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CO2 Challenge (co2 + challenge)
Selected AbstractsThe effects of acute exercise and high lactate levels on 35% CO2 challenge in healthy volunteersACTA PSYCHIATRICA SCANDINAVICA, Issue 5 2002G. Esquivel Objective:, To test the possible antipanic effects of acute exercise in healthy volunteers exposed to an inhalation of 35% CO2 challenge. Method:, Twenty healthy subjects in a randomized separate group design, performed exercise in a bicycle ergometer reaching >6 mm of blood lactate and a control condition of minimal activity in the same fashion with no lactate elevation. Immediately afterwards an inhalation of a vital capacity using a mixture of 35% CO2/65% O2 through a mask was given on both conditions. Results:, Subjects under the exercise condition reported less panic symptoms than controls after a CO2 challenge on the diagnostic statistical manual-IV (DSM-IV) Panic Symptom List but no difference on the Visual Analogue Anxiety Scale. Conclusion:, Subjects under the exertion condition had lactate levels comparable with those of lactate infusions but an inhibitory rather than accumulative effect was seen when combined with a CO2 challenge. [source] Corticosteroids and the cardiovascular response to stress: a pilot study of the 35% CO2 challenge in Addison's diseaseCLINICAL ENDOCRINOLOGY, Issue 3 2006J. M. Kaye Summary Objective, Glucocorticoids play an essential role in the neuroendocrine response to stress, influencing both the hypothalamic,pituitary,adrenal (HPA) axis and the sympatho-adrenomedullary (SAM) axis at several levels. In this pilot study, a clinical model of primary adrenocortical failure (Addison's disease, AD) has been used to evaluate the role of circulating glucocorticoids in both the autonomic and psychological response to stress. Design and subjects, Five subjects with known AD underwent a randomized, double-blind, placebo-controlled investigation in which they received fixed glucocorticoid plus mineralocorticoid hormone replacement or placebo for 48 h prior to a 35% CO2 challenge. Measurement, Psychological responses immediately before and after CO2 exposure were assessed by questionnaire. Systolic blood pressure (SBP) and heart rate were measured automatically at 1-min intervals for 5 min before and 5 min after the CO2 exposure. Results, While on hormone replacement, all subjects had an identical response to CO2 to that recorded in normal volunteers (initial bradycardia, an increase in blood pressure and subjective feelings of anxiety). On no replacement, however, the bradycardia and anxiety responses were not significantly altered, but the pressor response was markedly attenuated (+15·6 ± 5 mmHg on replacement compared with +4·2 ± 3·3 mmHg off replacement; P = 0·043). Conclusions, These data provide further evidence that the CO2 -induced bradycardia is a direct , presumably parasympathetic , response to CO2 independent of the pressor effect, and that the pressor response itself is dependent on the presence of the circulating corticosteroid. [source] Abnormal heart rate response to hypercapnia in boys with an apparent life-threatening eventACTA PAEDIATRICA, Issue 12 2002A Edner Aim: To determine instantaneous cardiac variability responses to increased carbon dioxide (CO2) during quiet sleep in infants who may be at risk for the Sudden Infant Death syndrome (SIDS). Methods: The cardiac rate variability before, during and after a CO2 challenge was examined in 41 infants who had experienced an apparent life-threatening event (ALTE) and 41 gender- and age-matched control infants. Results: The ALTE infants responded to CO2 breathing with a significant increase in R-R intervals, i.e. decreases in heart rate, compared to the controls (45.1% increase in R-R intervals vs. 41.4%; p= 0.005). The differences between ALTE infants and controls depended primarily on the boys' responses. Conclusion: ALTE infants, particularly ALTE boys, have an autonomic dysfunction,lower sympathetic stimulation and/or inhibited vagal withdrawal when stressed with CO2. The outcome might provide clues to the mechanisms underlying the cardiovascular processes contributing to the terminal event in SIDS. [source] |