[Neutrophile apoptosis in patients with chronic rheumatic heart disease].
The purpose of the investigation was to study peculiarities of the functioning of neutrophile granulocytes in chronic rheumatic disease (CRD) complicated by cardiovascular pathology. The subjects of the study were 80 patients with CRD of the heart with valvular defects, accompanied by arterial hypertension (AH) and cardiac arrhythmias: 37 men (mean age 53.6 +/- 9.7 years) and 43 women (mean age 56.2 +/- 9.6 years). The control group consisted of 25 healthy donors. Isolated peripheral blood neutrophiles were cultivated during 6 hours. The level of nitric oxide (NO) production was measured. Functional cell activity was studied by chemoluminiscent assay. The degree of apoptotic readiness was studied by immunocytochemical method, determining bak marker expression on cell membrane surface. In CRD the processes of oxygen-dependent neutrophile metabolism were found to be intensified, which was accompanied by intensified reserve abilities and decreased NO synthesis and apoptotic activity. Functional cell activity in patients with a background of AH was characterized by lowered granulocyte NO production. Intensified production of active oxygen metabolites, observed in paroxysmal cardiac fibrillation, evidences the hyperactivity of the pro-oxidative system, leads to fast myocardial cell membrane lesion and the development of structural changes forming abnormal automatism and trigger activity. Neutrophiles isolated from patients with CRD were in a state of priming, the feature of which was high biocide cell potential. The lowering of apoptotic readiness evidences high mobilization abilities of neutrophiles. The synthesis of NO as one of autoregulation factors is a protective mechanism directed against the cytotoxic activity of phagocytes. The stimulation of granulocyte NO production can lower the oxidative stress intensity and leukocyte aggression and stabilize the course of the disease.
Il'in
M V
MV
Khrustalev
A O
AO
Korshunov
N I
NI
D000328:Adult; D000368:Aged; D017209:Apoptosis / Q000502:physiology*; D002478:Cells, Cultured; D002908:Chronic Disease; D005260:Female; D005500:Follow-Up Studies; D006801:Humans; D007150:Immunohistochemistry; D008297:Male; D008875:Middle Aged; D009504:Neutrophils / Q000378:metabolism / Q000473:pathology*; D009569:Nitric Oxide / Q000096:biosynthesis; D018384:Oxidative Stress; D012214:Rheumatic Heart Disease / Q000097:blood / Q000473:pathology*
D009569:Nitric Oxide