Ординатура / Хирургия / Библиотека им академика М.И. Перельмана / Книга_896_Библиотеки_им_академика_М_И_Перельмана

Diabetes is characterized by chronic hyperglycemia result­ing either from a lack of insulin production (type 1) or from insulin resistance (type 2). Over the past decades, there has

The circulatory system of the human body is mainly divided between atrial, venous, and lymphatic vessels. The arterial walls are well-organized structures that consist of the tunica intima, tunica media, and tunica adventitia.

In diabetes, the levels of circulating platelets may actually be elevated, contributing to increased aggregation. However, not only are their more platelets but their mechanism is altered as well. Normally, prostaglandin 2 (PGI2) and NO produced by the endothelium prevent platelet aggregation [40]. However, patients with diabetes have decreased NO production but also have decreased PGI2 [41]. With decreased PGI2 and NO as well as elevated platelet counts, patients with diabetes are at a higher risk of prothrombotic events that can lead to coronary disease and stroke.

Researchers have known for decades that patients with dia­betes have notable differences in their arteries. Structural abnormalities of the arterioles were observed in the mid­twentieth century in the retina and the kidneys in patients with diabetes [46]. Such arteriolar remodeling was con­rmed decades later in patients with type 2 diabetes, who had systemic structural alterations of subcutaneous small resistance arteries, as indicated by an increased media-to­lumen ratio. Notably there was hypertrophic remodeling which was associated with impaired endothelium-dependent vasodilation invitro. Of note, it is important to realize that these changes are seen in diabetic patients with and without hypertension [47].

The failure of the microcirculation to vasodilate in response to injury has been described as a functional ischemia and has been demonstrated to be a result of a number of factors at play in the microcirculation of patients with diabetes. These functional changes in the microcirculation include reduced elasticity of capillaries and impaired cellular migration as well as nutrient exchanges. These abnormalities are thought to be due to endothelial dysfunction, smooth muscle cell dysfunction, and impairment of the nerve-axon reex. This impairment of the microcirculation has been attributed to reduced expression of endothelial nitric oxide synthetase and poly polymerase [56]. Furthermore, expression of endothe­lial nitric oxide synthetase is reduced in peripheral neuropa­thy, suggesting a relationship between neuropathy and endothelial dysfunction. Under conditions of stress such as pain and trauma, the C bers secrete peptides such as substance P, neuropeptide Y, neurotensin, and others that exert vasodilation and increase vessel permeability. This rep­resents a protective mechanism, and it has been shown to be impaired in patients with diabetes irrespective of having neu­ropathy [12] with the largest reduction observed in neuro­pathic feet. This characteristic impairment at the foot level can also be considered as a functional ischemia, and it may be another possible mechanism that explains poor wound healing in DFU.

Surgeons and interventionalists will often start with an endovascular rst approach to open up stenotic vessels; how­ever, if that fails, patients may ultimately require an arterial bypass. However, even if the revascularization improves blood ow, the effect of a successful lower extremity arterial revascularization on the impaired foot microcirculation with diabetes is not clear [59]. Some studies have shown that impaired vasodilation in the diabetic neuropathic lower extremity leads to functional ischemia, which improves con­siderably but is not completely corrected with successful bypass grafting surgery. This could be an explanation to why patients with diabetes and neuropathy may still be at high risk for the development of foot ulceration despite adequate correction of large vessel blood ow [60].