Thoracic reflexes stabilizing loaded ventilation in normal and cord-injured man.
The ability to regulate tidal volume was quantified in 24 cervical cord-injured patients by comparing the "effective" elastance (E'rs) observed during single-breath elastic loads to the passive respiratory elastance (Ers) measured separately with relaxed muscles. Thirteen patients, the majority of whom had an abnormal subjective perception of loading, usually failed to demonstrate any tidal volume compensation under load conditions (i.e. E'rs less than or equal to Ers). This impaired tidal volume defense, which could not be attributed either to diaphragmatic paralysis or rib cage instability, was accompanied by a markedly shortened inspiratory duration and, hence, a prematurely terminated phrenic motoneuron output. Conversely, those patients who developed a larger then previously reported "effective" elastance (i.e., E'rs greater than or equal to 2Ers) described loading as an inspiratory obstruction, as did all our normal subjects, and usually prolonged loaded inspiratory duration, probably by a consciously mediated mechanism. These findings are consistent with the hypothesis that, in spontaneously breathing intact man, thoracic sensory receptors normally maintain phrenic motoneuron output under load conditions and thereby promote tidal volume stability.
D000293:Adolescent; D000328:Adult; D005260:Female; D005652:Functional Residual Capacity; D006801:Humans; D008168:Lung / Q000503:physiopathology; D008170:Lung Compliance; D008297:Male; D008433:Mathematics; D012018:Reflex; D012119:Respiration; D011984:Sensory Receptor Cells; D013119:Spinal Cord Injuries / Q000503:physiopathology*; D013990:Tidal Volume