Proceedings of The Physiological Society

Europhysiology 2018 (London, UK) (2018) Proc Physiol Soc 41, PCB339

Poster Communications

Exploring the effect of an oral glucose load on the cutaneous microvascular dynamics with the wavelet transform

J. Šorli1, H. Silva2,3, H. Lenasi1

1. Institute of Physiology, Faculty of Medicine, University of Ljubljana, Ljubljana, Slovenia. 2. U Lusófona, School of Health Sc & Technologies, CBiOS (Research Center for Biosciences and Health Technologies), Lisboa, Portugal. 3. Pharmacol. Sc Depart, U Lisboa, Faculty of Pharmacy, Lisboa, Portugal.

Chronic hyperglycemia leads to microvascular dysfunction associated with several cardiovascular and metabolic complications. It has also been established that acute hyperglycemia impacts endothelial function by increasing the level of oxidative stress and reducing NO bioavailability, as well as interfering with the activity of the sympathetic nervous system. On the other hand, hyperinsulinemia has been shown to increase the endothelium-dependent vasodilation. How these mechanisms integrate at the level of microcirculation is less well investigated and contradictory results have been found in in vivo studies where both physiological stimuli are present. Our objective was to explore the effect of a standard oral glucose load (OGL) on the reactivity of the cutaneous microcirculation. 16 healthy subjects (21.4±1.3 yr.; 11 males, 5 females) participated in the study after informed consent was obtained. Preliminary experiment where plasma glucose dynamics was traced spectrophotometrically (HemoCue, Glucose201+) for 2 h by a 5 min blood sampling revealed that the highest plasma conc. was achieved after 35 min (8.9±1.2 mmol/L). After fasting for 12 h, microcirculation was assessed on the finger pulp and on the volar surface of the forearm by using laser Doppler fluxmetry (LDF), quantified in arbitrary units (AU). To test microvascular reactivity, we induced post-occlusive reactive hyperemia (PORH: 5 min baseline tracing, 3 min occlusion of the brachial artery, 7 min post-occlusion) before (pre-load) and after OGL (75 g/250 mL). As a control experiment, subjects performed the same protocol after receiving 250 mL of bottled water. The main spectral components of the LDF signal (cardiac, respiratory, myogenic, sympathetic and endothelial NO-dependent) were obtained after decomposition with the wavelet transform, and their contribution to the overall signal was expressed as percent ratio (%). Nonparametric tests were applied and a p<0.05 adopted. The post-pre PORH perfusion difference was significantly lower with glucose than with water (glucose: -2.0±4.9 AU; water: 5.4±7.9 AU; p=0.001) for the forearm. The glucose load significantly affected the sympathetic activity of the forearm region. On the post-load PORH, this activity was significantly lower than control during the reactive hyperemia phase (glucose: 20.3±8.4 %; water: 26.0±4.1 %; p=0.006), but significantly higher during the recovery phase (glucose: 20.4±6.7 %; water: 18.4±7.8 %; p=0.039). These changes were not noted on the pre-load PORH and in neither of the control experiments. No changes in the PORH response profile were detected for the finger. These results suggest that, in healthy subjects, an oral glucose load might affect the local cutaneous microvascular response to a PORH test through modulation of the sympathetic activity, rather than through endothelium-dependent vasodilation.

Where applicable, experiments conform with Society ethical requirements