ABSTRACT
It is believed that hyperemia in the skin, resulting from applied weak mechanical pressure delays the development of ischemia, and that it is a defensive neurovascular reaction against the local pressure, which can be considered as a critical point in terms of prevention of ischemia and, respectively, the risk for development of bedsores. Taking into account that nitric oxide can be released from autonomic nerves and make a significant contribution to the functioning of the mechanism of neurogenic vasodilation in different tissues, and the fact that the same role can also play the calcitonin gene-related peptide, the aim of this study was to clarify the role of each of these factors in the development of local hyperemia caused by non-painful, mechanical pressure on the skin. In experiments on white rats with a quantitative measurement of the intensity of skin blood flow, it was confirmed that in case of non-painful pressure acting on the skin, two-phase reaction of local blood flow appears - at first there is an increase in its level, and then an exponential decrease with stabilization at a level below the initial one. Analysis of received data allow to make conclusion that in relization of this phenomenon the role of trigger element belongs to nitric oxide, and the role of the executing unit - to calcitonin gene-related peptide. The effectiveness of this combined mechanism is limited by development of dominance of pressor-induced mechanical compression of cutaneous vessels over its vasodilator effect.
