency-pressure curves prior to, 5 minutes post CL, and 30 minutes post CL. Mean airway opening pressures were 100.12 ± 3.26% and 116 ± 4.68% of control values(N.S.) at 5 and 30 minutes post CL respectively. Under these experimental conditions, there is no CL induced force decrement indicative of damage to the intact rabbit diaphragm.
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