Grassi G, Dell'Oro R, Quarti-Trevano F, Scopelliti F, Seravalle G, Paleari F, Gamba P L, Mancia G
Department of Internal Medicine, Prevention and Medicine Biotechnologies, University Milano-Bicocca, Milan, Italy.
Diabetologia. 2005 Jul;48(7):1359-65. doi: 10.1007/s00125-005-1798-z. Epub 2005 Jun 3.
AIMS/HYPOTHESIS: Previous studies have shown that alterations in vascular, metabolic, inflammatory and haemocoagulative functions characterise the metabolic syndrome. Whether this is also the case for sympathetic function is not clear. We therefore aimed to clarify this issue and to determine whether metabolic or reflex mechanisms might be responsible for the possible adrenergic dysfunction.
In 43 healthy control subjects (age 48.2+/-1.0 years, mean+/-SEM) and in 48 untreated age-matched subjects with metabolic syndrome (National Cholesterol Education Program's Adult Treatment Panel III Report criteria) we measured, along with anthropometric and metabolic variables, blood pressure (Finapres), heart rate (ECG) and efferent postganglionic muscle sympathetic nerve activity (microneurography) at rest and during baroreceptor manipulation (vasoactive drug infusion technique).
Compared with control subjects, subjects with metabolic syndrome had higher BMI, waist circumference, blood pressure, cholesterol, triglycerides, insulin and homeostasis model assessment (HOMA) index values but lower HDL cholesterol values. Sympathetic nerve traffic was significantly greater in subjects with metabolic syndrome than in control subjects (61.1+/-2.6 vs 43.8+/-2.8 bursts/100 heartbeats, p<0.01), the presence of sympathetic activation also being detectable when the metabolic syndrome did not include hypertension as a component. Muscle sympathetic nerve traffic correlated directly and significantly with waist circumference (r=0.46, p<0.001) and HOMA index (r=0.49, p<0.001) and was inversely related to baroreflex sensitivity (r=-0.44, p<0.001), which was impaired in the metabolic syndrome.
CONCLUSIONS/INTERPRETATION: These data provide evidence that the metabolic syndrome is characterised by sympathetic activation and that this abnormality (1) is also detectable when blood pressure is normal and (2) depends on insulin resistance as well as on reflex alterations.
目的/假设:既往研究表明,血管、代谢、炎症和血液凝固功能改变是代谢综合征的特征。交感神经功能是否如此尚不清楚。因此,我们旨在阐明这一问题,并确定代谢或反射机制是否可能是导致可能的肾上腺素能功能障碍的原因。
在43名健康对照者(年龄48.2±1.0岁,均值±标准误)和48名未治疗的年龄匹配的代谢综合征患者(符合美国国家胆固醇教育计划成人治疗小组第三次报告标准)中,我们除测量人体测量学和代谢变量外,还在静息状态和压力感受器操作(血管活性药物输注技术)期间测量了血压(Finapres)、心率(心电图)和节后肌肉交感神经传出活动(微神经ography)。
与对照者相比,代谢综合征患者的体重指数、腰围、血压、胆固醇、甘油三酯、胰岛素和稳态模型评估(HOMA)指数值更高,但高密度脂蛋白胆固醇值更低。代谢综合征患者的交感神经活动明显高于对照者(61.1±2.6对43.8±2.8次爆发/100次心跳,p<0.01),当代谢综合征不包括高血压作为组成部分时,也可检测到交感神经激活。肌肉交感神经活动与腰围(r=0.46,p<0.001)和HOMA指数(r=0.49,p<0.001)直接且显著相关,与压力反射敏感性呈负相关(r=-0.44,p<0.001),压力反射敏感性在代谢综合征中受损。
结论/解读:这些数据提供了证据,表明代谢综合征的特征是交感神经激活,并且这种异常(1)在血压正常时也可检测到,(2)取决于胰岛素抵抗以及反射改变。