Effects of carotid body excision on recovery of respiratory function in C2 hemisected adult rats

In a previous study, we described the spontaneous recovery of respiratory motor function in adult rats subjected to a left C2 hemisection 6-16 weeks post-injury without any therapeutic intervention. We extend the previous findings by demonstrating in the present study that rats subjected to a left C2 hemisection with bilateral carotid body excision will also recover respiratory-related activity in the paralyzed ipsilateral hemidiaphragm. However, in this instance, recovery is significantly accelerated; i.e., it is evident as early as 2 weeks after spinal cord injury. Two experimental groups (and noninjured and sham-operated controls) of rats were employed in the study. H-CBE animals were subjected to a left C2 hemisection plus bilateral carotid body excision while H-CBI animals were subjected to a left C2 hemisection only. Carotid body excision was confirmed by the sodium cyanide test. The animals were allowed to survive for 2 weeks after hemisection. Thereafter, electrophysiologic assessment of respiratory activity was conducted in all animals. Spontaneous recovery of respiratory-related activity in the paralyzed hemidiaphragm (indicated by left phrenic nerve activity) was detected in all H-CBE animals while H-CBI animals did not express spontaneous recovery of diaphragmatic activity. The magnitude of recovered activity when expressed as a function of contralateral phrenic nerve activity was 48.8 +/- 3.8%. When expressed as a function of the homolateral phrenic nerve in noninjured animals, the magnitude amounted to 25.6 +/- 2.8%. Although the mechanisms responsible for the apparent early onset of spontaneous recovery are unknown, it is likely that a reorganization of the respiratory circuitry in the CNS may be involved. The significance of the findings is that it may be feasible to modulate the onset of functional recovery following cervical spinal cord injury by specifically targeting peripheral chemoreceptors. (c) 2005 Elsevier Inc. All rights reserved.