Effect of acute systemic hypoxia on human cutaneous microcirculation and endothelial, sympathetic and myogenic activity.

The regulation of cutaneous vascular tone impacts vascular vasomotion and blood volume distribution as a challenge to hypoxia, but the regulatory mechanisms yet remain poorly understood. A skin has a very compliant circulation, an increase in skin blood flow results in large peripheral displacement of blood volume, which could be controlled by local and systemic regulatory factors. The aim of this study was to determine the acute systemic hypoxia influence on blood flow in skin, local regulatory mechanism fluctuations and changes of systemic hemodynamic parameters. Healthy subjects (n=11; 24.9±3.7years old) participated in this study and procedures were performed in siting position. After 20min of acclimatization 15min of basal resting period in normoxia (pO2=21%) was recorded, followed by 20min in acute systemic hypoxia (pO2=12%), and after 15min of recovery period in normoxia (pO2=21%). HRV was used to evaluate autonomic nervous system activity to heart from systemic hemodynamic parameters which continuously evaluated cardiac output, total peripheral resistance and mean arterial blood pressure. Regional blood flow was evaluated by venous occlusion plethysmography and skin blood flow by laser-Doppler flowmetry. To evaluate local factor influences to cutaneous circulation wavelet analysis was used; fluctuations in the frequency intervals of 0.0095-0.021, 0.021-0.052, and 0.052-0.145Hz correspondingly represent endothelial, sympathetic, and myogenic activities. Our results from HRV data suggest that acute systemic hypoxia causes statistically significant increase of sympathetic (LF/HF; N1=0.46±0.25 vs. H=0.67±0.36; P=0.027) and decrease of parasympathetic (RMSSD; 80.0±43.1 vs. H=69.9±40.4, ms; P=0.009) outflow to heart. Acute hypoxia causes statistically significant increase of heart rate (RR interval; N1=960.3±174.5 vs. H=864.7±134.6, ms; P=0.001) and cardiac output (CO; N1=5.4 (5.2; 7.9) vs. H=6.7±1.4, l/min; P=0.020). Regional blood flow and vascular conductance were not changed during acute systemic hypoxia, but forearm skin blood flow (skin blood flow; N1=39.7 (34.0; 53.2) vs. H=51.6±13.9, PU; P=0.002) increases however local regulatory factor activity was not changed by acute systemic hypoxia. Acute systemic hypoxia causes sympathetic stimulation to heart which results in increased heart rate and larger cardiac output which could be the reason of forearm skin blood flow increase in acute systemic hypoxia without impact of local regulatory factors.

Two-stage multi-Gaussian fitting of conduit artery photoplethysmography waveform during induced unilateral hemodynamic events.

Photoplethysmography (PPG) is an optical technique with high diagnostic potential, yet clinical applications remain underdeveloped. Standardization of signal recording and quantification of waveform are essential prerequisites for broader clinical use. The aim of this study was to utilize a two-stage multi-Gaussian fitting technique in order to examine the parameters of conduit artery PPG waveform recorded during increasing the unilateral regional vascular resistance (RVR). This study was conducted on 14 young and healthy volunteers; various external compressions (ECs) were performed by inflating a tight cuff at 0, 40, 80, and 200 mmHg, while registering femoral PPG (wavelength 880 nm), diameter, blood flow linear velocity (vascular ultrasound), and the arterial pressure (Finapres) during the states of the baseline, partial, and total arterial occlusion, and resultant reactive hyperemia. An increase of the EC elevated the arterial stiffness (AS) and the unilateral distal RVR, and caused a shift of the fitted multi-Gaussian parameters: a decreased delay between reflected and traverse wave components and an increased ratio of their amplitudes. It was concluded that two-stage multi-Gaussian waveform quantification demonstrates an approach potentially extending the use of arterial site PPG in the assessment of diagnostically useful markers e.g., the RVR and the AS.

Nail fold capillary diameter changes in acute systemic hypoxia.

The present study was undertaken to determine the effect of arterial blood hypoxemia induced by acute systemic hypoxia (pO2=12%) on capillary recruitment and diameter, and red blood cell (RBC) velocity in human nail fold capillaries during rest, arterial post-occlusive reactive hyperemia (PRH), and venous occlusion (VO) using intravital video-capillaroscopy. Capillary recruitment was unchanged in acute systemic hypoxia (H) versus normoxia (N). There was no difference in RBC velocity measurements between normoxia and hypoxia (P<0.63). However, a statistically significant increase in nail fold capillary total width (N, 39.9±9.1 vs. H, 42.7±10.3 µm; P<0.05), apical diameter (N, 15.5±4.3 vs. H, 16.8±4.3 µm; P<0.05), arterial diameter (N, 11.9±3.5 vs. H, 13.9±4.1 µm; P<0.05), and venous diameter (N, 15.5±4.3 vs. H, 17.2±4.8 µm; P<0.05) was observed and continued to be significant most often during post-occlusive reactive hyperemia (PRH) and venous congestion (VO). These data suggest that acute systemic hypoxia does not increase capillary recruitment, but instead increases capillary diameter, resulting in increased capillary blood flow.

Relation of inflammatory chemokines to insulin resistance and hypoadiponectinemia in coronary artery disease patients.

BACKGROUND: Although many studies have shown that the metabolic syndrome (MS) and type 2 diabetes mellitus (T2DM) both are associated with chronic inflammatory state and are risk factors for coronary artery disease (CAD), it is still unclear which condition is a more important contributor to the increased production of inflammatory chemokines. The purpose of this study was to assess monocyte chemoattractant protein-1 (MCP-1) and interleukin-8 (IL-8) levels and their association with insulin resistance and adiponectin concentrations in CAD patients, who were categorized as having T2DM, MS, or neither. METHODS: CAD male patients were categorized into three groups: 24 non-obese patients with T2DM (D), 24 obese patients with MS (M) and 24 patients without T2DM or MS (W). 20 healthy subjects were selected as controls (C). Insulin resistance was assessed by the HOMA-IR method, but serum MCP-1, IL-8, and adiponectin levels were measured by xMAP technology. RESULTS: Serum levels of MCP-1 and IL-8 in D and M groups were increased in comparison with W and C groups (p<0.001, p<0.01), but the increase in the M group was significantly higher than that in the D group (p<0.05, p<0,001), besides MCP-1 and IL-8 concentrations were correlated with HOMA-IR indexes (r=0.52; r=0.49, p<0.0001) and adiponectin levels (r=-0.59, p<0.0001). The M group demonstrated a diminution in the adiponectin level (p<0.01) and pronounced increase of HOMA-IR in comparison with the other three groups (p<0.01). CONCLUSION: Obese CAD patients with MS have a more pronounced increase of MCP-1, IL-8 and HOMA-IR and more decreased adiponectin levels than non-obese CAD patients without MS.