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At least 19 recordsLinked to original sources
PubMed2004

The role of nitric oxide in the development of diabetic angiopathy.

Diabetic angiopathy is the main cause of morbidity and mortality in patients with diabetes mellitus. Clinical manifestations and pathophysiological mechanisms of diabetic angiopathy can be traced back to the development of endothelial cell dysfunction with alterations in the eNOS/NO system production or availability as the primum movens in its natural history. Hyperglycemia per se or through the accumulation of AGEs, increased oxidative stress, leading to NOS uncoupling and NO-quenching by excess superoxide and peroxynitrite, and individual genetic background are thought to be responsible for this NO metabolism imbalance. The complex interplay of these mechanisms results in a perturbation of the physiological properties of NO in the maintenance of endothelial homeostasis, such as vasodilation, anticoagulation, leukocyte adhesion, smooth muscle cell proliferation, and antioxidant capacity. Hence, abnormality in NO availability results in generalized accelerated atherosclerosis, hyperfiltration, glomerulosclerosis, tubulointerstitial fibrosis and progressive decline in glomerular filtration rate, and apoptosis and neovascularization in the retina. Indeed, the parallel development of nephropathy, retinopathy, and macroangiopathy may be considered as manifestations of endothelial dysfunction at distinct vascular sites. Given this scenario, intervention targeting any of the pathways involved in the NOS/NO system cascade may prove potential therapeutic targets in the prevention of long-term diabetic complications.

Animals↗
PubMed1998

Von Willebrand factor in diabetic angiopathy.

Diabetes mellitus is a complex disease characterised by chronic hyperglycaemia responsible for complications affecting the kidneys, eyes, peripheral nerves and micro- and macrovascular systems. Von Willebrand factor (vWf), a multimeric glycoprotein mainly synthesised by endothelial cells, is involved in platelet adhesion and aggregation and acts as the carrier of coagulation factor VIII in plasma. Increased levels of vWf, reflecting activation of or damage to endothelial cells, have been described in association with atherosclerosis and diabetes. vWf appears to be a predictive marker of diabetic nephropathy and neuropathy, although not of retinopathy, which suggests that endothelial dysfunction precedes the onset of diabetic microangiopathy. This dysfunction could be especially involved in the pathogenesis of renal abnormalities of diabetes. vWf is not a predictive marker of macroangiopathy when diabetes is associated with atherosclerotic risk factors. In the presence of chronic diabetic complications, vWf levels are not associated with any grade of retinopathy but increase with the severity of nephropathy and would appear to be a risk factor for macrovascular mortality in these patients. The endothelial dysfunction of diabetes can generate atherosclerotic lesions responsible for damage to the arterial wall, atheroma and formation of platelet microaggregates. Concomitant with high vWf levels, other possible mechanisms of endothelial damage include reduced synthesis or release of nitric oxide, hyperglycaemic pseudohypoxia and protein kinase-C activation, increased synthesis of proteins bearing advanced glycosylation end-products or transforming growth factor-beta (TGF-beta) activation of coagulation and inhibition of fibrinolysis. At present, it is not known whether high vWf levels are inherent to the physiopathology of diabetes, nor whether diabetes induces endothelial dysfunction through other pathways. However, since angiopathy resulting from endothelial dysfunction is the main cause of morbidity and mortality in diabetic patients, appropriate therapy is necessary to reduce these complications. Glycaemic control seems to be insufficient to normalise plasma vWf, whereas a decrease can be obtained by ingestion of diets rich in oleic acid or by treatment with statins. Inhibition of the binding of vWf to the GPlba receptor by synthetic peptides, aurin tricarboxylic acid or monoclonal antibodies has been proposed to prevent the thrombosis induced by high levels of plasma vWf. Thus, vWf probably represents an interesting target for the inhibition of thrombosis in diabetes.

Arteriosclerosis↗
PubMed1998

[Accuracy of the term "diabetic angiopathy of the lower limbs". II. Possibilities of the morphological assessment of the stage of diabetic angiopathy of the lower limbs and the choice of treatment tactics].

In 40 patients with diabetic angiopathy of lower extremities of terminal stage the foot tissue biopsies were studied up using electron and light microscopy. A skin was supposed to be most acceptable substrate for biopsy because there was established morphological changes of tissues, occurring in a single direction and in a single type. Morphological criteria of the angiopathy stages were delineated, permitting to make a differentiative choice of the treatment tactics.

