Olsen H, Länne T
Department of Endocrinology, Lund University, Malmö University Hospital, Sweden.
Diabetologia. 2000 Sep;43(9):1178-84. doi: 10.1007/s001250051510.
AIMS/HYPOTHESIS: Patients with Type I (insulin-dependent) diabetes mellitus have a reduced transcapillary fluid absorption from skeletal muscle and skin and thus defective plasma volume regulation during hypovolaemia. Our aim was to find whether a defective capillary filtration coefficient or impaired transcapillary driving force are aetiologic factors for this reduction.
We investigated 11 diabetic patients (diabetes duration 6.9 +/- 1.1 years, age 26 +/- 1 years), without complications and 12 control subjects (26 +/- 1 years). Their capillary filtration coefficient was measured in the upper arm using a volumetric technique at rest and during lower body negative pressure (LBNP). We calculated the driving force for transcapillary fluid transfer.
The increase in heart rate and the decrease in systolic blood pressure during lower body negative pressure were similar in diabetic and control subjects. The resting capillary filtration coefficient was decreased in the diabetic subjects, 0.033 +/- 0.003 vs 0.051 +/- 0.007 ml x 100 ml(-1) x min(-1) x mmHg(-1) (p < 0.05). During lower body negative pressure, the capillary filtration coefficient increased 35 % in both groups compared with resting capillary filtration coefficient and was still decreased in diabetes; 0.046 +/- 0.004 compared with 0.069 +/- 0.006 ml x 100ml(-1) x min(-1) x mmHg(-1) (p < 0.01). The established driving force during lower body negative pressure was 1.37 +/- 0.11 vs 1.30 +/- 0.15 mmHg (NS) in diabetic and control subjects, respectively.
CONCLUSIONS/INTERPRETATION: Our study indicates that a reduced capillary filtration coefficient rather than defective regulation of transcapillary driving force, is the reason for the reduced transcapillary fluid absorption during hypovolaemic circulatory stress found in Type I diabetic patients.
目的/假设：I型（胰岛素依赖型）糖尿病患者骨骼肌和皮肤的跨毛细血管液体吸收减少，因此在血容量不足时血浆容量调节存在缺陷。我们的目的是确定毛细血管滤过系数缺陷或跨毛细血管驱动力受损是否是这种减少的病因。
我们研究了11名无并发症的糖尿病患者（糖尿病病程6.9±1.1年，年龄26±1岁）和12名对照受试者（26±1岁）。使用体积技术在静息状态和下体负压（LBNP）期间测量他们上臂的毛细血管滤过系数。我们计算了跨毛细血管液体转移的驱动力。
糖尿病患者和对照受试者在下体负压期间心率的增加和收缩压的降低相似。糖尿病患者静息毛细血管滤过系数降低，为0.033±0.003 vs 0.051±0.007 ml×100 ml⁻¹×min⁻¹×mmHg⁻¹（p<0.05）。在下体负压期间，两组的毛细血管滤过系数与静息毛细血管滤过系数相比均增加了35%，但糖尿病患者仍降低；分别为0.046±0.004与0.069±0.006 ml×100ml⁻¹×min⁻¹×mmHg⁻¹（p<0.01）。糖尿病患者和对照受试者在下体负压期间确定的驱动力分别为1.37±0.11与1.30±0.15 mmHg（无显著性差异）。
结论/解读：我们的研究表明，毛细血管滤过系数降低而非跨毛细血管驱动力调节缺陷，是I型糖尿病患者在血容量不足循环应激期间跨毛细血管液体吸收减少的原因。
