Respiratory physiology & neurobiology
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Respir Physiol Neurobiol · Nov 2013
ReviewRespiration following spinal cord injury: evidence for human neuroplasticity.
Respiratory dysfunction is one of the most devastating consequences of cervical spinal cord injury (SCI) with impaired breathing being a leading cause of morbidity and mortality in this population. However, there is mounting experimental and clinical evidence for moderate spontaneous respiratory recovery, or "plasticity", after some spinal cord injuries. ⋯ While the extent of spontaneous recovery remains limited, it is possible that enhancing or facilitating neuroplastic mechanisms may have significant therapeutic potential. The next generation of treatment strategies for SCI and related respiratory dysfunction should aim to optimize these recovery processes of the injured spinal cord for lasting functional restoration.
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Respir Physiol Neurobiol · Nov 2013
ReviewActivation of inspiratory muscles via spinal cord stimulation.
Diaphragm pacing is a clinically useful modality providing artificial ventilatory support in patients with ventilator dependent spinal cord injury. Since this technique is successful in providing full-time ventilatory support in only ~50% of patients, better methods are needed. In this paper, we review a novel method of inspiratory muscle activation involving the application of electrical stimulation applied to the ventral surface of the upper thoracic spinal cord at high stimulus frequencies (300 Hz). ⋯ Since this method results in an asynchronous pattern of EMG activity and mean peak firing frequencies similar to those observed during spontaneous breathing, HF-SCS is a more physiologic form of inspiratory muscle activation. Further, ventilation can be maintained on a long-term basis with repetitive stimulation at low stimulus amplitudes (<1 mA). These preliminary results suggest that HF-SCS holds promise as a more successful method of inspiratory muscle pacing.
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Respir Physiol Neurobiol · Nov 2013
ReviewCommon mechanisms of compensatory respiratory plasticity in spinal neurological disorders.
In many neurological disorders that disrupt spinal function and compromise breathing (e.g. ALS, cervical spinal injury, MS), patients often maintain ventilatory capacity well after the onset of severe CNS pathology. In progressive neurodegenerative diseases, patients ultimately reach a point where compensation is no longer possible, leading to catastrophic ventilatory failure. ⋯ We propose that a suite of mechanisms, operating at distinct sites in the respiratory control system, underlies compensatory respiratory plasticity, including: (1) increased (descending) central respiratory drive, (2) motor neuron plasticity, (3) plasticity at the neuromuscular junction or spared respiratory motor neurons, and (4) shifts in the balance from more to less severely compromised respiratory muscles. To establish this framework, we contrast three rodent models of neural dysfunction, each posing unique problems for the generation of adequate inspiratory motor output: (1) respiratory motor neuron death, (2) de- or dysmyelination of cervical spinal pathways, and (3) cervical spinal cord injury, a neuropathology with components of demyelination and motor neuron death. Through this contrast, we hope to understand the multilayered strategies used to "fight" for adequate breathing in the face of mounting pathology.
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Respir Physiol Neurobiol · Oct 2013
Corrections of Enghoff's dead space formula for shunt effects still overestimate Bohr's dead space.
Dead space ratio is determined using Enghoff's modification (VD(B-E)/VT) of Bohr's formula (VD(Bohr)/VT) in which arterial is used as a surrogate of alveolar PCO₂. In presence of intrapulmonary shunt Enghoff's approach overestimates dead space. In 40 lung-lavaged pigs we evaluated the Kuwabara's and Niklason's algorithms to correct for shunt effects and hypothesized that corrected VD(B-E)/VT should provide similar values as VD(Bohr)/VT. ⋯ Uncorrected VD(B-E)/VT (mean ± SD of 0.70 ± 0.10) overestimated VD(Bohr)/VT (0.59 ± 0.12) (p < 0.05), over the entire range of shunts. Mean (K) VD(B-E)/VT was significantly higher than VD(Bohr)/VT (0.67 ± 0.08, bias -0.085, limits of agreement -0.232 to 0.085; p < 0.05) whereas (N)VD(B-E)/VT showed a better correction for shunt effects (0.64 ± 0.09, bias 0.048, limits of agreement -0.168 to 0.072; p < 0.05). Neither Kuwabara's nor Niklason's algorithms were able to correct Enghoff's dead space formula for shunt effects.
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Respir Physiol Neurobiol · Oct 2013
High tidal volume ventilation does not exacerbate acid-induced lung injury in infant rats.
The impact of mechanical ventilation with high V(T)-low PEEP in infant rats with preinjured lungs is unknown. After tracheal instillation of saline or acid, two week old rats were ventilated with V(T) 7 mL/kg and PEEP 5 cm H₂O or V(T) 21 mL/kg and PEEP 1cm H₂O for 4 h. Airway resistance and the coefficient of tissue elastance, measured via low-frequency forced-oscillation technique, and quasi-static pressure-volume curves deteriorated less with high V(T)-low PEEP when compared with low V(T)-high PEEP. ⋯ Moreover, differences in BALF protein concentration and histological lung injury scores were independent of applied ventilation strategies. In contrast to experimental studies with adult rats, short-term mechanical ventilation with high V(T)-low PEEP is not deleterious when compared to low V(T)-high PEEP in both healthy and pre-injured infant rat lungs. Our results call for caution when extrapolating data from adult studies and highlight the need for age-specific animal models.