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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The following microscopical aspects were found in the small intramural arteries in the myocardium of 30 diabetic patients: endothelial proliferations with focal protuberances leading to partial narrowing of the lumen, increased thickness of the arterial wall due to fibrosis and accumulations of neutral mucopolysaccharides: alteration of elastic fibres. Morphometrically, the arterial wall thickness and the arterial diameter were increased whereas the arterial density decreased in the diabetic heart. In 25 rats with streptozotocin-induced diabetes the small intramyocardial arteries were investigated at 11 to 40 weeks of diabetic state. Using morphometrical analysis a constant increase of arterial wall thickness paralleling the diabetes duration was found. Microscopically, the lesions consist in endothelial proliferation with bridging across the vascular lumen and slight perivascular and diffuse fibrosis. Ultrastructurally, the capillary basal lamina was thickened in the diabetic myocardium. In order to investigate the morphometrical data we used symbolic-logic as a decision method, by applying an original computer program based on the Quine-McCluskey algorithm. All our results together with the final symbolic-logic expression suggest that damage of the small intramyocardial arteries plays an important role in the pathogenesis of diabetic cardiomyopathy.
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PMID:The myocardial microangiopathy in human and experimental diabetes mellitus. (A microscopic, ultrastructural, morphometric and computer-assisted symbolic-logic analysis). 373 4

The mechanism of heart failure in patients with diabetic cardiomyopathy is not clear. Previous studies suggested that vascular lesions specific for diabetes mellitus were present and that the lesions could be the basis for impaired cardiac function. We have investigated the histologic and histochemical characteristics of intramyocardial vessels (20 to 500 microns) in a group of diabetics using comparable groups of patients with hypertension, patients with hypertension and diabetes mellitus, and, as controls, patients with neither hypertension nor diabetes mellitus. Analysis of multiple blocks taken from the 42 study patients disclosed no lesions specific for diabetes mellitus or hypertension. The discrepancy between our findings and earlier reports is probably due to a lack of controls and the use of non-perfusion-fixed material in the earlier studies.
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PMID:Diabetic cardiomyopathy. A morphological study of intramyocardial arteries. 375 19

The use of insulin by diabetics has largely removed the threat of death from ketotic coma but cardiovascular dysfunction remains a major cause of death in patients with diabetes. Recent research has indicated a generalized membrane defect, which may cause abnormalities of calcium metabolism in nerves, cardiac and smooth muscle as well as endothelial cells and thus may lead respectively to the development of neuropathy, primary cardiomyopathy, microangiopathy and atherosclerosis in the diabetic population. Each of these pathogenic processes, which are associated with insulin deficiency, alone or in combination with others, may result in cardiac dysfunction in chronic diabetes. Activation of the sympathetic nervous system and abnormalities in catecholamine metabolism have been identified in diabetes; their involvement in the genesis of cardiac pump failure as well as large and small vessel disease is likely. The membrane defects as indicated by changes in both plasma membrane and glycocalyx in diabetic cardiomyopathy appear to be complex and may involve alterations in the metabolism of lipids and pyrimidine nucleotides. It seems that intracellular calcium overload is intimately involved in the development of diabetic cardiomyopathy; however, a concentrated research effort is required to understand the primary biochemical lesion in the pathogenesis of cardiac dysfunction in diabetes. In the meantime, a heightened awareness on the part of clinicians concerning the susceptibility of diabetic patients to cardiovascular problems may help in reducing mortality and morbidity in the diabetic population.
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PMID:Pathogenesis of cardiac dysfunction in diabetes mellitus. 385 Jul 73

