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

We report a case of hypertensive-diabetic cardiomyopathy demonstrating left ventricular regional wall motion abnormality, with a normal coronary artery documented on coronary arteriography. Dipyridamole-infusion 201Tl scintigraphy demonstrated transient perfusion defects in the infero-posterior wall of the left ventricle, where reduced wall motion was demonstrated on contrast left ventriculography. Myocardial SPECT (single photon emission tomography) imaging with [123I] beta-methyliodophenylpentadecanoic acid (BMIPP) and 201Tl demonstrated reduced [123I]BMIPP uptake compared with 201Tl uptake in the infero-posterior wall of left ventricle. These results suggest that the impairment of myocardial free fatty acid metabolism is an etiologic or contributory factor for regional wall motion abnormality, together with small-vessel coronary artery disease, in this patient.
Diabetes Care 1996 Aug
PMID:A case of hypertensive-diabetic cardiomyopathy demonstrating left ventricular wall motion abnormality. 911 86

In order to determine if cardiac membrane Ca(2+)-transport activities are altered in chronic diabetes induced by alloxan, rats were given an intravenous injection of 65 mg/kg and the hearts were used 8 weeks later. Some 4 weeks, diabetic animals were injected with insulin (3 U/day) for 4 weeks. Both sarcolemmal (SL) and sarcoplasmic reticulum (SR) membranes were isolated from the ventricular tissue and their Ca(2+)-transporting activities were determined. SL Na(+)-dependent Ca2+ uptake, ATP-dependent Ca2+ uptake and Ca(2+)-stimulated ATPase activities were depressed in the diabetic heart. Likewise, SR ATP-dependent Ca2+ uptake activity in the diabetic heart was markedly decreased in comparison to the control preparations. These defects in diabetic SL and SR Ca(2+)-transport activities were prevented by treatment of diabetic animals with insulin. The results from the alloxan-rat model of diabetes support the view that membrane abnormalities with respect to Ca2+ handling may lead to the occurrence of intracellular Ca2+ overload and the development of diabetic cardiomyopathy.
Diabetes Res Clin Pract 1996 Jul
PMID:Cardiac membrane Ca(2+)-transport in alloxan-induced diabetes in rats. 886 44

Abundant information is now available about changes in subcellular organelles that are responsible for the impaired intracellular calcium homeostasis in diabetic cardiomyopathy. Some of these changes concern heart sarcolemma and include decrease in the following variables: calcium binding, influx of calcium through the L-type calcium channels, (Na,K)-ATPase activity and its affinity to sodium, Na(+)-Ca2+ exchange, H(+)-Na+ exchange, etc. Diabetic hearts also exhibited increased tolerance to calcium, but none of the above membrane perturbations were clearly identified as the source of this effect. The present study was undertaken in order to identify those alterations appearing in diabetes which are specific for the diabetic heart only. Our interest was focused on changes in sarcolemmal ATPase activities, particularly those of the (Na,K)-ATPase and its activation by increasing concentrations of sodium and potassium. Studies were performed in the acute (8 days) and chronic (63 days) phase of development of insulin-dependent diabetic cardiomyopathy. Wistar rats were made diabetic by administration of streptozotocin. To test the effect of excess calcium, the well-established model of calcium paradox was used. From the results obtained the following conclusions have been made: (a) diabetic hearts exceed normal hearts in their tolerance to calcium overload. In this respect the effect of chronic diabetes is more pronounced than the effect of acute diabetes; (b) the activities of sarcolemmal ATPases in diabetic hearts remain relatively well preserved. For this reason and with respect to modulation of calcium tolerance, the changes in specific properties of the ATPases, particularly those in the (Na,K)-ATPase, outweigh the importance of perturbations in their activities; (c) the enormous decrease in affinity of the (Na,K)-ATPase to sodium (increased K(m) value) monitored in calcium paradox in acute diabetic hearts was absolutely missing in "calcium-tolerant" chronic diabetic hearts. This observation pointed to a possible relation that may exist between the specific properties (Na,K)-ATPase adapted to work in chronic diabetic hearts and the enhanced calcium tolerance of those hearts; (d) the specific mechanism responsible for improved activation of the (Na,K)-ATPase by sodium and also partially responsible for potassium ions, which is clearly manifested in chronic diabetic hearts upon calcium paradox, still remains to be elucidated. Nevertheless, it could be assumed that the same mechanism may be also co-responsible for the enhanced tolerance of diabetic hearts to calcium.
Diabetes Res Clin Pract 1996 Jul
PMID:Diabetic cardiomyopathy in rats: biochemical mechanisms of increased tolerance to calcium overload. 886 47

