The combined operation of mitral valve prosthetics with the applying biological prosthesis and simultaneous radio-frequency surgical ablation is a radical method of treating acquired mitral valve defects with associated atrial fibrillation at elderly patients. The presence of biological prosthesis and steady sinus rhythm makes it possible to cancel the anticoagulant therapy in half a year after operation, which excludes the risk of hemorrhagic complication development.

The aim of this work was to evaluate contribution of released membrane particles (RMP) to the development of systemic inflammatory response (SIR) after aortocoronary bypass grafting (ACBG). The number of RMP carrying surface adhesion molecules, CD62L, CD62P, CD62E, was shown to increase in the early postoperative period in parallel with the enhancement of lymphocyte plasma membrane blebbing and elevation of cytokine levels in peripheral blood. It is concluded that (1) activation of plasma membrane blebbing in peripheral blood cells underlies the appearance of RMP in circulation; (2) increased number of RMP expressing CD62L, CD62P, CD62E is a marker of intercellular communication associated with the development of SIR and suggests new mechanisms of RMP involvement in the reaction of organism to massive surgical injury.

The pathogenesis of neuronal dysfunction was evaluated from the viewpoint of cellular disturbances in NAD(+) metabolism and changes in activity of NAD(+)-utilizing enzymes (e g., ADP-ribosyl cyclase/CD38). S-100B concentration and CD38 expression on peripheral blood lymphocytes were altered in patients after surgery for coronary heart disease with extracorporeal circulation. These changes in patients during the early postoperative period correlated with variations in CD38 expression on neuronal cells from postischemic rats with cognitive dysfunction.

The currently available data on the pathogenesis of a systemic inflammatory reaction (SIR) are reviewed in terms of dys-regulation of membrane-cytoskeletal interactions, cellular adhesion, membrane particle release, and development of endothelial dysfunction as a key factor in the genesis of SIR. Key words: systemic inflammatory reaction, membrane particles, blebbing, selectines, cytokines.

The present views of the pathogenesis of neuronal dysfunction in critical conditions are analyzed, by taking into account of impairments of cellular NAD+ metabolism, the activity of NAD+-converting enzymes, including ADP-ribosyl cyclase/CD38, the possibilities of developing new neuroprotective strategies. Key words: neuronal dysfunction, ADP-rybosyl cyclase/CD38, NAD+, critical condition.

Objective: to study the mechanism that is responsible for impaired neuronal cell electroexcitability and viability, which is associated with modification of ADP-ribosyl cyclase in cerebral ischemic lesion, as well as the possibilities of pathogenet-ically correcting these disorders. Materials and methods. Acute cerebral ischemia was simulated in vivo on noninbred albino male rats, by ligating the right common carotid artery under general anesthesia. y-Interferon was intraperitoneally administered to the mammal in a dose of 5000 IU/kg body weight once daily for 3 days until unilateral extravasal occlusion of the common carotid artery occurred. The activity of ADP-ribosyl cyclase was evaluated by the fluorometric technique. CD38 expression in the brain cells was immunohistohemically detected. The severity of neurological symptoms was evaluated using the international NSS scale for laboratory animals. Cognitive dysfunction was recorded employing the standard test — the Morris water maze. The validity of differences was assessed by Student’s t-test and T-test, by applying STATISTICA version 6.0 (StatSoft-Russia, 1999) and BIOSTATISTICA programs. Results. Progressive neurological and cognitive deficit-induced changes occurred in the activity and expression of ADP-ribosyl cyclase/CD38 in the neuronal and glial cells in the course of brain ischemia. Neuroprotection and prevention of postischemic cognitive dysfunction were achieved by the use of y-interferon as a modifier of the brain cell expression of CD38/ADP-ribosyl cyclase.