## 3 Results
Red and blue lines show BPA averaged in the ROIs located at the forehead in the area of the compress application and marked by the red and blue squares in panels (A–C), respectively. Black and magenta lines in graph (**D**) show BPA dynamics estimated in the black and magenta ROIs located in the nose and cheek, respectively. The application of the compress lasted from the fifth to the eleventh minute of the experiment. during the whole period of the thermal impact, and in the most cases, it continues at this level even after the termination of the impact. The observed BPA increase reflects the vasomotor response of the skin to a local temperature increase, the physiological equivalent of which is an increase in the number of functioning capillaries. Therefore, most likely, BPA is a measure of the intensity of blood flow in the upper layers of the skin. As seen in Figure 3, the amplitude of the PPG waveform in the skin exposed to the thermal impact (red and blue curves in Figure 3D) displays different dynamics than that in the non-exposed areas (black and magenta curves). While a significant increase in BPA was observed in the compress application area, no such dynamics was observed in the reference ROIs. A significant BPA difference between the heated and unheated facial areas before and during compress application was observed for all subjects (\(p<0.0001\)), as shown in Figure 4. Hereinafter, a paired-sample \(t\)-test is used to evaluate the statistical significance of the difference between these data groups. The intensity of the thermal impact denoted as heating grade and measured as the difference in the skin temperature in the forehead before and after application of the compress was different for different subjects (see Table 2). Periods of the compress application denoted as heating time were also slightly different. The duration of the vasomotor reaction of skin vessels to the heat exposure was determined as a period during which BPA exceeds its mean level plus the standard deviation (STD) measured in the baseline. The mean heating time was \(6.2\pm 1.5\) min whereas the mean duration of the vasomotor reaction in the entire cohort of subjects was \(8.9\pm 2.6\) min. The example of BPA dynamics in Figure 3D shows that its initial growth occurs immediately with increasing temperature and takes the same time (30-40 s). A similar reaction was observed in all studied subjects. After removing the compress, BPA in the forehead remained significantly higher than in the baseline in 10 of 17 subjects, despite the fact that the skin temperature of the forehead always dropped to the initial level. We explain this observation by differences in the heating grade, which was different in different experiments. A simultaneous drop in BPA and skin temperature was observed in subjects for whom the heating grade was less than 3.5 \({}^{\circ}\)C (with the exception for KVO), as seen in Table 2. More pronounced heating of the skin was accompanied by a longer reaction of the vascular system. Table 2 also shows the mean BPA (\(\pm\)STD) in the forehead before, during and after the thermal impact for each subject. As one can see, there is a significant increase in the parameter BPA for all  
Figure 4: Vasomotor response to the thermal impact applied to the forehead, measured as the relative increase of BPA in different locations before and during compress application, and presented as a “box-and-whiskers” type diagram for all studied subjects. Red and blue are ROIs located on the forehead, black is ROI located in the bridge of the nose and magenta in the cheek. measured subjects during the warm compress application. Correlation analysis of the data has revealed that both mean BPA after the impact and its absolute increase in respect to the baseline positively correlate with the heating grade: \(r=0.73\), \(p=0.001\) and \(r=0.77\), \(p<0.001\), respectively. Nevertheless, no correlation of the BPA increase with age, gender, blood pressure and the mass index was observed within our cohort of subjects.