van Gurp P J, Willemsen J J, Lenders J W M, Ross H A, Sweep C G J, Smits P, Tack C J
Division of General Internal Medicine, Department of Medicine, Radboud University Nijmegen Medical Centre, the Netherlands.
Eur J Clin Invest. 2006 Oct;36(10):674-81. doi: 10.1111/j.1365-2362.2006.01707.x.
According to the 'haemodynamic hypothesis', increased tissue perfusion predisposes to microangiopathy in diabetic patients. We hypothesized that the typical haemodynamic changes underlying the increased tissue perfusion can be explained by a decreased sympathetic nerve activity caused by chronic hyperglycaemia. In this study we investigated sympathetic activity in patients with uncomplicated type 1 diabetes mellitus (DM).
In 15 DM patients (DM duration 6.3 +/- 3.8 year; HbA1c 7.9 +/- 1.3%) and 16 age- and sex-matched healthy volunteers (Control), sympathetic nervous system activity was measured at rest (baseline) and during sympathoneural stimulation (lower body negative pressure (LBNP)) by means of interstitial and plasma noradrenaline (NA) sampling and power spectral analysis. Muscle sympathetic nerve activity (MSNA) was measured before (baseline) and during a cold pressure test. Forearm blood flow was measured during forearm vascular alpha- and beta-adrenergic receptor blockade.
At baseline, forearm vascular resistance (FVR), plasma NA concentrations, MSNA and heart rate variability were similar in both groups. LBNP-induced vasoconstriction was significantly attenuated in the DM group compared with the Control group (DeltaFVR: 12 +/- 4 vs. 19 +/- 3 arbitrary units, P < 0.05). The responses of plasma NA and heart rate variability did not differ.
Baseline FVR and sympathetic nerve activity are normal in patients with uncomplicated type 1 diabetes. However, the forearm vasoconstrictor response to sympathetic stimulation is attenuated, which cannot be attributed to an impaired sympathetic responsiveness.
根据“血流动力学假说”,组织灌注增加易使糖尿病患者发生微血管病变。我们推测,组织灌注增加背后典型的血流动力学变化可由慢性高血糖导致的交感神经活动降低来解释。在本研究中,我们调查了无并发症的1型糖尿病(DM)患者的交感神经活动。
对15例DM患者(DM病程6.3±3.8年;糖化血红蛋白7.9±1.3%)和16例年龄及性别匹配的健康志愿者(对照组),通过组织间液和血浆去甲肾上腺素(NA)采样及功率谱分析,在静息状态(基线)和交感神经刺激期间(下体负压(LBNP))测量交感神经系统活动。在冷压试验前(基线)和试验期间测量肌肉交感神经活动(MSNA)。在前臂血管α和β肾上腺素能受体阻断期间测量前臂血流量。
在基线时,两组的前臂血管阻力(FVR)、血浆NA浓度、MSNA和心率变异性相似。与对照组相比,DM组LBNP诱导的血管收缩明显减弱(ΔFVR:12±4对19±3任意单位,P<0.05)。血浆NA和心率变异性的反应无差异。
无并发症的1型糖尿病患者的基线FVR和交感神经活动正常。然而,前臂对交感神经刺激的血管收缩反应减弱,这不能归因于交感反应性受损。