Vigili de Kreutzenberg S, Kiwanuka E, Tiengo A, Avogaro A
Department of Clinical and Experimental Medicine, University of Padova, Padova, Italy.
Eur Heart J. 2003 Jul;24(13):1210-5. doi: 10.1016/s0195-668x(03)00206-9.
Endothelial dysfunction has been described in obesity. This study examines the impact of visceral obesity on nitric oxide-independent relaxation in the human forearm.
In ten viscerally obese and ten matched controls forearm blood flow (FBF) was measured by venous occlusion plethysmography during intrabrachial infusion of: (1) sodium nitroprusside; (2) bradykinin, before and after inhibition of vasoactive prostaglandins and nitric oxide; (3) potassium; (4) ouabain (Na(+)/K(+)ATPase inhibitor) alone or (5) in combination with BaCl(2)(K(IR)inhibitor). Baseline FBF and endothelium-independent vasodilatation were similar in the two groups. In obese patients, bradykinin-induced increase of FBF was significantly less than in controls (P<0.01). Irrespective of prostaglandins and nitric oxide inhibition, bradykinin response was lower in the viscerally obese. Intrabrachial potassium determined a significantly blunted response (P<0.05). Ouabain caused a similar, moderate decrease in basal FBF in the two groups; the coinfusion of BaCl(2)caused a more intense decline in FBF which was significantly relevant in obese (-24+/-5%, P<0.01).
In obese patients there is a blunted nitric oxide-independent relaxation determined by a decreased response of inwardly rectifying potassium channels.
肥胖症中已发现存在内皮功能障碍。本研究探讨内脏肥胖对人前臂非一氧化氮依赖性舒张功能的影响。
对10名内脏肥胖者和10名匹配的对照者，通过静脉阻塞体积描记法测量前臂血流量（FBF），测量期间经肱动脉输注：（1）硝普钠；（2）缓激肽，在抑制血管活性前列腺素和一氧化氮之前及之后；（3）钾；（4）哇巴因（钠/钾ATP酶抑制剂）单独使用或（5）与氯化钡（内向整流钾通道抑制剂）联合使用。两组的基线FBF和内皮依赖性血管舒张功能相似。在肥胖患者中，缓激肽诱导的FBF增加显著低于对照组（P<0.01）。无论前列腺素和一氧化氮是否受到抑制，内脏肥胖者的缓激肽反应均较低。经肱动脉输注钾导致反应显著减弱（P<0.05）。哇巴因使两组的基础FBF出现相似的中度下降；联合输注氯化钡导致FBF下降更为明显，在肥胖者中具有显著相关性（-24±5%，P<0.01）。
在肥胖患者中，内向整流钾通道反应降低导致非一氧化氮依赖性舒张功能减弱。