Adult↗
PubMed1998

[On the legal aspects of the term "diabetic angiopathy of the lower extremities". Part I. Clinico-morphological parallels of the lower diabetic angiopathy].

The clinico-morphological data analysis was done in 100 examined patients with diabetic angiopathy of the lower extremities. The morphological changes revealed have corresponded to severity of the disease clinical symptoms in 70% only. Purulent affection of extremities have characterized not the end stage of angiopathy only but it was observed in another stages of the disease.

Diabetic Angiopathies↗
PubMedDate not supplied

Possible pathophysiological mechanisms for diabetic angiopathy in type 2 diabetes.

The expression of large and small vessel disease in type 2 diabetes differs from that observed in type 1, with a higher prevalence of atherosclerosis and hypertension, maculopathy rather than proliferative retinopathy, and nephropathy of a more complex nature. Such differences are mirrored by differences in vascular pathophysiology with an early impairment of microvascular vasodilatory reserve being a prominent feature. The defect appears to be endothelium dependent and in conjunction with evidence of endothelium activation suggests that the endothelium plays a crucial role in the pathogenesis of vascular disease in type 2 diabetes and may even be an intrinsic feature or common antecedent of the insulin resistance syndrome. Several cellular mechanisms may be proposed linking insulin resistance and endothelial dysfunction including (i) abnormalities of common signal transduction mechanisms, (ii) alterations in cell membrane fluidity altering the expression and/or presentation of a wide range of receptors, or (iii) changes in oxidative stress. It is intuitively unlikely that the alteration of a single signal transduction mechanism could be a common cause, particularly as aspects of endothelial dysfunction implicate different mechanisms. Accordingly, changes in oxidative stress, either stemming from glucose-mediated increased free-radical generation and/or reduction of antioxidant capacity, are strong contender mechanisms. Not only may increased oxidative stress result in the quenching of nitric oxide, neutralizing its many protective functions, but it may also damage DNA, protein structure, and membrane properties. Elucidating the links between oxidative stress, endothelial function, and insulin resistance has important implications for the prevention of diabetic angiopathy and perhaps for the prevention of diabetes itself.

Diabetes Mellitus, Type 2↗
PubMed2004

Impact of adiposity and plasma adipocytokines on diabetic angiopathies in Japanese Type 2 diabetic subjects.

AIMS: Adipocytokines, products from adipose tissue, have biological activities on the vascular system, and may affect diabetic angiopathy. In this study, we assessed the relationship between adiposity and plasma adipocytokine levels, and investigated the clinical significance of adiposity and plasma adipocytokine levels on diabetic micro- and macroangiopathy in Type 2 diabetic subjects. METHODS: We studied 231 Japanese Type 2 diabetic subjects (135 men and 96 women, aged 60.4 +/- 12.3 years, body mass index 24.8 +/- 5.2 kg/m2). We measured adipocytokine [adiponectin, leptin, resistin, and tumour necrosis factor (TNF)-alpha] levels, lipid profiles and urine albumin excretion. We also performed optic fundus examination and measured carotid intramedia thickness (IMT) using B-mode ultrasonography, and the localization of fat with abdominal computed tomography. A group of 93 subjects with microalbuminuria or overt proteinuria was compared with the other 148 to assess the effect on nephropathy. A group of 191 eyes with simple retinopathy or more advanced changes was compared with 263 eyes without retinal changes to assess the effect on retinopathy. RESULTS: Plasma adiponectin level was negatively correlated with both visceral (r = -0.37, P < 0.01) and subcutaneous (r = -0.25, P < 0.01) fat areas. Resistin concentration was positively related with visceral fat area (r = 0.15, P < 0.05). Adiponectin concentration was positively correlated with age (r = 0.26, P < 0.01). TNF-alpha was correlated with IMT (r = 0.16, P < 0.05) after correction for age. Logistic regression analysis indicates a 4085 times greater chance of having retinopathy with a one unit increase in TNF-alpha (pmol/l) and a 30.64 times greater chance of having nephropathy with one unit increase in leptin (nmol/l). CONCLUSIONS: The present observations suggest that visceral and subcutaneous fat has an impact on microangiopathy as well as macroangiopathy, possibly through different adipocytokines.

