Flynn M D, Tooke J E
Department of Diabetes and Endocrinology, Bristol Royal Infirmary, Exeter, UK.
Diabet Med. 1992 May;9(4):320-9. doi: 10.1111/j.1464-5491.1992.tb01790.x.
Neuropathy, mechanical stress, and macrovascular disease are involved in the pathogenesis of diabetic foot ulceration. Implicit in the development of gangrene and ulceration is the recognition that these factors interact with the microcirculation, resulting in the failure of skin capillary flow to meet nutritive requirements. There is little evidence to associate structural microangiopathy with foot microcirculatory failure. Significant functional abnormalities of the microcirculation have been defined. In accord with the haemodynamic hypothesis early hyperaemia and capillary hypertension promote more sinister late functional abnormalities with increasing duration of diabetes. These late functional abnormalities include loss of autoregulation and reduced hyperaemic responses which interact with loss of neurogenic flow regulation, disturbed endothelial function, and abnormal rheology to produce the familiar clinical picture of the diabetic foot. Ischaemia secondary to multi-segment arterial disease induces additional abnormalities of microcirculatory function which are superimposed on the pre-existing diabetic microvascular structural and functional microangiopathy.
神经病变、机械应力和大血管疾病参与了糖尿病足溃疡的发病机制。坏疽和溃疡的发展意味着这些因素与微循环相互作用，导致皮肤毛细血管血流无法满足营养需求。几乎没有证据表明结构性微血管病变与足部微循环衰竭有关。微循环的显著功能异常已得到明确。根据血流动力学假说，早期充血和毛细血管高血压随着糖尿病病程的延长会促进更严重的晚期功能异常。这些晚期功能异常包括自动调节功能丧失和充血反应减弱，它们与神经源性血流调节丧失、内皮功能紊乱和异常流变学相互作用，形成了糖尿病足常见的临床表现。多节段动脉疾病继发的缺血会诱发微循环功能的额外异常，这些异常叠加在已有的糖尿病微血管结构和功能性微血管病变之上。
