BACKGROUND AND AIMS: The hypothesis of this study was that microvascular FID and AChID is impaired in visceral (VAT) compared to SAT arterioles in morbidly obese women. An Additional aim was to determine the mechanisms contributing to FID and AChID in VAT and SAT arterioles. METHODS AND RESULTS: Arterioles were obtained from SAT and VAT biopsies from women (BMI > 35 kg/m(2) ) undergoing bariatric surgery. Microvessels were cannulated for reactivity measurements in response to flow (pressure gradients of 10-100 cmH2 O) and to ACh (10(-9) -10(-4 ) M) with and without l-NAME, INDO, and PEG-catalase. NO and H2 O2 generation were detected in arterioles by fluorescence microscopy. FID and AChID of arterioles from VAT were reduced compared to SAT arterioles. In SAT arterioles, l-NAME, INDO, and PEG-catalase significantly reduced FID and AChID but had no effect individually on VAT arterioles' vasodilator reactivity. INDO +l-NAME reduced FID in VAT arterioles. NO-fluorescence was greater in arterioles from SAT compared to VAT arterioles. Vascular H2 O2 generation during flow was similar in both VAT and SAT. CONCLUSION: Our results suggest that VAT arterioles display reduced vasodilator reactivity to flow and ACh compared to SAT arterioles, mediated by different regulatory mechanisms in human obesity.
BACKGROUND AND AIMS: The hypothesis of this study was that microvascular FID and AChID is impaired in visceral (VAT) compared to SAT arterioles in morbidly obesewomen. An Additional aim was to determine the mechanisms contributing to FID and AChID in VAT and SAT arterioles. METHODS AND RESULTS: Arterioles were obtained from SAT and VAT biopsies from women (BMI > 35 kg/m(2) ) undergoing bariatric surgery. Microvessels were cannulated for reactivity measurements in response to flow (pressure gradients of 10-100 cmH2 O) and to ACh (10(-9) -10(-4 ) M) with and without l-NAME, INDO, and PEG-catalase. NO and H2 O2 generation were detected in arterioles by fluorescence microscopy. FID and AChID of arterioles from VAT were reduced compared to SAT arterioles. In SAT arterioles, l-NAME, INDO, and PEG-catalase significantly reduced FID and AChID but had no effect individually on VAT arterioles' vasodilator reactivity. INDO +l-NAME reduced FID in VAT arterioles. NO-fluorescence was greater in arterioles from SAT compared to VAT arterioles. Vascular H2 O2 generation during flow was similar in both VAT and SAT. CONCLUSION: Our results suggest that VAT arterioles display reduced vasodilator reactivity to flow and ACh compared to SAT arterioles, mediated by different regulatory mechanisms in humanobesity.
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