Respiratory physiology & neurobiology
-
Respir Physiol Neurobiol · Sep 2003
ReviewMechanisms of inflammation-mediated airway smooth muscle plasticity and airways remodeling in asthma.
Recent evidence points to progressive structural change in the airway wall, driven by chronic local inflammation, as a fundamental component for development of irreversible airway hyperresponsiveness. Acute and chronic inflammation is orchestrated by cytokines from recruited inflammatory cells, airway myofibroblasts and myocytes. Airway myocytes exhibit functional plasticity in their capacity for contraction, proliferation, and synthesis of matrix protein and cytokines. ⋯ Functional plasticity of airway smooth muscle (ASM) is regulated by an array of environmental cues, including cytokines, which mediate their effects through receptors and a number of intracellular signaling pathways. Despite numerous studies of the cellular effects of cytokines on cultured airway myocytes, few have identified how intracellular signaling pathways modulate or induce these cellular responses. This review summarizes current understanding of these concepts and presents a model for the effects of inflammatory mediators on functional plasticity of ASM in asthma.
-
Respir Physiol Neurobiol · Aug 2003
The effect of diffusion in the respiratory tree on the alveolar amplitude response technique (AART).
Theoretical data for the alveolar amplitude response technique (AART) (J. Appl. Physiol. 41 (1976) 419-424) for assessing lung function was simulated using a single path lung model. ⋯ The data was inserted into previously published parameter recovery techniques that may be used to estimate dead-space volume, alveolar volume and cardiac output. These parameter recovery techniques are based on much simpler mathematical models that do not allow stratified inhomogeneities in gas concentrations. It was found that: (i) recovered dead-space volume depended significantly on the ventilation pattern and on the distribution of volume within of the conducting airways; (ii) alveolar volume was recovered to a good degree of accuracy; and (iii) the recovered value of cardiac output was highly dependent on both the choice of inert gas and parameter recovery technique.
-
Respir Physiol Neurobiol · Aug 2003
Hypothermia-induced respiratory arrest and recovery in neonatal rats.
To examine the changes in breathing that occur during progressive hypothermia and rewarming in neonatal rats, we cooled and rewarmed rat pups during the first 6 days of life. During cooling, breathing stopped when rectal temperature (Tr) fell below 10.7+/-0.24 degrees C, and recovered spontaneously during rewarming when Tr reached 13.3+/-0.38 degrees C, regardless of age. During cooling, breathing frequency declined progressively, whereas tidal volume increased until Tr fell below 15 degrees C whence it declined to, but never below, normothermic levels. ⋯ There were no effects of age observed over the range studied on the changes in respiratory variables associated with hypothermia or rewarming. Breathing restarted spontaneously on rewarming with no evidence that gasping was required to initiate this process. The overall breathing pattern was episodic during the early stages of rewarming, however, suggesting that the respiratory rhythm is only periodically expressed during the initial stages of recovery from hypothermia.
-
Respir Physiol Neurobiol · Jul 2003
ReviewSleepiness and residual sleepiness in adults with obstructive sleep apnea.
Sleepiness is a common, but not necessary symptom of the obstructive sleep apnea syndrome (OSA) and is a frequent chief complaint of patients with OSA who seek medical attention. While sleepiness may seem simple in nature, the underlying mechanisms producing daytime sleepiness in OSA are complex and poorly characterized. Moreover, the meaningful assessment of pathological sleepiness is frequently far from straightforward. ⋯ An unknown percentage of treated OSA patients, however, remain sleepy during waking hours. The assessment and treatment of residual sleepiness in treated OSA can range from simple to difficult, depending on the nature and causes of the continued sleepiness. Recently, however, data from clinical trials have been generated which provide direction in the evaluation and management of the OSA patient suffering residual daytime sleepiness.
-
Respir Physiol Neurobiol · May 2003
ReviewGenetic aspects of breathing: on interactions between hypercapnia and hypoxia.
Indeed, specific genes in humans and mice regulate breathing pattern at baseline and breathing control during chemical stimulation. The current review addresses the question of coupling plausible candidate genes to physiological variation in control of breathing. That is, can genes discovered in mice be candidates assigned to similar physiological mechanisms as genetic control of breathing in humans? As an illustration, this review examines the interaction of hypoxia in affecting the hypercapnic ventilatory sensitivity (HCVS) curve in humans and mice. ⋯ As a mechanism associated with the chemical control of breathing in humans, the absence of CO(2) potentiation in mice suggests that specific genes interact to establish variation in complex breathing traits among mouse strains and between species. If future studies support the current evidence, the absence of CO(2) potentiation in mice compared with humans suggest a clearly defined species difference, which may depend on alternative hypoxic interactions such as hypometabolic and central neuronal depressive mechanisms in mice. Because the complexity of breathing mechanisms varies with modest adjustments in the environment, gene-targeting strategies that achieve 'one-gene, one-phenotype' results must be complimented with alternative strategies that consider integrating complex respiratory mechanisms with gene-to-gene interactions.