Avogaro A, Nosadini R, Doria A, Fioretto P, Velussi M, Vigorito C, Saccà L, Toffolo G, Cobelli C, Trevisan R
Istituto di Medicina Interna, Policlinico Universitario, Padua, Italy.
Am J Physiol. 1990 Apr;258(4 Pt 1):E606-18. doi: 10.1152/ajpendo.1990.258.4.E606.
Eleven insulin-dependent diabetes mellitus (IDDM) patients with angiographically normal coronary arteries and a normal hemodynamic response to an echocardiographic-dipyridamole test and 12 normal controls were studied at rest and after atrial pacing simultaneously sampling arterial and coronary sinus blood. In IDDM patients, despite hyperglycemia [10.0 +/- 2.0 (SE) mmol/l], myocardial glucose uptake was slightly lower than in controls. This process was significantly activated in both groups during atrial pacing. The isotopically calculated net flux of lactate across myocardium, in agreement with the net balance value based on unlabeled lactate-pyruvate arteriovenous differences, showed a net uptake in controls (3.5 +/- 0.6 mumol.min-1.1.73 m-2) and a net release in IDDM (12.4 +/- 2.6; P less than 0.01). Atrial pacing stimulated lactate uptake in both groups. Myocardial uptake of ketone bodies was significantly higher in IDDM (37.0 +/- 6.3 mumol.min-1.1.73 m-2) than in controls (10.1 +/- 3.4 mumol.min-1.1.73 m-2; P less than 0.01). Free fatty acid uptake was also significantly greater in IDDM than in controls (44.1 +/- 7.0 vs. 24.1 +/- 5.1 mumol.min-1.1.73 m-2; P less than 0.01). Alanine and branched amino acids were released by diabetic but not by control hearts at rest. The normalization of blood glucose concentrations restored normal patterns of lactate and ketone body kinetics across diabetic myocardium. In conclusion, 1) at rest, myocardial lactate and amino acid uptake is markedly impaired in IDDM without coronary artery disease, and 2) the metabolic abnormalities of the diabetic myocardium are not a primary phenomenon but rather a consequence of hypoinsulinemia and hyperglycemia because insulin administration, resulting in euglycemia, restored normal patterns of cardiac metabolism.
对11名胰岛素依赖型糖尿病（IDDM）患者和12名正常对照者进行了研究。这些IDDM患者冠状动脉造影显示正常，且对超声心动图-潘生丁试验的血流动力学反应正常。研究人员让他们在静息状态下以及心房起搏后同时采集动脉血和冠状窦血。在IDDM患者中，尽管血糖水平较高[10.0±2.0（标准误）mmol/L]，但其心肌葡萄糖摄取量略低于对照组。在心房起搏期间，两组的这一过程均被显著激活。通过同位素计算的乳酸跨心肌净通量，与基于未标记乳酸-丙酮酸动静脉差值的净平衡值一致，显示对照组有净摄取（3.5±0.6μmol·min⁻¹·1.73 m⁻²），而IDDM患者有净释放（12.4±2.6；P<0.01）。心房起搏刺激了两组对乳酸的摄取。IDDM患者心肌对酮体的摄取量（37.0±6.3μmol·min⁻¹·1.73 m⁻²）显著高于对照组（10.1±3.4μmol·min⁻¹·1.73 m⁻²；P<0.01）。IDDM患者对游离脂肪酸的摄取也显著高于对照组（44.1±7.0对24.1±5.1μmol·min⁻¹·1.73 m⁻²；P<0.01）。静息时，糖尿病患者的心脏释放丙氨酸和支链氨基酸，而对照组心脏不释放。血糖浓度正常化后，糖尿病心肌的乳酸和酮体动力学模式恢复正常。总之，1）在静息状态下，无冠状动脉疾病的IDDM患者心肌对乳酸和氨基酸的摄取明显受损；2）糖尿病心肌的代谢异常不是原发性现象，而是低胰岛素血症和高血糖的结果，因为给予胰岛素导致血糖正常后，心脏代谢模式恢复正常。