Adipocytes↗
PubMed2000

Long-term effects of the endothelin(A) receptor antagonist LU 135252 and the angiotensin-converting enzyme inhibitor trandolapril on diabetic angiopathy and nephropathy in a chronic type I diabetes mellitus rat model.

Diabetic angiopathy is a serious problem in antidiabetic therapy. We wanted to investigate whether treatment with the endothelin(A) receptor antagonist LU 135252 or with the angiotensin-converting enzyme inhibitor trandolapril might prevent angiopathy in long-term type I diabetes mellitus. Six groups of male Wistar rats were investigated: untreated age-matched control rats, healthy controls treated with trandolapril (0.3 mg/kg), healthy controls treated with LU 135252 (100 mg/kg), untreated diabetic rats, and diabetic rats treated with either trandolapril or LU 135252. Rats were rendered diabetic by injection of streptozotozin. Duration of the disease was 6 months. Thereafter, rats were sacrificed, and hearts, kidneys, and a mesenterial loop were removed. Hearts and kidneys were processed histologically; the mesenterial loop was perfused with saline at constant pressure for investigation of microvessels using microvideoangiometry while treated with either 30 mM KCl, 1 microM acetylcholine, or 1 microM sodium nitroprusside. All diabetic rats developed hyperglycemia without differences among these three groups. Diabetic rats exhibited marked anemia, which was significantly antagonized by both treatments. The heart capillaries/muscle fibers ratio was decreased significantly in diabetic animals, which was prevented fully by both treatments. Renal glomerular diameter was increased in diabetic rats. This was significantly antagonized by LU 135252 but not by trandolapril. Deposition of homogeneous eosinophilic material within the glomeruli was nearly completely prevented by LU 135252. The acetylcholine-induced vasodilation in mesenteric microvessels was significantly attenuated in diabetic rats, which was significantly antagonized by both treatments. We conclude that both angiotensin and endothelin seem to contribute to the development of diabetic angiopathy and that, in addition to angiotensin-converting enzyme inhibition, blockade of endothelin(A) receptors may be an interesting new approach to antiangiopathic therapy.

Angiotensin-Converting Enzyme Inhibitors↗
PubMedDate not supplied

[Pathogenesis of lower limb diabetic angiopathies in patients with non-insulin-dependent diabetes mellitus].

Some indices of the system of homeostasis, lipid metabolism, lipid peroxidation (LPO), the levels of IRI, C-peptide, glycosylated Hb and glycemia (on an empty stomach) were investigated in 131 patients with noninsulin dependent diabetes mellitus (the patients ranged in age from 40 to 60). Correlation analysis has shown that derangements in the system of homeostasis, lipid metabolism and LPO are correlated and interrelated, resulting in disorder of the arterial blood flow in the lower limbs and hence to the development and progression of diabetic angiopathies. The authors have proposed a scheme of LPO involvement in the development of lower limb diabetic angiopathies.

Adult↗
PubMed2000

[Diabetic angiopathy--etiopathogenesis and clinical manifestations (hypersyndrome X)].

Diabetic angiopathy is a generalised systemic disease of the vascular system which afflicts both distribution vessels (diabetic macroangiopathy) and microcirculation (diabetic microangiopathy). The diabetic angiopathy, as well as other angiostenotic diseases (obliterations, obstructions, occlusions) result in one common consequence--ischaemia. This study is based on an analysis of a large group of patients (71,662 angiologic consultant examinations which took place during the 25-year period of the existence of the Comenius University Faculty Hospital). The author indicates that the clinical course of angio-organic ischaemic syndromes determined by diabetic angiopathy is multiform, remarkably severe and unfavourable. The author has suggested the term "X hypersyndrome" referring to cases with simultaneous occurrence of various pathophysiologic abnormalities and clinical units which finally increase the risk of origin and development of diabetic angiopathy. (Tab. 7, Ref. 47.)

Diabetic Angiopathies↗
PubMed1976

[Diabetes mellitus and microcirculation. Significance of diabetic angiopathy for the prognosis and course of diabetes mellitus, possibilities and bases of angiologic therapy].

