Sundell J, Laine H, Nuutila P, Rönnemaa T, Luotolahti M, Raitakari O, Knuuti J
Turku PET Centre, Department of Medicine, University of Turku, Turku, Finland.
Diabetologia. 2002 Jun;45(6):775-82. doi: 10.1007/s00125-002-0819-4. Epub 2002 Apr 25.
AIMS/HYPOTHESIS: Insulin enhances coronary vasodilation in healthy subjects. We tested whether insulin is able to induce coronary vasodilation in Type I (insulin-dependent) diabetic mellitus patients. Additionally, the effect of short-term hyperglycaemia on myocardial perfusion was studied.
Myocardial blood flow was quantitated basally and during adenosine infusion (140 microg/kg per min i.v.) with or without simultaneous insulin infusion (1 mU/kg per min for 60 min) in nine non-smoking Type I diabetic males (HbA(1c) 7.4+/-1.0%) without diabetic complications and 10 healthy non-diabetic otherwise matched males using positron emission tomography and (15)O-water. Diabetic patients were studied on two occasions, once during normoglycaemia (plasma glucose ~6 mmol/l) and once during hyperglycaemia (approximately 10 mmol/l) induced by reducing the dose of insulin for two days.
Resting myocardial blood flow was similar in the studied groups (NS). Hyperaemic adenosine stimulated flow was 23% lower in diabetic than in non-diabetic subjects (3.09+/-0.72 vs 4.0+/-1.13 ml x g(-1) x min(-1), p<0.05). Insulin increased significantly adenosine stimulated flow by 23% in diabetic and 17% in non-diabetic subjects (NS between the groups). Hyperglycaemia for two days had no effect on flow values when compared to the values during normoglycaemia (NS).
CONCLUSION/INTERPRETATION: Insulin has similar vasodilative effects on coronary arteries in diabetic and non-diabetic subjects. Short-term hyperglycaemia does not alter myocardial blood flow or abolish insulin induced vasodilation in these patients. Insulin induced coronary vasodilation might contribute to the known beneficial effect of intensive insulin therapy on myocardial ischaemia in diabetic patients.
目的/假设:胰岛素可增强健康受试者的冠状动脉舒张功能。我们测试了胰岛素是否能够诱导I型(胰岛素依赖型)糖尿病患者的冠状动脉舒张。此外,还研究了短期高血糖对心肌灌注的影响。
采用正电子发射断层扫描和(15)O-水,对9名无糖尿病并发症的非吸烟I型糖尿病男性(糖化血红蛋白7.4±1.0%)和10名健康的非糖尿病且其他条件匹配的男性,在基础状态下以及在输注腺苷(140微克/千克每分钟静脉注射)时,无论有无同时输注胰岛素(1毫单位/千克每分钟,持续60分钟)的情况下,定量测定心肌血流量。糖尿病患者分两次进行研究,一次在血糖正常时(血浆葡萄糖约6毫摩尔/升),一次在通过减少胰岛素剂量两天诱导的高血糖时(约10毫摩尔/升)。
研究组的静息心肌血流量相似(无显著性差异)。糖尿病患者中腺苷刺激的充血性血流量比非糖尿病受试者低23%(3.09±0.72对4.0±1.13毫升×克-1×分钟-1,p<0.05)。胰岛素使糖尿病患者腺苷刺激的血流量显著增加23%,非糖尿病受试者增加17%(两组间无显著性差异)。与血糖正常时的值相比,两天的高血糖对血流量值无影响(无显著性差异)。
结论/解读:胰岛素对糖尿病和非糖尿病受试者的冠状动脉具有相似的舒张作用。短期高血糖不会改变这些患者的心肌血流量,也不会消除胰岛素诱导的血管舒张。胰岛素诱导的冠状动脉舒张可能有助于强化胰岛素治疗对糖尿病患者心肌缺血的已知有益作用。