[Impaired production of platelet-endothelial cell adhesion molecules as an early diagnostic marker of heart transplant rejection]. / Narushenie produktsii molekul trombotsitarno-endotelial'noi kletochnoi adgezii kak rannii diagnosticheskii marker ottorzheniya serdechnogo transplantata.

OBJECTIVE: Reveal the involvement of platelet-endothelial cell adhesion molecules PECAM-1 in the transplanted heart rejection pathogenesis and determine the CD31 marker significance for biopsy diagnostics of the process form and degree. MATERIAL AND METHODS: Sections from endomyocardial biopsies of 56 heart transplant recipients were stained with hematoxylin and eosin. The streptavidin-biotin method was used to determine the expression of T-lymphocytes (CD3), B-lymphocytes (CD20), macrophages (CD68) and the C4d component of complement to determine the form and degree of graft rejection. Additionally, the expression of platelet-endothelial cell adhesion molecules PECAM-1 (CD31) was detected. Using computer morphometry in digital images, the area of pathological changes and the area of CD31 expression was measured with the calculation of the staining area coefficient. RESULTS: The highest levels of PECAM-1 expression were found in the absence of a heart transplant rejection. The degree of rejection of 1R is characterized by a decrease in expression by 1.3 times, when there are no significant signs of necrosis in the myocardium, the area of which increases sharply at degree 2R by 163.7 times, and at 3R by 570.7 times compared with 1R. The process proceeds in parallel with a further decrease in the level of CD31 expression and is accompanied by the development of hemorrhagic manifestations. The intensity of hemorrhages in the myocardium increases by 7.3 times with grade 3R compared with 1R. CONCLUSION: Expression of PECAM-1 reflects the state of the vascular bed of the heart transplant. Its decrease can be considered as an early pathomorphological marker of transplanted heart rejection. The expression of CD31 continues to decrease with increasing severity of rejection and is accompanied by the progressive development of necrosis and hemorrhages in the graft heart muscle.

Index of phagocyte activation based on luminescence of dehydrogenase coenzymes.

In the cytoplasm of activated neutrophils and monocytes of blood, as well as microphages and macrophages of festering wounds, the incubation with nitroblue tetrazolium results, in two types of autoluminescence. The blue luminescence as a result of reduced pyridine nucleotides (RP) characterizes the non-active state of phagocytes. The yellow-green luminescence due to oxygenated flavoproteins (OF) signifies the active state of phagocytes. The luminescence intensity ratio of OF to RP reflects the rate of energy output and is the energy index of phagocyte activation.