PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “endothelial dysfunction”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,585 records · Page 88Linked to original sources
PubMed2005

Arterial intima-media thickening and endothelial dysfunction in obese Chinese children.

UNLABELLED: We studied ultrasonographic signs of early atherosclerosis in relation to established risk factors of cardiovascular disease in 43 obese school-age children compared to 28 non-obese controls. The groups did not show significant differences in age, gender ratio and body height. Mean carotid intima-media-thickness (IMT), carotid haemodynamic parameters, flow-mediated dilatation of the brachial artery (FMD), and biochemical markers of dyslipidaemia were measured and correlated. IMT was significantly increased (0.62 mm vs. 0.46 mm, P <0.001) and FMD was markedly reduced (10.9% vs. 18.8%, P <0.001) in the obesity group. Differences in IMT and FMD persisted after adjustment for Body Mass Index (BMI) and blood pressure on ANCOVA. BMI was highly associated with increased IMT ( r =0.58, P <0.01) and reduced FMD ( r =-0.42, P <0.01), as were blood levels of total cholesterol, LDL cholesterol and Apo B. CONCLUSION: Childhood obesity seems to contribute to the development and progression of early atherosclerosis, particularly in combination with hypertension and dyslipidaemia. In order to prevent coronary atherosclerosis and other cardiovascular complications, it is vital to control obesity starting from childhood. Ultrasonography of the arterial wall may be used in a clinical setting to identify high-risk patients among severely obese children.

Analysis of Variance↗
PubMed1995

Endothelial dysfunction in venous pulmonary hypertension in the neonatal piglet.

In a group of neonatal piglets an increase in pulmonary arterial pressure was obtained within 2 weeks after a partial mechanical obstruction of the left atrium by a balloon catheter. Mean pulmonary artery pressure in the hypertensive animals (n = 6) was 24 +/- 2 mm Hg as compared (p < 0.01) with 15 +/- 1 mm Hg in controls (n = 6) or 9 +/- 2 mm Hg in sham-operated piglets (n = 6). Cardiac index was reduced in hypertensive versus control and sham groups: 0.15 +/- 0.01 versus 0.32 +/- 0.05 and 0.29 +/- 0.04 L.min-1.kg-1 (p < 0.05), respectively. There was no detectable difference on histologic examination in the pulmonary arteries between the three groups. Right ventricular hypertrophy was observed in the group with pulmonary hypertension. In hypertensive piglets, isolated conduit pulmonary arteries did not relax when stimulated with acetylcholine; they always relaxed to sodium nitroprusside. These data suggest that the first stages of perturbations reported during pulmonary venous hypertension occur at the level of the pulmonary vascular endothelium. This neonatal model of pulmonary hypertension is simple to perform and might be useful for further investigations.

Acetylcholine↗
PubMed1995

Prevention of endothelial dysfunction in small and large arteries in a model of chronic heart failure. Effect of angiotensin converting enzyme inhibition.

Chronic heart failure (CHF) impairs endothelium-dependent vasodilatation of large conductance arteries. We investigated whether a similar reduction also occurs in small arteries, and whether such a reduction can be prevented by the angiotensin converting enzyme inhibitor perindopril (P) in a rat model of CHF (left coronary artery ligation). After 1 month treatment with placebo or P (2 mg/kg/day), rats were anesthetized and arterial pressure, left ventricular end-diastolic pressure, and central venous pressure were measured with a micromanometer. Segments of aorta and mesenteric artery (mean diameter, 281 +/- 8 microns) were then isolated, cannulated, and perfused at constant pressure using an arteriograph. Responses to increasing concentrations of acetylcholine (Ach), nitroprusside, and to 10(-4) mol/L NG-nitro-L-arginine methyl ester (L-NAME) were studied after preconstriction by phenylephrine. Heart failure resulted in a decrease in systolic and diastolic pressures, an increase in left ventricular end-diastolic and central venous pressures, and a significant depression of Ach-induced dilatation of the mesenteric artery (maximal dilatation, from 90 +/- 4% to 63 +/- 4%, P < .05) but not of the aorta (from 56 +/- 8% to 45 +/- 5%, NS) without any modification in the endothelium-independent vasodilatation induced by nitroprusside. In the group treated by the angiotensin converting enzyme (ACE) inhibitor perindopril, systolic and diastolic pressures were slightly decreased, whereas left ventricular end diastolic, central venous pressures, and the endothelium-dependent vasodilating response to Ach were normalized. Responses to L-NAME were not affected by CHF or perindopril. Perindopril also decreased hypertrophy, as evidenced by a significantly lower heart weight in treated rats.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin-Converting Enzyme Inhibitors↗