**4. Conclusion**

*Basic and Clinical Understanding of Microcirculation*

the exact opposite effect is observed. How can we explain it?

This state can be formulated simply as "no outflow – no inflow".

The venular MVB itself deserves special attention. What is the physiological underpinning of the significantly larger vascular volume in the venular MVB than on the arteriolar side? This is what Nature intended, and therefore there is a physiological reason. Unlike arterioles, which only regulate blood inflow to the capillaries, many important functions are performed at the venular level. One is that mast cells are located in the immediate vicinity of venules with a diameter of 40–80 μm. This protective system reacts to various chemical and biological noxious agents entering the systemic circulation and it is situated in the venular section of the MVB. Postcapillary venules provide the exchange of macromolecules and protein-bound substances in the bloodstream by vesicular transport. Recognition, immobilization, "unpacking" of transport molecules, and vesicle formation require some time and are facilitated by the hemodynamic conditions in the venular section of MVB, since it has the slowest blood flow in the entire cardiovascular system. The venular section occupies a strategic position and is the first to receive

cardiac output. The cardiac output in AH patients may be elevated during venoconstriction [60]. Based on the significantly lower peripheral vascular resistance, the VP patients can be hypothesized to have a hyperkinetic circulation type, and their higher BP values are due to a combination of two factors – an increase in the cardiac output, as noted in other studies [48], and a disruption of the blood outflow from the capillary bed with an increase in PVR at the postcapillary (venular) level. Regardless of the reasons for the hindered blood outflow from the capillary bed, the mechanism that increases the amplitude of myogenic vasomotions in the precapillary arterioles and capillary sphincters is baffling. Normally, in a closed cardiovascular system, an increase in the venous pressure results in a consecutive rise in the capillary and precapillary arteriolar pressure. The smooth muscle cells of the resistive microvessels respond to increased pressure and distension by contracting by the Ostroumov-Bayliss mechanism, which should lead to a rise in their tone with a decrease in the amplitude of myogenic vasomotions (Am). But in the VP group,

It can be hypothesized that the precapillary arteriolar tone decline is of a compensatory nature, aimed at overcoming the raised resistance at the postcapillary level. The increase in the arterial blood inflow is aimed at overcoming the impaired venous outflow. But from the metabolic expediency point of view, this compensation mechanism is extremely unfavorable. This can be assumed to be a consequence of the functional features of the smooth muscle cells in VP patients. Falcone et al. established *in vivo* that an increase in venous pressure in the cremaster muscle of SHR caused a more pronounced constriction reaction of the 15–100 μm arterioles than in normotensive animals [61]. Another research group demonstrated on mesenteric arterioles (diameter 100–150 μm) *in vitro* that in SHR the smooth muscle cells (lacking sympathetic innervation) develop a significantly higher vasomotion amplitude in response to norepinephrine compared to normotensive animals [62]. The results of this pilot study suggest that the contribution of the venular MVB to PVR is more substantial, and the generally accepted vascular resistance scale requires adjustment. In previous studies on healthy normotensive volunteers it was demonstrated that the blood volume in the skin venular microvessels has a positive correlation with BP, and a negative correlation not only with the magnitude of nocturnal BP decline, but also with the dilation response of MVB during the heat test, the nociception system activation, and post-occlusive reactive hyperemia [63, 64]. MVB is anatomically located between the arterial and venous systems, and, as capillaries do not stretch, the disruptions in the outflow system naturally affect the inflow system to the exchange vessels with all the logical metabolic consequences.

**146**

metabolic information.

LDF is a relatively new technique for studying microcirculation in humans which is going through the stages of adoption, data accumulation, and interpretation of the obtained results. A review of the scientific literature over the past 20 years has identified only 143 studies of microcirculation in humans by LDF with wavelet analysis of blood flow oscillation. The total number of healthy subjects and patients with various organ and system diseases involved in the studies does not exceed 2600 [74].

The main aim of this pilot study was to evaluate the informativeness of LDF in assessing the functional state of the skin microvascular bed in patients with essential arterial hypertension. The study has many weaknesses, due to the retrospective data analysis and the inability to collect information on the central hemodynamic parameters and humoral status of the patients. Nevertheless, it can be concluded that the aim has been achieved. The obtained results are unexpected; however, they allow the microcirculatory blood flow problems in patients with AH to be viewed in an entirely new light.

Several quite precise conclusions can be made based on the study:


4.The role of the venular-venous vascular bed in AH is underestimated, and further studies in this area are required; this will contribute to solving many problems that cardiologists face today.
