On the intercostal muscle compensation for diaphragmatic paralysis in the dog.

Abstract

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.

Contribution of the spontaneous crossed-phrenic phenomenon to inspiratory tidal volume in spontaneously breathing rats

“…These compensatory responses remain robust after vagotomy, suggesting that vagally mediated lung afferents are not essential to this process (46). Rather, the increased output of other respiratory muscles after diaphragm paralysis appears to reflect a diminished influence of inhibitory phrenic afferent neurons with additional contribution from arterial hypercapnia (3,46). It is difficult, however, to compare the time course (e.g., onset time) of the compensatory responses across studies since prior work has induced diaphragm paralysis with selective anesthesia (e.g., lidocaine, bupivacaine, and vecuronium; Refs.…”

“…Changes in V T following diaphragm paralysis or paresis are mitigated by compensatory increases in the activity of other respiratory muscles (3,28,40,43,51). For example, both rostral (1st space) and caudal (6 -10th space) intercostal muscle EMG activity is substantially increased following bilateral phrenicotomy in rats (43).…”

“…It is difficult, however, to compare the time course (e.g., onset time) of the compensatory responses across studies since prior work has induced diaphragm paralysis with selective anesthesia (e.g., lidocaine, bupivacaine, and vecuronium; Refs. 3,26,46). Accordingly, the onset of diaphragm paralysis will have a slower time course compared with phrenicotomy, and to our knowledge prior studies have not attempted to examine immediate (i.e., next breath) changes in V T .…”

Enhanced recovery of breathing capacity from combined adenosine 2A receptor inhibition and daily acute intermittent hypoxia after chronic cervical spinal injury

“…Spontaneous VT recovery may occur from recruitment of less affected (contralateral) respiratory muscles (Brichant and De Troyer, 1997; Johnson and Mitchell, 2013; Katagiri et al, 1994; Teitelbaum et al, 1993), removal of inhibitory sensory inputs to phrenic motor neurons (Goshgarian, 1981) or spontaneous plasticity, partially restoring function in the most affected muscles. Since rats with C2HS maintain normal blood gases (Goshgarian et al, 1986), spontaneous compensation does not result from persistent chemoreceptor stimulation.…”

Adenosine 2A Receptor Inhibition Enhances Intermittent Hypoxia-Induced Diaphragm but Not Intercostal Long-Term Facilitation

“…One factor that may shift the balance of contributions from ipsilateral to contralateral respiratory muscles is the loss of inhibitory sensory inputs onto uninjured (e.g., contralateral) respiratory motorneurons. [35][36][37] Similar mechanisms may also (at least partially) restore the contributions of affected (ipsilateral) motor pools.…”