COMPARISON OF EFFECTS OF ENALAPRIL AND UNCONTROLLED ANTIHYPERTENSIVE THERAPY ON INSULIN RESISTANCE, ENDOTHELIUM FUNCTION, MARKERS OF INFLAMMATION AND PLATELET ACTIVITY IN PATIENTS WITH METABOLIC SYNDROME

Aim. To assess influence of enalapril and uncontrolled antihypertensive therapy on insulin resistance, endothelium function, markers of inflammation, and platelet activity in patients with metabolic syndrome (MS). Material and methods. 41 patients with MS (21 women and 20 men, aged 58±2 years) were included into open parallel controlled study. MS was defined according to III report of USA Educational Program on cholesterol (2001). Patients were divided into 2 groups. Patients of the 1st group received enalapril (Enam, Dr. Reddy’s) 10 mg daily with further dose titration to 20 mg daily. Patients of the  2nd group continued receiving the same antihypertensive therapy as before (15% - inhibitors of angiotensin converting enzymes, 15% - в-blockers, 15% - diuretics, and 20% of patients - combined therapy). Study duration was 12 weeks. Results. Therapy with enalapril during 3 months resulted into significant decrease in systolic and diastolic blood pressure (BP) by 13 and 9% respectively. BP level decreased insignificantly (by 4,5 and 2% respectively) in controlled group. Ratio of plasma concentration of glucose to insulin in the 1st group increased by 14% before glucose load, and by 25% (p<0,05) 2 hours after peroral glucose load, while in the 2nd group decrease in these figures was noted by 12 and 5% respectively. This shows that treatment with enalapril, unlike uncontrolled antihypertensive therapy, lead to decrease in insulin resistance. Cuff test revealed significant increase in growth of brachial artery diameter in the group of patients, who received enalapril (12% before treatment, and 17% after treatment). Regular antihypertensive therapy didn’t change this parameter significantly (13 and 13,8% respectively). C-reactive protein level decreased by 48% (p<0,05) in the 1st group. Insignificant increase of this marker’s level was observed in the 2nd group. Platelet functional activity in both groups didn’t change significantly. Conclusion.  Together with strong antihypertensive effect, enalapril monotherapy is more efficient than regular antihypertensive therapy in reducing insulin resistance and chronic subclinical inflammation, as well as it has priority in improving endothelium depending vasodilatation

MOULDING MIXTURES HARDENING PROCESS BASED ON LIGNIN-BASE SULPHONATE BINDER

Hardening of agglutinant sands on lignosulphonate binding agent is the result of two processes: oxidation-reduction in the system lignosulphonate acids — persulfuric natrium in the early stages of hardening and hydration of cement in the latter stages

Perindopril and hydrochlorthiazide effects on endothelium-dependent vasodilatation and angiotensin-converting enzyme activity in patients with mild to moderate arterial hypertension

Aim. During 12-week perindopril (PR) and hypothiazide (HT) therapy, to study its antihypertensive efficacy, as well as its influence on endothelial function (EF) and angiotensin-converting enzyme (ACE) serum activity, in patents with essential arterial hypertension (EAH). Material and methods. The study included 20 males (mean age 48.8±8.4 years) with mild to moderate AH. Antihypertensive efficacy was assessed during office BP measurement (Korotkoff method) and 24-hour blood pressure monitoring (BPM). EF was assessed by endothelium-dependent vasodilatation (EDVD) during reactive hyperemia test (RHT). Results. According to office BP measurements, target BP level (<140/90 mm Hg) was achieved in 75% patients on PR monotherapy, and 65% on HT monotherapy. According to 24-hour BPM, PR influenced BP levels more beneficially than HT. During PR and HT monotherapy, antihypertensive effect was more pronounced in patients with moderate AH (p=0.06). PR monotherapy caused some EDVD increase in patients with moderate AH (by 10%; NS), but did not affect EDVD in individuals with mild AH. HT treatment substantially increased EDVD in patients with mild AH (by 24%, from 7.13 to 9.18) and even more in participants with moderate AH (by 54%, from 6.52 to 10.02). PR therapy significantly reduced ACE activity, increased at baseline, to 28.1 nmol/min•ml (-43%, p<0.01). In patients with initially low ACE activity, it remained at the same level (reduction to 21.16 nmol/min•ml, NS). HT treatment did not affect this parameter in participants with low or high initial ACE activity. Conclusion. PR and HT antihypertensive effects were associated with EDVD correction. PR and HT antihypertensive efficacy depended on baseline ACE activity. Both drugs could be used for BP correction in individuals with low ACE activity; for patients with initially high ACE activity, PR is more effective