Diabetes mellitus is associated with a specific cardiomyopathy. This is evident from the clinical-pathological work and the epidemiologic data from the Framingham study. Noninvasive studies of diabetics have shown alterations in systolic and diastolic function that may ultimately lead to clinical heart failure. The relationship of these cardiac changes to the type of diabetes, its duration, and its severity is not settled. However, a correlation between changes in heart function and other complications of diabetes has been demonstrated. Insufficient prospective data is available from noninvasive studies to establish the frequency of progression from subclinical cardiac dysfunction to overt congestive failure. The pathogenesis of this disorder is still uncertain. Pathological studies have shown changes in the intramural arteries, arterioles, and capillaries but their functional significance is uncertain. Experimental studies have shown interstitial changes leading to an apparently less compliant left ventricle in the diabetic dog and monkey. In the diabetic rat reversible changes were found in myocardial function, related to changes in contractile proteins and intracellular calcium metabolism. In both species, the response to anoxia or ischemia was altered in the presence of diabetes. However, irreversible depression of the contractile element was not found in most animal studies of isolated diabetes. In contrast, the combination of hypertension and diabetes leads to substantial cardiac damage and circulatory congestion, both in clinical and experimental investigations. Clearly much more work must be carried out to understand the pathogenesis, treatment, and ultimately the prevention of diabetic cardiomyopathy.
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PMID:Diabetic cardiomyopathy. 388 Sep 19

Diabetes mellitus is associated with severe and premature cardiovascular disease. The reasons for this have not been identified. It is now apparent that diabetics often have elevated circulating insulin levels compared to non-diabetics. In non-insulin dependent diabetes this is due to the associated obesity while in insulin treated diabetics exogenous insulin is responsible for hyperinsulinaemia between meals and at night. Two reports of high insulin levels in non-insulin dependent diabetics with cardiovascular disease are consistent with clinical and epidemiological studies linking hyperinsulinaemia with coronary, cerebral and peripheral arterial disease in non-diabetics. The arterial wall is an insulin sensitive tissue. Insulin promotes proliferation of arterial smooth muscle cells and enhances lipid synthesis and low density lipoprotein receptor activity. Insulin also promotes experimental atherosclerosis in a number of species. The evidence linking hyperinsulinaemia to the cardiovascular complications and diabetes is suggestive but incomplete and much more information on predictive factors for arterial disease in diabetes is urgently required. Diabetes mellitus is associated with severe and premature cardiovascular disease (reviewed by Stout 1982). Ischaemic heart disease, stroke and peripheral vascular disease are all more common in diabetics, particularly diabetic women. Although there is evidence for the existance of a specific diabetic cardiomyopathy, much of the cardiovascular disease in diabetics is due to atherosclerosis and its complications. Arterial disease in diabetics in distinct from microvascular disease affecting capillaries, and does not differ morphologically or biochemically from atherosclerosis in non-diabetics. The reason for the increased incidence of atherosclerosis in diabetes has not been established. Both non-insulin dependent and insulin dependent diabetes appear to be associated with cardiovascular disease.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hyperinsulinaemia--a possible risk factor for cardiovascular disease in diabetes mellitus. 390 79

Non-invasive cardiac studies using systolic time intervals were performed on 89 diabetic Nigerians and 45 non-diabetic controls, to investigate possible preclinical abnormality of left ventricular function. There was no significant difference in the pre-ejection period to left ventricular ejection time ratio (PEP/LVET) between the patients and controls: 0.373 +/- 0.011 vs 0.365 +/- 0.013 (P = 0.688). Patients at higher risk for developing significant vascular disease i.e. those with peripheral vascular insufficiency, those in higher socio-economic class and those with disease duration of 10 or more years had the highest mean values of PEP/LVET (0.403, 0.403 and 0.412 respectively). However, these values did not reach a level of significance. There was no correlation between PEP/LVET and age, body mass index, duration of diabetes, total or HDL cholesterol and the HDL to total cholesterol ratio. Because recent reports have related diabetic cardiomyopathy to angiopathic disease in diabetes, these results suggest that Nigerian patients, who like most other black African diabetics show little susceptibility to severe vascular complications of diabetes may enjoy some protection from a preclinical abnormality of left ventricular function as well.
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PMID:Non-invasive cardiac study in diabetic Nigerians using systolic time intervals. 403 78

