Iino K, Yoshinari M, Doi Y, Shinohara N, Iwase M, Fujishima M
Second Department of Internal Medicine, Faculty of Medicine, Kyushu University, Fukuoka city, Japan.
Diabetes Res Clin Pract. 1997 Jan;34(3):163-8. doi: 10.1016/s0168-8227(96)01349-6.
Relationship of transcutaneous oxygen pressure (TcP(O2)) to glycemic control and diabetic complications was investigated in patients with non-insulin dependent diabetes mellitus. TcP(O2) was measured in 103 patients with non-insulin dependent diabetes mellitus. Correlation of TcP(O2) to HbA1c, 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 (HbA1c < 7.0%), fair control group (HbA1c, 7.0-8.9%) and poor control group (HbA1c > or = 9.0). We compared TcP(O2) of these three groups with 19 non-diabetic controls. In 103 patients, TcP(O2) at baseline correlated with HbA1c, 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. TcP(O2) 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 TcP(O2) (55 +/- 10 mmHg) comparing to non-diabetic control (P < 0.005) and good control group (P < 0.005). Furthermore, in an independent study, TcP(O2), arterial oxygen pressure (Pa(O2)), oxygen pressure of dorsal pedal vein (PV(O2)) and erythrocyte 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 TcP(O2) and Pa(O2) (P < 0.001 and P < 0.005, respectively). However, two patients without improvement of hyperglycemia had no change in TcP(O2) 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 TcP(O2).
我们对非胰岛素依赖型糖尿病患者经皮氧分压(TcP(O2))与血糖控制及糖尿病并发症之间的关系进行了研究。对103例非胰岛素依赖型糖尿病患者测量了TcP(O2)。检测了TcP(O2)与糖化血红蛋白(HbA1c)、空腹血糖(FBS)、年龄、糖尿病病程、血脂、高血压及糖尿病并发症之间的相关性。我们根据血糖控制情况将患者分为三组:良好控制组(HbA1c < 7.0%)、一般控制组(HbA1c,7.0 - 8.9%)和较差控制组(HbA1c ≥ 9.0)。我们将这三组患者的TcP(O2)与19名非糖尿病对照者进行了比较。在103例患者中,基线时的TcP(O2)与HbA1c、FBS及年龄相关(分别为P < 0.001、P < 0.01和P < 0.05),但与糖尿病病程、神经病变、肾病或视网膜病变无关。良好控制组和一般控制组的TcP(O2)与非糖尿病对照者相比未降低(分别为63 ± 11、59 ± 10和64 ± 12 mmHg)。较差控制组的TcP(O2)(55 ± 10 mmHg)与非糖尿病对照者相比显著降低(P < 0.005),与良好控制组相比也显著降低(P < 0.005)。此外,在一项独立研究中,对8例血糖控制较差的患者的TcP(O2)、动脉血氧分压(Pa(O2))、足背静脉血氧分压(PV(O2))及红细胞2,3 - 二磷酸甘油酸(2,3 - DPG)进行了前瞻性随访。6例血糖控制改善的患者TcP(O2)和Pa(O2)显著升高(分别为P < 0.001和P < 0.005)。然而,2例血糖未改善的患者TcP(O2)和Pa(O2)无变化。6例患者红细胞的PV(O2)和2,3 - DPG水平未改变。这些发现提示,糖尿病患者的组织氧合因高血糖而恶化,且血糖控制可使其逆转。Pa(O2)的改善可能部分有助于TcP(O2)的升高。