The enzymatic histochemical and ultrastructural alterations of the rat heart during development of streptozotocin (STZ) induced diabetic cardiomyopathy were studied. Moreover, the response of the isolated diabetic hearts to Ca overload-Ca paradox-was investigated. In the early stage of diabetes (1 week of diabetes), no apparent histochemical changes were observed but gentle alterations of the ultrastructure of the myocytes and particularly capillaries were found. Structural changes of the myocytes and microangiopathy accompanied by decreased activities of some enzymes (phosphorylase, various dehydrogenases, ATPase) progressed with time and were more pronounced late in diabetes (9 weeks). Ca paradox induced severe structural damage of the majority of cardiomyocytes and loss of the cellular integrity, and marked decrease in activities of all enzymes. However, in acute diabetic heart only partial Ca paradox was observed. It was manifested by transmural heterogeneity of structural and enzymatic histochemical changes. Evident preservation of the ultrastructure and enzyme activities of the myocardium was revealed in late stage (9 weeks) of diabetes. It can be concluded that diabetes results in prevention of the Ca overload in rat myocardium in vitro. Disturbances in coronary perfusion associated with microangiopathy as well as altered Ca handling and depressed heart function may account for delayed development of Ca paradox in diabetic heart.
Diabetes Res Clin Pract 1996 Jul
PMID:Resistance of diabetic rat hearts to Ca overload-related injury. Histochemical and ultrastructural study. 886 49

Diabetes mellitus is a complex group of diseases that has hyperglycemia as a common metabolic abnormality. Although it is well-known that diabetic patients are susceptible to the effects of large vessel atherosclerosis with specific cardiac and cerebral complications, the association of diabetes mellitus with cardiac dysfunction caused by cardiomyopathy in the absence of significant coronary artery disease has been recognized for many years. However, the pathogenesis of diabetic cardiomyopathy remains unknown and has been somewhat controversial. Specifically, whether diabetes mellitus with its metabolic effects is sufficient to account for cardiomyopathy remains to be proven. This paper reviews the evidence for and against a metabolic etiology. In addition, we review the clinical and experimental evidence that supports the view that diabetes mellitus acts together with hypertension to produce structural damage in the heart that manifests as ventricular dysfunction and ultimately congestive heart failure. The concomitant effects of the metabolic derangements of diabetes and the vascular abnormalities associated with hypertension may lead to microvascular-induced tissue injury. Findings supporting this hypothesis are presented, along with observations suggesting that treatment with vasodilating calcium channel blockers or angiotensin converting enzyme inhibitors may be beneficial in regard to tissue pathology and mortality in experimental models. Recent clinical studies also support a role for the microcirculation in diabetics. Finally, it is suggested that if the microcirculation is pathogenetically involved in diabetic cardiomyopathy, then agents that improve microcirculatory flow along with tight control of hypertension may be as beneficial in the treatment or prevention of diabetic cardiomyopathy as strict metabolic control of hyperglycemia.
Diabetes Res Clin Pract 1996 Jul
PMID:Myocardial alterations in diabetes and hypertension. 886 52