Secretin stimulation of adenylate cyclase activity in heart membranes was selectively altered in streptozotocin-diabetic adult male rats suffering from moderately severe diabetes, 40 days after i.v. streptozotocin administration (40 mg/kg body weight). The efficacy of secretin was reduced by 55% whilst its potency was unaffected. By contrast, the stimulation of adenylate cyclase by NaF, GTP, Gpp(NH)p, D,L-isoproterenol, and glucagon remained normal. The present data, together with the markedly reduced secretin response of cardiac adenylate cyclase in genetically obese (fa/fa) Zucker rats might indicate that hypoinsulinemia and insulin resistance both reduce the number of secretin receptors coupled to the adenylate cyclase system, an alteration whose contribution to diabetic cardiomyopathy remains to be determined.
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PMID:Selective alteration of secretin-stimulated cardiac adenylate cyclase activity in streptozotocin-diabetic rats. 622 63

The effect of chronic experimental diabetes on the adrenergic receptors in the rat heart was investigated. Diabetes was induced by streptozotocin (65 mg/kg; i.v.) administration, animals were sacrificed 8 weeks later, and positive as well as negative dF/dt values were determined in isolated papillary muscle preparations. Stimulation of the contractile force generation by isoproterenol and methoxamine was attenuated in diabetic preparations. Beta- and alpha-adrenergic receptor bindings were determined in cardiac membranes by employing 3H-dihydroalprenolol and 3H-dihydroergocryptine respectively. Reduced number of beta- and alpha-receptor binding sites without changes in the affinity constants were observed in diabetic myocardium. Such a decrease in alpha- and beta-receptor density in the heart may account for the depressed contractile responsiveness to adrenergic stimuli in diabetic cardiomyopathy.
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PMID:Cardiac alpha- and beta-adrenergic receptor alterations in diabetic cardiomyopathy. 629 54

Heart failure seems to occur in adult-onset diabetics with a greater frequency than in the nondiabetic population, particularly in women. A number of such patients do not have significant occlusive disease of the major coronary arteries, or convincing small-vessel disease. A subclinical abnormality of myocardium in experimental diabetes and asymptomatic human diabetics supports the concept of a diabetic cardiomyopathy.
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PMID:Congestive heart failure in the diabetic. 634 54

In order to determine whether diabetic cardiomyopathy in rats is associated with altered contractile proteins, male and female rats were made diabetic with intravenous streptozotocin (STZ). Calcium ATPase activity of cardiac actomyosin was significantly decreased after 1 week of diabetes and was depressed by 60% by 2 weeks. Rats pretreated with 3-O-methyl glucose to prevent the hyperglycemia caused by STZ had normal Ca2+-actomyosin ATPase activities, and non-diabetic rats whose food was restricted to keep their body and heart weights similar to those found in diabetic animals had only a slight fall in actomyosin ATPase activity. Ca2+-ATPase and actin-activated ATPase activities of pure myosin were similarly depressed in preparations from hearts of diabetic animals. Sodium dodecylsulfate gel electrophoresis and isoelectric focusing failed to reveal differences in the patterns of contractile proteins or light subunits between diabetics and controls, but pyrophosphate gels showed a shift in the myosin pattern. Because of depressed circulating thyroid hormone levels in diabetic animals, cardiac contractile proteins were also studied in preparations from thyroidectomized rats. Calcium activities of actomyosin and myosin ATPase were lower than values found in hearts of diabetic rats. When diabetic animals were kept euthyroid with thyroid replacement, actomyosin ATPase activity was still depressed. Thus STZ diabetes causes a significant decrease in cardiac contractile protein ATPase activity. This may be related to altered proportions of myosin isoenzymes.
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PMID:The effect of streptozotocin-induced diabetes in rats on cardiac contractile proteins. 645 19


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