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短期高血糖对1型糖尿病患者血流动力学的影响。

Effect of short-term hyperglycaemia on haemodynamics in type 1 diabetic patients.

作者信息

Jacobsen P, Rossing K, Hansen B V, Bie P, Vaag A, Parving H-H

机构信息

Steno Diabetes Center, Gentofte, Denmark.

出版信息

J Intern Med. 2003 Nov;254(5):464-71. doi: 10.1046/j.1365-2796.2003.01216.x.

Abstract

OBJECTIVES

Mechanisms underlying glucose-mediated development and progression of diabetic complications are incompletely understood. We tested the impact of short-term hyperglycaemia on systemic blood pressure and regulatory hormones in type 1 diabetic patients.

DESIGN AND METHODS

We included 18 patients [13 men, mean (SEM) diabetes duration 10 (1) years] without signs of autonomic neuropathy or renal complications in a randomized single-blinded cross-over trial using insulin-glucose clamp technique. Patients were clamped for 90 min to blood glucose of 5 mmol L(-1) (euglycaemia) and 15 mmol L(-1) (hyperglycaemia) in random order. Blood pressure was measured noninvasively every 5 min (Takeda TM2421 device). Regulatory hormones were determined at the end of each clamp period.

RESULTS

Systolic blood pressure increased [mean (95% CI)] 3 (1, 5) mmHg during hyperglycaemia from 123 (SEM 2) during euglycaemia, P=0.01. Diastolic blood pressure remained unchanged at 78 (2) mmHg. Hyperglycaemia reduced plasma concentrations of: renin [14 (4, 23)%, P=0.02], angiotensin II [17 (8, 25)%, P<0.01] and adrenaline [20 (10, 29)%, P<0.01]. Plasma concentration of atrial natriuretic peptide increased by 11 (6, 17) pg mL(-1) (P<0.01) from 43 (2) pg mL(-1). We calculated a median (range) increase in extracellular volume and plasma volume (PV) of 2.6 (0.7-5.3)% and 5.0 (-4.7 to 8.6)%, respectively.

CONCLUSIONS

In type 1 diabetic patients without signs of autonomic neuropathy short-term hyperglycaemia induced a modest increase in systolic blood pressure and suppression of the renin-angiotensin system, possibly caused by PV expansion because of fluid shift from intra- to extracellular compartment.

摘要

目的

葡萄糖介导的糖尿病并发症发生和发展的潜在机制尚未完全明确。我们测试了短期高血糖对1型糖尿病患者全身血压和调节激素的影响。

设计与方法

我们纳入了18例患者[13名男性,平均(标准误)糖尿病病程10(1)年],这些患者无自主神经病变或肾脏并发症迹象,采用胰岛素 - 葡萄糖钳夹技术进行随机单盲交叉试验。患者随机依次被钳夹至血糖水平为5 mmol/L(正常血糖)和15 mmol/L(高血糖),持续90分钟。每5分钟无创测量一次血压(武田TM2421设备)。在每个钳夹期结束时测定调节激素。

结果

高血糖期间收缩压升高[平均(95%置信区间)]3(1,5)mmHg,从正常血糖时的123(标准误2)mmHg升高,P = 0.01。舒张压维持在78(2)mmHg不变。高血糖降低了血浆中肾素[14(4,23)%,P = 0.02]、血管紧张素II[17(8,25)%,P < 0.01]和肾上腺素[20(10,29)%,P < 0.01]的浓度。心房利钠肽的血浆浓度从43(2)pg/mL增加了11(6,17)pg/mL(P < 0.01)。我们计算细胞外液量和血浆量(PV)的中位数(范围)分别增加了2.6(0.7 - 5.3)%和5.0( - 4.7至8.6)%。

结论

在无自主神经病变迹象的1型糖尿病患者中,短期高血糖导致收缩压适度升高并抑制肾素 - 血管紧张素系统,这可能是由于液体从细胞内室转移到细胞外室导致PV扩张所致。

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