Clinica Medica, Dipartimento di Medicina Clinica, Prevenzione e Biotecnologie Sanitarie, Università Milano-Bicocca, Ospedale San Gerardo, Milan, Italy.
Obesity (Silver Spring). 2010 Jan;18(1):92-8. doi: 10.1038/oby.2009.195. Epub 2009 Jun 11.
Obese persons are at increased cardiovascular risk and exhibit increased arterial stiffness and impaired endothelial function of large- and medium-size arteries. We hypothesized that normotensive subjects suffering from severe obesity would also present remodeling and endothelial dysfunction of small resistance arteries. A total of 16 lean (age: 49.6 +/- 2.9 years, BMI: 22.9 +/- 0.3 kg/m(2), mean +/- s.e.m.) and 17 age-matched severely obese (BMI: 41.1 +/- 2.3 kg/m(2)) normotensive subjects were investigated. None had glucose or lipid metabolic abnormalities except for insulin resistance. Resistance arteries, dissected from abdominal subcutaneous tissue, were assessed on a pressurized myograph. For superimposable blood pressure, the media thickness, media cross-sectional area (CSA), and media-to-lumen ratio values of resistance arteries were markedly and significantly greater in obese compared to lean subjects (media thickness 26.3 +/- 0.6 vs. 16.2 +/- 0.6 microm, CSA 22,272 +/- 1,339 vs. 15,183 +/- 1,186 microm(2), and media-to-lumen ratio 0.113 +/- 0.006 vs. 0.059 +/- 0.001, respectively, P < 0.01). Acetylcholine-induced relaxation was impaired in vessels from obese subjects compared to the lean individuals (-40.4 +/- 1.3%, P < 0.01), whereas endothelium-independent vasorelaxation was similar in all groups. Stiffness of small arteries as assessed by the stress/strain relationship was similar in lean and severely obese subjects. We conclude that severe human obesity is associated with profound alterations in structural and functional characteristics of small arteries, which may be responsible for the presence of elevated cardiovascular risk and increased incidence of coronary, cerebrovascular and renal events reported in obesity.
肥胖者心血管风险增加，表现为大动脉和中动脉僵硬和内皮功能受损。我们假设患有严重肥胖症的正常血压患者也会出现小阻力动脉的重构和内皮功能障碍。共研究了 16 名瘦（年龄：49.6 +/- 2.9 岁，BMI：22.9 +/- 0.3 kg/m(2)，平均值 +/- s.e.m.）和 17 名年龄匹配的严重肥胖（BMI：41.1 +/- 2.3 kg/m(2)）正常血压者。除胰岛素抵抗外，无葡萄糖或脂质代谢异常。从腹部皮下组织分离出阻力血管，并在加压肌描记器上进行评估。为了使血压可叠加，与瘦个体相比，肥胖个体的阻力血管的中膜厚度、中膜横截面积（CSA）和中膜-腔比显著增加（中膜厚度 26.3 +/- 0.6 对 16.2 +/- 0.6 微米，CSA 22,272 +/- 1,339 对 15,183 +/- 1,186 微米(2)，中膜-腔比 0.113 +/- 0.006 对 0.059 +/- 0.001，P < 0.01）。与瘦个体相比，乙酰胆碱诱导的血管舒张在肥胖个体的血管中受损（-40.4 +/- 1.3%，P < 0.01），而所有组之间的内皮非依赖性血管舒张相似。通过应力/应变关系评估的小动脉僵硬在瘦和严重肥胖个体中相似。我们得出结论，严重的人类肥胖与小动脉结构和功能特征的深刻改变有关，这可能是肥胖患者心血管风险增加和冠心病、脑血管病和肾病发生率增加的原因。
