Respiratory physiology & neurobiology
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Respir Physiol Neurobiol · Apr 2011
ReviewExperimental protocols and preparations to study respiratory long term facilitation.
Respiratory long-term facilitation is a form of neuronal plasticity that is induced following exposure to intermittent hypoxia. Long-term facilitation is characterized by a progressive increase in respiratory motor output during normoxic periods that separate hypoxic episodes and by a sustained elevation in respiratory activity for up to 90min after exposure to intermittent hypoxia. This phenomenon is associated with increases in phrenic, hypoglossal or carotid sinus nerve inspiratory-modulated discharge. ⋯ Initially, the models and protocols used to study LTF in animals other than humans will be discussed, followed by a section specifically focused on human studies. Each section will begin with a discussion of various factors that must be considered when selecting an experimental preparation and intermittent hypoxia protocol to examine LTF. Model and protocol design recommendations will follow, with the goal of presenting a prevailing model and protocol that will ultimately ensure standardized comparisons across studies.
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The generation of reactive oxygen species (ROS) plays a major role in endothelial signaling and function. Of the several potential sources of ROS in the vasculature, the endothelial NADPH oxidase (Nox) family of proteins, Nox1, Nox2, Nox4 and Nox5, are major contributors of ROS. Excess generation of ROS contributes to the development and progression of vascular disease. ⋯ Physiological concentrations of ROS function as signaling molecule in the endothelium; however, excess ROS production leads to pathological disorders like inflammation, atherosclerosis, and lung injury. Regulation of Nox proteins is unclear; however, antioxidants, MAP Kinases, STATs, and Nrf2 regulate Nox under normal physiological and pathological conditions. Studies related to redox regulation of Nox should provide a better understanding of ROS and its role in the pathophysiology of vascular diseases.
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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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Respir Physiol Neurobiol · Nov 2009
ReviewThe crossed phrenic phenomenon and recovery of function following spinal cord injury.
This review will focus on neural plasticity and recovery of respiratory function after spinal cord injury and feature the "crossed phrenic phenomenon" (CPP) as a model for demonstrating such plasticity and recovery. A very brief summary of the earlier literature on the CPP will be followed by a more detailed review of the more recent studies. Two aspects of plasticity associated with the CPP that have been introduced in the literature recently have been spontaneous recovery of ipsilateral hemidiaphragmatic function following chronic spinal cord injury and drug-induced persistent recovery of the ipsilateral hemidiaphragm lasting long after animals have been weaned from drug treatment. ⋯ Both models provide an opportunity to sort out the intracellular signaling cascades that may be involved in motor recovery in the respiratory system after spinal cord injury. Finally, the review will examine developmental plasticity of the CPP and discuss how the expression of the CPP changes in neonatal rats as they mature to adults. Understanding the underlying mechanisms behind the spontaneous expression of the crossed phrenic pathway either in the developing animal or after chronic spinal cord injury in the adult animal may provide clues to initiating respiratory recovery sooner to alleviate human suffering and eventually eliminate the leading cause of death in human cases of spinal cord injury.
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Respir Physiol Neurobiol · Nov 2009
ReviewIntermittent hypoxia induces functional recovery following cervical spinal injury.
Respiratory-related complications are the leading cause of death in spinal cord injury (SCI) patients. Few effective SCI treatments are available after therapeutic interventions are performed in the period shortly after injury (e.g. spine stabilization and prevention of further spinal damage). ⋯ Early experiments suggest that intermittent hypoxia also enhances respiratory motor output in experimental models of cervical SCI (cervical hemisection) and that the capacity to induce functional recovery is greater with longer durations post-injury. Available evidence suggests that intermittent hypoxia-induced spinal plasticity has considerable therapeutic potential to treat respiratory insufficiency following chronic cervical spinal injury.