TY - JOUR
T1 - Vascular endothelial dysfunction tested by blunted response to endothelium-dependent vasodilation by salbutamol and its related factors in uncomplicated pre-menopausal obese women
AU - Suh, H. S.
AU - Park, Y. W.
AU - Kang, J. H.
AU - Lee, S. H.
AU - Lee, H. S.
AU - Shim, K. W.
N1 - Funding Information:
The pulse analyzer (Pulse Wave Analysis, SphygmoCor) used in the present study was donated by AtCor Medical Pty Ltd. The present study was funded by a research grant provided by Ewha Womans University.
PY - 2005/2
Y1 - 2005/2
N2 - BACKGROUND: Vascular endothelial dysfunction (VED) plays a pivotal role in the pathogenesis of atherosclerosis and is associated with insulin resistance and visceral obesity. We examined the predicting factors of VED in uncomplicated premenopausal obese women using analysis of endothelium-dependent vasodilation by radial artery pulse wave obtained through applanation tonometry. METHODS: The subjects included a group of 33 obese women body mass index ((BMI)≥25) and another age-matched control group of 25 nonobese women (BMI: 18.5-22.9) of Asian origin. All uncomplicated premenopausal (20-45y) obese women were sedentary (<1 h/week of physical activity). Anthropometric measurements were performed, and regional distributions of adipose tissue and metabolic variables were measured. Endothelial function was measured by pulse wave analysis after salbutamol administration, which reflects endothelium-mediated vasodilation, contributed partially by nitric oxide release from β2-adrenergic stimulation. Radial artery wave forms were recorded and from a derived aortic wave forms augmentation index (Alx, defined as the pressure difference between the first and second peaks of the central arterial wave form, expressed as a percentage of the pulse pressure) was calculated. The subjects received sublingual nitroglycerine (NTG) (0.6 mg), followed by nebulized salbutamol (2.5 mg). RESULTS: Alx fell significantly after the administration of salbutamol, which causes endothelium-dependent vasodilatation. This value was significantly reduced in obese women compared with the controls (10.3 ± 6.7 vs 17.2 ± 6.8%, P = 0.0003). NTG, which causes endothelium-independent vasodilatation, did not produce significant changes (P= 0.917). As for our obese subjects, the visceral adipose tissue area was a significant predictor of VED independent of BMI, percent body fat, and other metabolic variables including high-sensitivity C-reactive protein (β = -0.141, P=0.002, Adj-R2 = 0.41). CONCLUSION: Increased abdominal adiposity is a powerful independent predictor of VED in uncomplicated obese women. Further studies are warranted to determine the pathophysiological link between visceral adipose tissue and VED.
AB - BACKGROUND: Vascular endothelial dysfunction (VED) plays a pivotal role in the pathogenesis of atherosclerosis and is associated with insulin resistance and visceral obesity. We examined the predicting factors of VED in uncomplicated premenopausal obese women using analysis of endothelium-dependent vasodilation by radial artery pulse wave obtained through applanation tonometry. METHODS: The subjects included a group of 33 obese women body mass index ((BMI)≥25) and another age-matched control group of 25 nonobese women (BMI: 18.5-22.9) of Asian origin. All uncomplicated premenopausal (20-45y) obese women were sedentary (<1 h/week of physical activity). Anthropometric measurements were performed, and regional distributions of adipose tissue and metabolic variables were measured. Endothelial function was measured by pulse wave analysis after salbutamol administration, which reflects endothelium-mediated vasodilation, contributed partially by nitric oxide release from β2-adrenergic stimulation. Radial artery wave forms were recorded and from a derived aortic wave forms augmentation index (Alx, defined as the pressure difference between the first and second peaks of the central arterial wave form, expressed as a percentage of the pulse pressure) was calculated. The subjects received sublingual nitroglycerine (NTG) (0.6 mg), followed by nebulized salbutamol (2.5 mg). RESULTS: Alx fell significantly after the administration of salbutamol, which causes endothelium-dependent vasodilatation. This value was significantly reduced in obese women compared with the controls (10.3 ± 6.7 vs 17.2 ± 6.8%, P = 0.0003). NTG, which causes endothelium-independent vasodilatation, did not produce significant changes (P= 0.917). As for our obese subjects, the visceral adipose tissue area was a significant predictor of VED independent of BMI, percent body fat, and other metabolic variables including high-sensitivity C-reactive protein (β = -0.141, P=0.002, Adj-R2 = 0.41). CONCLUSION: Increased abdominal adiposity is a powerful independent predictor of VED in uncomplicated obese women. Further studies are warranted to determine the pathophysiological link between visceral adipose tissue and VED.
KW - Augmentation index
KW - High-sensitivity CRP (C-reactive protein)
KW - Pulse wave analysis
KW - Salbutamol
KW - Vascular endothelial dysfunction
KW - Visceral adipose tissue area
UR - http://www.scopus.com/inward/record.url?scp=13244259255&partnerID=8YFLogxK
U2 - 10.1038/sj.ijo.0802642
DO - 10.1038/sj.ijo.0802642
M3 - Article
C2 - 15570314
AN - SCOPUS:13244259255
SN - 0307-0565
VL - 29
SP - 217
EP - 222
JO - International Journal of Obesity
JF - International Journal of Obesity
IS - 2
ER -