Earlier we reported that probucol treatment subsequent to the induction of diabetes can prevent diabetes-associated changes in myocardial antioxidants as well as function at 8 weeks. In this study, we examined the efficacy of probucol in the reversal of diabetes induced myocardial changes. Rats were made diabetic with a single injection of streptozotocin (65 mg/kg, i.v.). After 4 weeks of induction of diabetes, a group of animals was treated on alternate days with probucol (10 mg/kg i.p.), a known lipid lowering agent with antioxidant properties. At 8 weeks, there was a significant drop in the left ventricle (LVSP) and aortic systolic pressures (ASP) in the diabetic group. Hearts from these animals showed an increase in the thiobarbituric acid reacting substances (TBARS), indicating increased lipid peroxidation. This was accompanied by a decrease in the myocardial antioxidant enzymes activities, superoxide dismutase (SOD) and glutathione peroxidase (GSHPx). Myocardial catalase activity in the diabetic group was higher. In the diabetic + probucol group both LVSP and ASP showed significant recovery. This was also accompanied by an improvement in SOD and GSHPx activities and there was further increase in the catalase activity. Levels of the TBARS was decreased in this group. These data provide evidence that diabetic cardiomyopathy is associated with an antioxidant deficit which can be reversed with probucol treatment. Improved cardiac function with probucol may be due to the recovery of antioxidants in the heart.
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PMID:Probucol treatment reverses antioxidant and functional deficit in diabetic cardiomyopathy. 890 84

It has been suggested that alterations in intracellular Ca2+ homeostasis may be responsible for the development of diabetic cardiomyopathy. We have studied the effects of streptozotocin-induced diabetes on intracellular Ca2+ concentration ([Ca2+]i) in enzymically isolated rat ventricular myocytes. [Ca2+]i was measured using indo 1 or fluo 3. Both diastolic and peak systolic [Ca2+]i were reduced in diabetic compared with normal myocytes (by 52 and 43%, respectively). The decay phase of the systolic [Ca2+]i transient was slower in the diabetic myocyte compared with normal (time constant = 89.6 +/- 3.4 ms, n = 23, normal vs. 105.2 +/- 4.05 ms, n = 20, diabetic; P < 0.01). This led to a significant prolongation of the [Ca2+]i transient duration in the diabetic myocyte. In both normal and diabetic myocytes, increasing the frequency of electrical stimulation decreased peak systolic [Ca2+]i. The relationship between stimulation frequency and normalized peak systolic [Ca2+]i was the same for both normal and diabetic myocytes. We also found that the caffeine-induced Ca2+ release [used as an index of sarcoplasmic reticulum (SR) Ca2+ content] was significantly reduced in diabetic myocytes. These data indicate that SR Ca2+ content is decreased by diabetes. In the presence of thapsigargin (2.5 microM, an inhibitor of SR Ca(2+)-adenosinetriphosphatase), the magnitude and time course of stimulus-evoked [Ca2+]i transients were identical in both groups of myocytes, suggesting that Ca2+ influx and/or efflux across the plasma membrane is not significantly affected in diabetes. We conclude that 1) diabetes is associated with significant alterations in [Ca2+]i homeostasis and 2) the decrease in systolic [Ca2+]i and lengthening of the systolic [Ca2+]i transient result primarily from dysfunction of the SR.
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PMID:Altered Ca2+ handling in ventricular myocytes isolated from diabetic rats. 892 57

