Di Carli M F, Bianco-Batlles D, Landa M E, Kazmers A, Groehn H, Muzik O, Grunberger G
Department of Internal Medicine, Positron Emission Tomography Center Detroit, MI, USA.
Circulation. 1999 Aug 24;100(8):813-9. doi: 10.1161/01.cir.100.8.813.
C ardiac sympathetic signals play an important role in the regulation of myocardial perfusion. We hypothesized that sympathetically mediated myocardial blood flow would be impaired in diabetics with autonomic neuropathy.
We studied 28 diabetics (43+/-7 years old) and 11 age-matched healthy volunteers. PET was used to delineate cardiac sympathetic innervation with [(11)C]hydroxyephedrine ([(11)C]HED) and to measure myocardial blood flow at rest, during hyperemia, and in response to sympathetic stimulation by cold pressor testing. The response to cardiac autonomic reflex tests was also evaluated. Using ultrasonography, we also measured brachial artery reactivity during reactive hyperemia (endothelium-dependent dilation) and after sublingual nitroglycerin (endothelium-independent dilation). Based on [(11)C]HED PET, 13 of 28 diabetics had sympathetic-nerve dysfunction (SND). Basal flow was regionally homogeneous and similar in the diabetic and normal subjects. During hyperemia, the increase in flow was greater in the normal subjects (284+/-88%) than in the diabetics with SND (187+/-80%, P=0.084) and without SND (177+/-72%, P=0.028). However, the increase in flow in response to cold was lower in the diabetics with SND (14+/-10%) than in those without SND (31+/-12%) (P=0.015) and the normal subjects (48+/-24%) (P<0.001). The flow response to cold was related to the myocardial uptake of [(11)C]HED (P<0.001). Flow-mediated brachial artery dilation was impaired in the diabetics compared with the normal subjects, but it was similar in the diabetics with and without SND.
Diabetic autonomic neuropathy is associated with an impaired vasodilator response of coronary resistance vessels to increased sympathetic stimulation, which is related to the degree of SND.
心脏交感神经信号在心肌灌注调节中起重要作用。我们假设自主神经病变的糖尿病患者交感神经介导的心肌血流会受损。
我们研究了28例糖尿病患者（43±7岁）和11名年龄匹配的健康志愿者。使用正电子发射断层显像（PET）用[（11）C]羟基麻黄碱（[（11）C]HED）描绘心脏交感神经支配情况，并测量静息、充血时以及冷加压试验交感神经刺激后的心肌血流。还评估了对心脏自主神经反射试验的反应。使用超声检查，我们还测量了反应性充血（内皮依赖性舒张）期间和舌下含服硝酸甘油后（内皮非依赖性舒张）肱动脉的反应性。基于[（11）C]HED PET，28例糖尿病患者中有13例存在交感神经功能障碍（SND）。糖尿病患者和正常受试者的基础血流在区域上是均匀的且相似。充血期间，正常受试者的血流增加幅度（284±88%）大于有SND的糖尿病患者（187±80%，P = 0.084）和无SND的糖尿病患者（177±72%，P = 0.028）。然而，有SND的糖尿病患者对冷刺激的血流增加幅度（14±10%）低于无SND的糖尿病患者（31±12%）（P = 0.015）和正常受试者（48±24%）（P < 0.001）。对冷刺激的血流反应与[（11）C]HED的心肌摄取有关（P < 0.001）。与正常受试者相比，糖尿病患者血流介导的肱动脉舒张受损，但有SND和无SND的糖尿病患者相似。
糖尿病自主神经病变与冠状动脉阻力血管对交感神经刺激增加的血管舒张反应受损有关，这与SND的程度相关。
