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Based on literary data we carried out the analysis of the influence vascular endothelium on maintaining the haematological and circulatory balance in the organism. Particular attention was paid on its active metabolic and secretory role in this process.
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OBJECTIVE: The aim of this study is to investigate the role of high doses of atorvastatin (80 mg per day) in the treatment of endothelium dysfunction of the coronary arteries. MATERIAL AND METHODS: Intracoronary acethylcholine test was performed for 28 (16 in treatment group and 12 in control group) patients who had normal coronary angiogram or minimal lesions (stenosis <50%) and symptomatic coronary heart disease. Acetylcholine was given into left coronary artery in three stages (2 min each) at estimated intracoronary concentrations 10(-6) mol/l, 3.3x10(-6) mol/l,and 10(-5) mol/l. Treatment group patients were given atorvastatin 80 mg per day. Intracoronary acetylcholine test was repeated after six months. The target segment was the segment that exhibited the maximal constrictive response at baseline in a given patient. RESULTS: Total cholesterol was reduced by 40.6+/-11.2% (p<0.001), low density lipoproteins cholesterol by 55.4+/-14% (p<0.001), triglycerides by 29.6% (p<0.05) and high density lipoproteins cholesterol was increased by 24.7% (p<0.05) in atorvastatin group after 6 months of therapy. No significant lipid changes were observed in the control group. Sixteen target segments in the treatment group and 12 segments in the control group were selected for primary efficacy parameter. The vasoconstrictor reaction to acetylcholine was similar at baseline in both groups: -16.8%+/-11.6% of diameter in atorvastatin group and -14.2%+/-13.7% in control group (p=0.58) at dose 10(-6) mol/l, -43.5%+/-21.2% in atorvastatin group and -41.2%+/-22.4% in control group (p=0.79) at dose 3.3x10(-6) mol/l, -64.5%+/-12.4% in atorvastatin group and -57.4%+/-15.6% in control group (p=0.35) at dose 10(-5) mol/l. Treatment with high doses of atorvastatin markedly decreased acetylcholine - induced vasoconstriction: -6.5%+/-14.5% of diameter in atorvastatin group versus -18.3%+/-14.0% in control group (p=0.04) at dose 10(-6) mol/l, -19.7%+/-22.8% in atorvastatin group versus -40.0%+/-25.0% in control group (p=0.034) at dose 3.3x10(-6) mol/l, -29.9%+/-21.3% in atorvastatin group (6 segments) versus -48.7%+/-19.0% in control group (3 segments, p=0.24) at dose 10(-5) mol/l. CONCLUSION: Treatment with high doses of atorvastatin significantly improves endothelium-mediated response to acetylcholine in the coronary arteries of the patients with minimal lesions.
In this pilot study, we sought to compare the vasodilatory and hemodynamic properties of the peripheral vasculature in the forearms of young, healthy African-American females to similarly matched white females. We used high-resolution ultrasound of the brachial artery to evaluate 11 African-American females and 8 white females. When normalized to nitrate-induced dilation, endothelium-dependent dilation was reduced in young African American females compared to white females (0.6 in African American females compared to 1.0 in white females). These results indicate the need for a larger study to examine this phenomenon.
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The study was conducted in St. John's Medical College Hospital and Department of Physiology, with the aim of studying the serum nitrate levels in pre-eclampsia and normal pregnancy. The total number of subjects studied in various groups were 159, control (n = 55), first trimester (n = 13), second trimester normal (n = 42), second trimester pre-eclampsia/PET (n = 5), third trimester normal (n = 32), third trimester pre-eclampsia/PET (n = 12). The serum nitrate was measured by one step enzymatic assay using Nitrate reductase from Aspergillus species. The nitrate levels in the third trimester pre-eclamptic group was found to be significant lower (P = 0.02), as compared to normal subjects, however the renal functions were normal in all the subjects.
The presence of an altered endothelium-mediated flow-dependent dilatation (FDD) of peripheral conduit arteries in insulin-dependent diabetic patients without microangiopathy is still controversial. We studied 10 normotensive and non atherosclerotic insulin-dependent diabetic patients (D group) without complication (neuropathy, microalbuminuria or neuropathy) and 10 control subjects (C group) matched for age, sex and BMI. Radial artery diameter (RAD, echotracking) and flow (RAF, Doppler) were measured at baseline and during FDD in response to distal hand skin heating (from 34 to 44 degrees C). a method developed to increase RAF by stable steps by decreasing gradually hand skin vascular resistance. Endothelium-independent dilatation was evaluated by administration of glyceryl trinitrate (GTN: 0.3 mg spray). At baseline, there was no difference between group for RAF (C: 18 +/- 5 vs D: 18 +/- 2 mL/min; NS) and RAD (C: 2.51 +/- 0.12 vs D: 2.54 +/- 0.07 mm; NS). Heating induced in the diabetic group a smaller increase in RAF (C: 473 +/- 126% vs D: 262 +/- 63%; p<0.05) and RAD (C: 22.6 +/- 2.6% vs D: 16.1 +/- 1.8%; p<0.01). This last result remains significant when the increase in RAF was included into the analysis of RAD variation during heating (p<0.05). GTN-induced dilatation was similar in the 2 groups. Our results obtained by use of the hand skin heating method demonstrate the presence of an abnormal arteriolar skin reactivity and an altered peripheral conduit artery endothelium-dependent dilatation in uncomplicated insulin-dependent diabetic patients. The early identification of these anomalies, with negative prognostic value, could contribute to the management of these patients.
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