Reduced tissue oxygenation and its reversibility by glycemic control in diabetic patients

Relationship of transcutaneous oxygen pressure (TcPo2) to glycemic control and diabetic complications was investigated in patients with non-insulin dependent diabetes mellitus. TcPo2 was measured in 103 patients with non-insulin dependent diabetes mellitus. Correlation of TcPo2 to HbA(1c), fasting blood sugar (FBS), age, duration of diabetes, serum lipids, hypertension, and diabetic complications were examined. We divided the patients into three groups according to their glycemic control: good control group (HbA(1c) < 7.0%), fair control group (HbA(1c), 7.0-8.9%) and poor control group (HbA(1c)greater than or equal to 9.0). We compared TcPO2 of these three groups with 19 non-diabetic controls. In 103 patients, TcPo2 at baseline correlated with HbA(1c), FBS and age (P < 0.001, P < 0.01 and P < 0.05, respectively), but did not correlate with duration of diabetes mellitus, neuropathy, nephropathy or retinopathy. TcPo2 of good and fair control group was not reduced comparing to the non-diabetic control (63 +/- 11, 59 +/- 10 and 64 +/- 12 mmHg, respectively). The poor control group had significantly reduced TcPo2 (55 +/- 10 mmHg) comparing to non-diabetic control (P < 0.005) and good control group (P < 0.005). Furthermore, in an independent study, TcPo2, arterial oxygen pressure (Pa-o2), oxygen pressure of dorsal pedal vein (Pv(o2)) and eiythrocyte 2,3-diphosphoglycerate (2,3-DPG) in eight patients with poor glycemic control were followed prospectively. Six patients with improvement of glycemic control showed a significant increase of TcPo2 and Pa-o2 (P < 0.001 and P < 0.005, respectively). However, two patients without improvement of hyperglycemia had no change in TcPo2 and Pa-o2. Pv(o2) and 2,3-DPG levels of erythrocytes were not changed in six patients. These findings suggest that tissue oxygenation in diabetic patients was deteriorated in relation to hyperglycemia and was reversed with glycemic control. Improvement of Pa-o2 might contribute partly to the increase of TcPO2. (C) 1997 Elsevier Science Ireland Ltd.