ArticleEuropean journal of medical research2009
Impairment of the baroreflex control of human respiratory resistance with age.
Article in European journal of medical research, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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4 authors at 2 institutions in 1 country.
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Abstract
backgroundThe mechanism responsible for the central baroreflex resetting with age are an area of limited knowledge. We previously demonstrated that in subjects aged above 50 the airway resistance did not change in response to baroreceptor activation, whereas in younger volunteers the airway resistance significantly decreased.
objectiveThe aim of the present study was to evaluate the effect of carotid baroreceptor inactivation on the reflex change of respiratory resistance, in the course of aging. MATERIAL AND
methods80 healthy men, divided in four groups: aged 20-30 (Group I), 31-40 (Group II), 41-50 (Group III), and 51-60 (Group IV) were included in the study. The selective inactivation of carotid baroreceptors was induced by generating a positive pressure of 40 mmHg for 5 s in two capsules placed bilaterally on the neck over the bifurcation of the carotid arteries. The oscillatory method (Siregnost FD5, Siemens) was used to measure continuously respiratory resistance.
resultsInactivation of carotid baroreceptors produced a short increase in respiratory resistance by 0.38 +/- 0.01SE mbar/l/s, i.e., 21.7% above the resting level in Group I and by 0.25 +/- 0.01 mbar/l/s in Group II. In the two older groups (III and IV) respiratory resistance did not change in response to baroreceptors inactivation.
conclusionsIn humans aged above 40, carotid baroreceptors do not contribute to bronchodilator tone, which causes imbalance between the activities of upper airway and chest wall inspiratory muscles leading to a collapsing effect on the upper airway.
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