The importance of diabetic angiopathy for prognosis and course of diabetes mellitus, possibilities and basis of angiological therapy Complications originating from the vascular system determine life expectancy of the diabetic patient. He is particularly endangered by apoplexy, heart attack, arteriosclerosis of the lower extremities, retino- and nephropathy. Microangiopathy is a specific diabetic problem, the development of which shows a clear dependency on the quality of metabolism. Conventional therapy of circulatory problems today is less concerned with the vascular system than with the qualities of blood viscosity. In this context, viscosity is of main concern. Particularly in microcirculation viscosity is dependent on blood factors such as: haematocrit, plasmaviscosity, erythrocytes and thrombocytes. Their changed behaviour results, in the case of diabetes mellitus, in an increase in viscosity partly dependent on metabolism. A promising concept of treatment is available by pharmaceutically influencing the alteration of erythrocytes.

Anticoagulants↗
PubMed1986

Lack of correlation of glycosylated haemoglobin level with the duration of diabetes or diabetic angiopathy.

Patients with severe diabetic angiopathy show an increased physiologic haemolysis. The aim of the present study was to evaluate the practical influence of the resulting reduced red cells half-life on the glycosylated haemoglobin (GHb) level as determined by a routine method. 168 diabetics, aged 55.7 +/- 1.3 years, were studied. The duration of disease ranged from 3 months to 34 years; 66 patients were insulin-treated and 87 had clinical features of arteritis and/or patent microangiopathy. A highly significant correlation was found between the mean plasma glucose level determined on the first day after admission and the GHb value. The slopes of regression curves of diabetics with and without angiopathies were similar. For a given mean glucose level there was no correlation between the GHb value and the duration of diabetes. So, in clinical practice, it is not necessary to take into account the duration of diabetes or the presence of angiopathies for explaining the GHb results.

Adult↗
PubMed1978

Diabetic angiopathy--its lessons in vascular physiology.

Progress in our understanding diabetic angiopathy has been slow, but we are now learning a number of lessons of interest to the cardiologist. Diabetic angiopathy is a collective term for conditions specific to the diabetic state and related to its duration more than to patient age. The angiopathy produces calcification of the media of larger arteries, but its major effects are in the microcirculation. Intense interest in one feature, skeletal muscle capillary basement membrane thickening, has dominated the last decade. Capillary basement membrane thickening, while characteristic of diabetes, is associated with little direct impairment of the microcirculatin. It appears to play no role in the pathogenesis of diabetes itself. The pathology of diabetic retinopathy and diabetic nephropathy suggests that arteriolar changes may be the major mediator of diabetic angiopathy. This concept is supported by the interactions between hypertension and diabetes in the eye and kidney. The course of diabetes of youthful onset differs from that of maturity onset. The relative frequency of diabetic angiopathy is higher, and of atherosclerotic complications is lower. This has made it difficult to demonstrate the potential value of preventive measures. Benefit to one type of problem may become hidden by worsening of the other. If the diabetic benefits from what is learned about how ischemic heart disease risk can be reduced, he will require even more effective management to prevent or control diabetic angiopathy.

Arteriosclerosis↗
PubMed1998

[Use of serotonin for treatment of patients with diabetic angiopathies].

In 26 patients (female 11, males--15) with diabetic angiopathy (necrosis of the foot or toes) local measurement of pO2 by transcutaneous mode was carried out before and during introduction of serotonine adipinate. Simultaneously with evaluation of pO2 in 14 patients electromyography (EMG) was made. Serotonine adipinate was introduced intravenously with a speed of 5.0-10.0 mg per hour. In this group mean age of the patients made up 57.4 years, mean values of initial pO2 25.6 mm Hg, and mean indices of pO2 at the moment of serotonine treatment 38.5 mm Hg. Average increase of pO2 during serotonine infusion was registered as 50.4% in comparison with mean initial data. In all 14 patients, who underwent simultaneous measurement of pO2 and registration of EMG, reinforcement of electrical activity of smooth muscles (SM) of various intensity and increase in tissue pO2 were detected. Improvement of microcirculation (increase of transcutaneous pO2, reinforcement of electrical activity of SM as a result of serotonine introduction) evidences that functional and morphological changes of serotonine receptors of SM are involead in genesis of diabetic angiopathy. The data obtained showed that in diabetes mellitus, besides insulin deficiency, insufficiency of such an endogenous factor as serotonine duclops. Thus, serotonin should be used for prophylaxis and treatment of diabetic angiopathies.

Adipates↗