Canadian journal of physiology and pharmacology
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Can. J. Physiol. Pharmacol. · Nov 1994
ReviewPotential role for phenotypic modulation of bronchial smooth muscle cells in chronic asthma.
Asthma is considered to be a chronic inflammatory disease of the airways and is highlighted by excessive airway narrowing in response to various stimuli. Subepithelial fibrosis and increased airway smooth muscle mass are characteristic pathological features of the disease. Airway remodelling in asthma involves cellular hyperplasia and hypertrophy of bronchial myocytes. ⋯ Recruitment and modulation of smooth muscle cells to functionally different phenotypes, which contribute to fibrosis by secreting extracellular matrix materials and promote cellular hyperplasia by producing growth factors, are known to occur in atherogenic blood vessels; and evidence suggests that airway smooth muscle cells might play a similar role in asthma. We report the identification of markers of differentiation for airway smooth muscle cells. These markers should be useful tools in the elucidation of phenotypic heterogeneity of smooth muscle in asthmatic airways and, thereby, allow for the definition of a clearer role for bronchial smooth muscle cells in the pathogenesis of chronic asthma.
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Can. J. Physiol. Pharmacol. · May 1991
ReviewThe pain-adaptation model: a discussion of the relationship between chronic musculoskeletal pain and motor activity.
Articles describing motor function in five chronic musculoskeletal pain conditions (temporomandibular disorders, muscle tension headache, fibromyalgia, chronic lower back pain, and postexercise muscle soreness) were reviewed. It was concluded that the data do not support the commonly held view that the pain of these conditions is maintained by some form of tonic muscular hyperactivity. Instead, it seems clear that in these conditions the activity of agonist muscles is often reduced by pain, even when this does not arise from the muscle itself. ⋯ As a consequence of these changes, force production and the range and velocity of movement of the affected body part are often reduced. To explain how such changes in the behaviour come about, we propose a neurophysiological model based on the phasic modulation of excitatory and inhibitory interneurons supplied by high-threshold sensory afferents. We suggest that the "dysfunction" that is characteristic of several types of chronic musculoskeletal pain is a normal protective adaptation and is not a cause of pain.
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Muscle pain and poor sleep commonly occur together. Whether pain induces poor sleep or vice versa is difficult to know. Muscle pain is also observed in the presence of some types of dyskinesia or movement disorders. The interaction between sleep, movement disorders, and some musculoskeletal pain appears to be complex and may be influenced by various concomitant psychological and (or) biological factors.
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Can. J. Physiol. Pharmacol. · Sep 1989
ReviewNew perspectives on cocaine addiction: recent findings from animal research.
Research with laboratory animals has provided several insights into the nature of cocaine abuse and addiction. First, the nature of drug addiction has been reevaluated and the emphasis has shifted from physical dependence to compulsive drug-taking behavior. Second, animal studies suggest that cocaine is at least as addictive as heroin and possibly even more addictive. ⋯ Fifth, although the biological consequences of repeated cocaine self-administration on central nervous system functioning are poorly understood, preliminary findings suggest that intravenous cocaine self-administration may decrease neural functioning in this brain reward system. This has important clinical implications because diminished functioning of an important brain reward system may significantly contribute to relapse into cocaine addiction. These and other findings from experimentation with laboratory animals suggest new considerations for the etiology and treatment of drug addiction.
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Can. J. Physiol. Pharmacol. · Jan 1986
ReviewThe physiologic reserve in oxygen carrying capacity: studies in experimental hemodilution.
The mechanisms by which the body attempts to avoid tissue hypoxia when total body oxygen delivery is compromised during acute anemia are reviewed. When the hematocrit is reduced by isovolemic hemodilution the compensatory adjustments include an increase in cardiac output, redistribution of blood flow to some tissues, and an increase in the whole body oxygen extraction ratio. These responses permit whole body oxygen uptake to be maintained until the hematocrit has been lowered to about 10%. ⋯ Overall, peripheral compensatory adjustments result in an increased oxygen extraction ratio during acute anemia which reflects a better matching of the limited oxygen supply to tissue oxygen demands. However, some areas such as muscle are relatively overperfused which limits an even more efficient utilization of the reduced oxygen supply. Studies of the response of the microcirculation and the extent to which sympathetic vascular controls are involved in peripheral blood flow regulation are necessary to further appreciate the complex pattern of physiological responses which help ensure survival of the organism during acute anemia.