The existence of a distinct diabetic cardiomyopathy, characterized by a raised left ventricular mass, has previously been suggested. However, as diabetes mellitus is associated with both left ventricular hypertrophy and hypertension a confounding effect of raised blood pressure in diabetic patients has to be considered. In the present cross-sectional study an echocardiographical examination was performed as part of a health screening survey in 582 males, aged 70 years. After the exclusion of subjects with coronary heart disease or those on regular antihypertensive treatment, 30 normotensive subjects with diabetes were compared with 10 subjects with non-insulin-dependent diabetes (NIDDM) and a diastolic blood pressure 90 mm Hg or more and 203 normotensive control subjects with normal glucose tolerance. Both groups with NIDDM showed a significantly increased left atrial diameter (4.4 +/- 0.7 vs 4.0 +/- 0.5 cm, p < 0.05) and an increased atrial component in diastole (A-wave, p < 0.01) compared to the control subjects. Left ventricular mass was, however, only marginally and not significantly elevated in the diabetic subjects when compared to the healthy control subjects (133 +/- 19 and 133 +/- 28 vs 128 +/- 25 g/m2). Only in the subjects with concomitant diabetes and a raised blood pressure was the intraventricular septum significantly enlarged (p < 0.05). Thus, in the present sample no distinct diabetic cardiomyopathy with an increased left ventricular mass, independent of the influence of hypertension could be detected. The myocardial alterations in these diabetic males were restricted to an increased left atrial size and an impaired diastolic function.
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PMID:Relationship between diastolic hypertension and myocardial morphology and function in elderly males with diabetes mellitus. 896 Aug 49

The regulatory myosin light chain (MLC) is phosphorylated in cardiac muscle by Ca2+/calmodulin-dependent MLC kinase (MLCK) and is considered to play a modulatory role in the activation of myofibrillar adenosine triphosphatase (ATPase) and the process of force generation. Since the depression in cardiac contractile function in chronic diabetes is associated with a decrease in myofibrillar ATPase activity, we investigated changes in MLC phosphorylation in diabetic heart. Rats were made diabetic by injecting streptozotocin (65 mg/kg intravenously), and the hearts were removed 8 weeks later; some 6-week diabetic animals were injected with insulin (3 U/d) for 2 weeks. Changes in the relative MLC and MLCK protein contents were measured by electrophoresis and immunoblot assay, whereas phosphorylated and unphosphorylated MLCs were separated on 10% acrylamide/urea gel and identified by Western blot. MLC and MLCK contents were decreased markedly (40% to 45%) and MLC phosphorylation was decreased significantly (30% to 45%) in the diabetic rat heart homogenate in comparison to control values. The changes in MLC and MLCK content in diabetic heart were partially reversible, whereas changes in MLC phosphorylation were normalized upon treatment with insulin. These results suggest that decreased protein contents of MLC and MLCK and phosphorylation of MLC may contribute to the depression of cardiac myofibriliar ATPase activity and heart dysfunction in diabetic cardiomyopathy.
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PMID:Myosin light-chain phosphorylation in diabetic cardiomyopathy in rats. 900 73

The vectorcardiographic (VCG) bites in diabetic patients were compared with those in nondiabetic control subjects using automated analysis of the conventional electrocardiogram (ECG). A 12-lead ECG was recorded from each of the 154 patients with non-insulin-dependent diabetes mellitus and 128 control subjects. The orthogonal leads X, Y, and Z were derived from the 12-lead ECG, from which a so-called 12-lead VCG was calculated for each of the 282 participants. A computer-based method for the detection and quantification of bites was applied to the 12-lead VCGs. Bite amplitudes in the horizontal loop had an average of 0.062 +/- 0.089 mV in the diabetic group, and 0.039 +/- 0.045 mV in the control group (P < .01). In the sagittal plane, the mean bite amplitude was also greater in the diabetic group than in the control group: 0.095 +/- 0.084 versus 0.069 +/- 0.058 mV, respectively (P < .01). A bite greater than 0.1 mV in the horizontal or sagittal planes was found in 56 diabetic patients (36%) and 27 control subjects (21%) with (P < .05) considered significant. In conclusion, the results of this study suggest that automated analysis of the 12-lead VCG can be valuable in diagnosing diabetic cardiomyopathy.
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PMID:Increased prevalence of large bites in 12-lead vectorcardiograms of diabetic patients. 914 2


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