On the intercostal muscle compensation for diaphragmatic paralysis in the dog

• Published in: The Journal of physiology Vol. 500; no. Pt 1; pp. 245 - 253
• Main Authors: Brichant, J F, De Troyer, A
• Format: Journal Article Web Resource
• Language: English
• Published: England The Physiological Society 01-04-1997; Blackwell
• Subjects: Anesthesia & intensive care; Anesthetics, Local; Anesthésie & soins intensifs; Animals; Carbon Dioxide - blood; Diaphragm - innervation; Diaphragm - physiology; Diaphragm - physiopathology; Dogs; Electromyography; Human health sciences; Inhalation; Intercostal Muscles - innervation; Intercostal Muscles - physiology; Intercostal Muscles - physiopathology; Paralysis - physiopathology; Partial Pressure; Phrenic Nerve - physiology; Respiration; Respiratory Muscles - physiology; Respiratory Muscles - physiopathology; Ribs; Sciences de la santé humaine; Tidal Volume
• ISSN: 0022-3751; 1469-7793; 1469-7793
• DOI: 10.1113/jphysiol.1997.sp022014

1. Paralysis of the diaphragm in the dog is known to cause a compensatory increase in activation of the inspiratory intercostal
muscles (parasternal intercostals, external intercostals, and levator costae). The present studies were designed to assess
the mechanism(s) of that compensation. 2. Complete, selective diaphragmatic paralysis was induced by injecting local anaesthetic
into small silicone cuffs placed around the phrenic nerve roots in the neck. 3. Paralysis produced a decrease in tidal volume
and an increase in arterial P(CO2) (P(a,CO2)). The increased hypercapnic drive was a primary determinant of the increased
inspiratory intercostal activity. 4. However, paralysis also produced an increased inspiratory cranial displacement of the
ribs. When this increased rib displacement was reduced to that seen before paralysis, it appeared that the increase in external
intercostal and levator costae inspiratory activity was commonly greater than anticipated on the basis of the increased P(a,CO2).
5. Diaphragmatic paralysis after bilateral vagotomy also elicited disproportionate increases in inspiratory intercostal activity,
thus indicating that these increases are not caused by vagal afferent inputs. 6. These observations are consistent with the
idea that the intercostal muscle compensation for diaphragmatic paralysis is, in part, due to the release of an inhibition
originating from the contracting diaphragm. This inhibition might arise in the diaphragmatic tendon organs.