ECE2007 Poster Presentations (1) (659 abstracts)
Background: The cardiovascular complication is the main cause of morbidity and mortality in obese patients. Endothelial dysfunction and atherosclerosis have the goal role in development of these diseases. The aim of our study was to reveal the role of nitric oxide during obesity associated arterial hypertension.
Subject and method: 200 obese patients (age 3555) were investigated. Control group comprised 25 healthy subjects. We calculated BMI, determined lipid profile, concentration of nitric oxide, activity of antioxidant enzymes superoxiddismutase and katalaze, evaluated arterial pressure.
Results: Systolic arterial pressure insignificantly increased in overweight group (n=50) compared to control group (124.3±5.6 mm/hg), but significantly (P<0,05) in patients with obesity of I (n=50) (134.4±11.7 mm/hg), II (n=50) (142.6±12.6 mm/hg) and III (n=50) (145.7±10.3 mm/hg) degree. Diastolic arterial pressure significantly (P<0.05) increased in patients with obesity of II (91.8±9.4 mm/hg) and III (95.6±7.2 mm/hg) degree compared to control group (81.4±6.2 mm/hg). According to weight gain the whole lipid profile (Chol, Trig, HDL, LDL) was damaged. Concentration of nitric oxide significantly reduced in obese subjects compared to control group. Significant decrease of nitric oxide in different BMI groups was revealed (overweight-11.875±0.427, I degree-11.2154±0.3113, II degree-10.2364±0.381, III degree-9.5±0.2823 P<0,001). Changes in concentration of NO correlated with decrease of antioxidant enzymes activity (enzymes activity decrease compared to control group and increase according to weight gain).
Conclusion: Hyper generation of oxygen causes inactivation of antioxidant enzymes and disorders in redox-status. NO oxidative degradation, stimulated by dyslipidemia, has the main role in the pathogenesis of arterial hypertension development during obesity.