Respiratory response to abdominal and rib cage muscle paralysis in dogs

Abstract

To assess the respiratory response to abdominal and rib cage muscle paralysis, we measured tidal volume, esophageal and gastric pressures, arterial blood gases, and the electromyogram (EMG) of the diaphragm during progressive epidural anesthesia (lidocaine 2%) in 35 supine anesthetized dogs. The EMG activity of the diaphragm was measured with fine-wire electrodes; the abdominal cavity was thus left intact. Paralysis of the abdominal muscles alone did not produce any alterations. In contrast, when all rib cage muscles were also paralyzed, there were substantial increases in the peak height and the rate of rise of diaphragmatic EMG activity that were associated with a decrease in tidal volume and an increase in arterial PCO2 (PaCO2); swings in transdiaphragmatic pressure, however, were unchanged. The increased diaphragmatic activation due to rib cage muscle paralysis persisted after bilateral cervical vagotomy and was well explained by the increased PaCO2. These observations indicate that in the dog 1) the rib cage muscles contribute significantly to tidal volume, and their paralysis causes, through the increased hypercapnic drive, a compensatory increase in diaphragmatic activation; and 2) the rib cage inspiratory muscles enhance the diaphragm's ability to generate pressure during breathing.