The aim of the present study was to assess circulating levels of VEGF (vascular endothelial growth factor), a biomarker with prognostic significance in cardiovascular disease, and markers of systemic inflammation in patients with stable and exacerbated COPD (chronic obstructive pulmonary disease). Lung function parameters, arterial blood gas analysis and circulating levels of VEGF, IL-6 (interleukin-6), TNF-alpha (tumour necrosis factor-alpha), CRP (C-reactive protein), fibrinogen and the peripheral blood neutrophil cell count were assessed in 30 patients on admission to the hospital for acute exacerbation of COPD, in 30 age-, gender- and BMI (body mass index)-matched patients with stable COPD, and 30 matched controls with normal lung function. Patients with acute exacerbated COPD had higher circulating concentrations of VEGF (P<0.001), IL-6 (P<0.05) and CRP (P<0.01) and an increased blood neutrophil cell count (P<0.05) compared with patients with stable COPD and healthy controls. VEGF levels in exacerbated COPD correlated with systemic inflammatory markers, such as CRP (r=0.61, P<0.005), IL-6 (r=0.46; P<0.01) and fibrinogen (r=0.39, P<0.05). In patients with stable COPD, there was a significant relationship between circulating VEGF levels and the percentage of the predicted FEV(1) (forced expiratory volume in 1 s) (r=0.47, P<0.01). Recovery from the exacerbation resulted in a significant decrease in both circulating VEGF levels and markers of systemic inflammation. In conclusion, circulating levels of VEGF and markers of systemic inflammation are up-regulated in patients with acute exacerbated COPD and decrease after recovery from the exacerbation.

. Heart rate variability and spontaneous baroreflex sequences in supine healthy volunteers subjected to nasal positive airway pressure. J Appl Physiol 99: [2137][2138][2139][2140][2141][2142][2143] 2005. First published July 7, 2005; doi:10.1152/japplphysiol.00003.2005.-To determine the dynamic effects of short-term nasal positive airway pressure (nPAP) on cardiovascular autonomic control, continuous recordings of noninvasively obtained hemodynamic measurements and heart rate variability (HRV) were obtained in 10 healthy subjects during frequency-controlled breathing (between 0.20 and 0.24 Hz) in supine posture under different pressures of nPAP ranging from 3 to 20 cmH 2O. HRV was assessed using spectral analysis of the R-R interval. The slope of the regression line between spontaneous systolic blood pressure and pulse interval changes was taken as an index of the sensitivity of arterial baroreflex modulation of heart rate (sequence method). Application of nPAP resulted in a pressure-dependent decrease of cardiac output and stroke volume (P Ͻ 0.05, ANOVA) and in an increase in total peripheral resistance (P Ͻ 0.03, ANOVA). Hemodynamic changes under increasing nPAP were accompanied by a decrease in total power of HRV despite mean R-R interval remaining unchanged. The overall decrease in HRV was accompanied by a reduction across all frequency bands when absolute units were used (P Ͻ 0.01). When the power of low frequency and high frequency was calculated in normalized units, a diminished high frequency and an increased low-to-high frequency ratio were observed (P Ͻ 0.05). Compared with low levels of nPAP, pressure levels of Ͼ10 cmH 2O were associated with a significant decline in the mean slope of spontaneous baroreceptor sequences (P Ͻ 0.04). These findings indicate that short-term administration of nPAP in normal subjects exerts significant alterations in R-R interval variability and spontaneous baroreflex modulation of heart rate. cardiac output; cardiovascular autonomic control; heart-lung interaction RESPIRATION SIGNIFICANTLY INFLUENCES autonomic cardiovascular control (12). During normal breathing, oscillatory changes of left ventricular stroke volume (SV) and arterial blood pressure (BP) are sensed by baroreceptors, which provoke parallel R-R interval changes by means of baroreflex physiology (27). Hemodynamic oscillations during normal (negative pressure) respiration are predominantly due to changes in intrathoracic pressure (ITP) (30). However, little is known about the effects of augmented positive ITP, which occurs with positive airway pressure (PAP) ventilation, on cardiovascular autonomic control. The application of PAP, both invasively or noninvasively, increases ITP and may result in a reduction in cardiac filling pressures (23,29,37,43). A reduction in cardiac filling pressures associated with PAP (or positive end-expiratory pressure) may induce a compensatory increase in vascular resistance to maintain systemic arterial pressure in the face of a reduced cardiac output (CO) (5, 41). The increase in...

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