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  • Title: Vascular endothelial dysfunction tested by blunted response to endothelium-dependent vasodilation by salbutamol and its related factors in uncomplicated pre-menopausal obese women.
    Author: Suh HS, Park YW, Kang JH, Lee SH, Lee HS, Shim KW.
    Journal: Int J Obes (Lond); 2005 Feb; 29(2):217-22. PubMed ID: 15570314.
    Abstract:
    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) > or = 25) and another age-matched control group of 25 nonobese women (BMI: 18.5-22.9) of Asian origin. All uncomplicated premenopausal (20-45 y) 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 beta2-adrenergic stimulation. Radial artery wave forms were recorded and from a derived aortic wave forms augmentation index (AIx, 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: AIx 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 (beta = -0.141, P=0.002, Adj-R(2)=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.
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