Respiratory physiology & neurobiology
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Respir Physiol Neurobiol · Nov 2009
ReviewPhrenic nerve stimulation in patients with spinal cord injury.
Phrenic nerve pacing (PNP) is a clinically useful technique to restore inspiratory muscle function in patients with respiratory failure secondary to cervical spinal cord injury. In this review, patient evaluation, equipment, methods of implementation, clinical outcomes, and the complications and side effects of PNP are discussed. Despite considerable technical development, and clinical success, however, current PNP systems have significant limitations. ⋯ Inadequate inspired volume generation may arise secondary to incomplete diaphragm activation, reversed recruitment order of motor units, fiber type conversion resulting in reduced force generating capacity and lack of coincident intercostal muscle activation. A novel method of pacing is under development which involves stimulating spinal cord tracts which synapse with the inspiratory motoneuron pools. This technique results in combined activation of the intercostal muscles and diaphragm in concert and holds promise to provide a more physiologic and effective method of PNP.
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Respir Physiol Neurobiol · Nov 2009
ReviewDescending bulbospinal pathways and recovery of respiratory motor function following spinal cord injury.
The rodent respiratory system is a relevant model for study of the intrinsic post-lesion mechanisms of neuronal plasticity and resulting recovery after high cervical spinal cord injury. An unilateral cervical injury (hemisection, lateral section or contusion) interrupts unilaterally bulbospinal respiratory pathways to phrenic motor neurons innervating the diaphragm and leads to important respiratory defects on the injured side. However, the ipsilateral phrenic nerve exhibits a spontaneous and progressive recovery with post-lesion time. ⋯ These pathways are located principally in the lateral part of the spinal cord and involve 30% of the medullary respiratory neurons. By contrast, in chronic post-lesion conditions, the medial part of the spinal cord becomes sufficient to trigger substantial ipsilateral respiratory drive. Thus, after unilateral cervical spinal cord injury, respiratory reactivation is associated with a time-dependent anatomo-functional reorganization of the bulbospinal respiratory descending pathways, which represents an adaptative strategy for functional compensation.
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Phox2b-expressing cells in the parafacial region of the ventral medulla are proposed to play a role in central chemoreception and postnatal survival. Recent findings in the adult rat and neonatal mouse suggest that the Phox2b-immunoreactive (ir) cell cluster in the rostral ventrolateral medulla is composed of glutamatergic neurons and expresses neurokinin 1 receptor (NK1R), indicating that the cluster may be identical to the retrotrapezoid nucleus. ⋯ Our findings suggest that Phox2b-expressing pFRG/Pre-I neurons play a role in respiratory rhythm generation as well as central chemoreception and thus are essential for postnatal survival. In this brief review, we focused on these recent findings and discuss the functional role of pFRG/Pre-I neurons.
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Respir Physiol Neurobiol · May 2009
Editorial ReviewPathophysiology of dyspnea evaluated by breath-holding test: studies of furosemide treatment.
Breath-holding is one of the most powerful methods to induce the dyspneic sensation, and the breath-holding test gives us much information on the onset and endurance of dyspnea. In conscious subjects, immediately after the start of breath-holding at functional residual capacity (FRC), there is a certain period of no particular respiratory sensation lasting for 20-30s, which is designated "no respiratory sensation period". This period is terminated by the onset of dyspnea and followed by a progressive increase in the intensity of dyspnea until the breaking point of breath-holding. ⋯ Alleviation of dyspnea with inhaled furosemide in conscious subjects is also consistent with the result of animal studies in which inhaled furosemide suppresses the escape behavior in the lightly anesthetized condition. The purpose of this article is to emphasize the usefulness of breath-holding test as a tool for evaluation of dyspnea. Furthermore, the possible mechanisms of alleviation of dyspnea with inhaled furosemide are highlighted.
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Respir Physiol Neurobiol · May 2009
Editorial ReviewMechanisms of activity-related dyspnea in pulmonary diseases.
Progressive activity-related dyspnea dominates the clinical presentation of patients afflicted by chronic obstructive and restrictive lung diseases. This symptom invariably leads to activity limitation, global skeletal muscle deconditioning and an impoverished quality of life. The effective management of exertional dyspnea remains an elusive goal but our understanding of the nature and mechanisms of this distressing symptom continues to grow. ⋯ Reductionist experimental approaches that attempt to partition, or isolate, the contribution of central and multiple peripheral sensory afferent systems to activity-induced dyspnea have met with limited success. Integrative approaches which explore the possible neurophysiological mechanisms involved in the two dominant qualitative descriptors of activity-related dyspnea in both diseases may prove to be more fruitful. In this review, we present a hypothetical model for exertional dyspnea that is based on current neurophysiological constructs that have been rigorously developed to explain the origins of perceptions of "effort," "air hunger" and the accompanying affective "distress" response.