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P-485: Insulin and chemoreceptors sensitivity
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P-485: Insulin and chemoreceptors sensitivity
P-485: Insulin and chemoreceptors sensitivity
Journal Article

P-485: Insulin and chemoreceptors sensitivity

2004
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Overview
Patients with obstructive sleep apnea frequently disclose obesity, hypertension, increased insulin levels and potentiation of peripheral chemoreflex sensitivity. We wanted to test the hypothesis that acute hyperinsulinemia increases chemoreflex sensitivity. In 12 healthy subjects (aged 24±3 years, mean±SD) we measured minute ventilation, end expiratory CO2, heart rate (HR) and arterial oxygen saturation during 5 minutes of normoxia, 5 minutes of isocapnic hypoxia (10% of oxygen and 90 % of nitrogen, stimulation of peripheral chemoreceptors) and 5 minutes of hypercapnic hyperoxia (7 % of CO2 and 93 % of oxygen) during insulin infusion (level of insulin 70±4 μU/ml) with stable glucose level and during infusion of NaCl 0.9 % (level of insulin 5±1 μU/ml). The infusions were administrated in a randomised order. Insulin increased minute ventilation (5.6±1.1 versus 6.5±1.2 L/min, p=0.0009), did not change HR (61±8 versus 62±7 bpm, p=0.17), saturation (98±1 versus 98±0 %, p=0.40) and end expiratory CO2 (39±2 versus 38±3, p=0.33) during normoxia. Insulin during hypoxia increased HR in comparison with placebo (76±12 versus 82±9, p=0.03), had a tendency to increase minute ventilation (7.7±2.1 versus 8.5±2.3, p=0.10), did not change saturation (88±4 versus 88±3, p=0.92) and end expiratory CO2 (37±1 versus 37±2, p=0.83). Peripheral chemoreflex sensitivity expressed by the ratio between minute ventilation and arterial oxygen saturation during normoxia and 5 minutes of hypoxia had a tendency to increase during insulin in comparison with placebo (82±22 versus 91±24 ml/% of saturation, p=0.07). Insulin did not change any parameter during hypercapnic hyperoxia in comparison with placebo. Insulin increases minute ventilation during normoxia and has a tendency to increase the sensibility of peripheral chemoreceptors. Am J Hypertens (2004) 17, 210A–210A; doi: 10.1016/j.amjhyper.2004.03.559
Publisher
Oxford University Press