Department of Internal Medicine, University of Pisa, Via Roma 67, 56100 Pisa, Italy.
Diabetologia. 2012 Jun;55(6):1559-63. doi: 10.1007/s00125-011-2445-5. Epub 2012 Jan 20.
The mechanisms responsible for the accelerated atherosclerosis observed in type 2 diabetes are not fully understood. One of the earliest events in the development of atherosclerosis is endothelial dysfunction, namely, a reduction in nitric oxide (NO) synthesis or its bioavailability within the peri-endothelial environment, where it is responsible for maintenance of vascular tissue integrity. The clinical evaluation of this pathway is hampered by the fact that in vivo NO cannot be directly measured; however, exploiting a novel, complex and elegant experimental setup, McVeigh and co-workers (Diabetologia 1992;35:771-776) were the first to document that NO bioavailability in type 2 diabetic patients is indeed reduced. In this edition of 'Then and now' that paper is reappraised not only for its originality, but also for the broad and extensive evaluation of the vascular functions explored, the complete clinical characterisation of patients enrolled and for the fact that all the major findings were subsequently replicated.
导致 2 型糖尿病患者动脉粥样硬化加速的机制尚未完全阐明。动脉粥样硬化发展过程中的最早事件之一是内皮功能障碍，即内皮细胞周围环境中一氧化氮（NO）合成或其生物利用度减少，而 NO 负责维持血管组织完整性。由于体内的 NO 无法直接测量，因此对该途径的临床评估受到阻碍；然而，通过利用新颖、复杂和精妙的实验设计，McVeigh 及其同事（1992 年《糖尿病学》；35:771-776）首次记录到 2 型糖尿病患者的 NO 生物利用度确实降低。在本期“彼时与此时”中，该论文不仅因其创新性，还因其广泛而深入地评估了所探索的血管功能、所纳入患者的全面临床特征，以及所有主要发现随后都得到了复制而受到重新评价。
