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The sympathetic nervous system has been reported to be activated in pulmonary arterial hypertension (PAH). We investigated the prognostic significance of muscle sympathetic nervous system activity (MSNA) in PAH. Thirty-two patients with PAH were included in the study and underwent a measurement of MSNA over a 6-year period of time. They had undergone a concomitant evaluation of New York Heart Association (NYHA) functional class, a 6-minute walk distance (6MWD), an echocardiographic examination, and a right heart catheterization for diagnostic or reevaluation purposes. The median follow-up time was 20.6 months (interquartile range, 45.8 mo). Clinical deterioration was defined by listing for transplantation or death. Seventeen patients presented with clinical deterioration. As compared with the 15 others, they had an increased MSNA (80 +/- 12 vs. 52 +/- 18 bursts/min; P < 0.001) and heart rate (88 +/- 17 vs. 74 +/- 12 bpm; P = 0.01), a lower 6MWD (324 +/- 119 vs. 434 +/- 88 m; P < 0.01) and a deteriorated NYHA functional class (3.6 +/- 0.5 vs. 2.9 +/- 0.8; P < 0.001). The hemodynamic variables were not different. MSNA was directly related to heart rate and inversely to 6MWD. A univariate analysis revealed that increased MSNA and heart rate, NYHA class IV, lower 6MWD, and pericardial effusion were associated with subsequent clinical deterioration. A multivariate analysis showed that MSNA was an independent predictor of clinical deterioration. For every increase of 1 burst/minute, the risk of clinical deterioration during follow-up increased by 6%. Sympathetic nervous system activation is an independent predictor of clinical deterioration in pulmonary arterial hypertension.

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

P-485 Key Words: Chemoreceptors, Insulin,