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In the brain, the levels of adenosine increase up to 100-fold during cerebral ischernia; however, the roles of specific cell types, enzymatic pathways and membrane transport processes in regulating intra- and extracellular concentrations of adenosine are poorly characterized. Rat primary cortical neurons and astrocytes were incubated with [(3)H]adenine for 30 min to radiolabel intracellular ATP. Cells were then treated with buffer, glucose deprivation (GD), oxygen-glucose deprivation (OGD), 100 micro M sodium cyanide (NaCN) or 500 micro M iodoacetate (IAA) for 1 h to stimulate the metabolism of ATP and cellular release of [(3)H]purines. The nucleoside transport inhibitor dipyridamole (DPR) (10 micro M), the adenosine kinase inhibitor iodotubercidin (ITU) (1 micro M), the adenosine deaminase inhibitor EHNA (1 micro M) and the purine nucleoside phosphorylase inhibitor BCX-34 (10 micro M) were tested to investigate the contribution of specific enzymes and transporters in the metabolism and release of purines from each cell type. Our results indicate that (a). under basal conditions astrocytes released significantly more [(3)H]adenine nucleotides and [(3)H]adenosine than neurons, (b). OGD, NaCN and IAA conditions produced significant increases in [(3)H]adenosine release from neurons but not astrocytes, and (c) DPR blocked [(3)H]inosine release from both astrocytes and neurons but only blocked [(3)H]adenosine release from neurons. These data suggest that, in these experimental conditions, adenosine was formed by an intracellular pathway in neurons and then released via a nucleoside transporter. In contrast, adenine nucleotide release and extracellular metabolism to adenosine appeared to predominate in astrocytes.
Dobutamine stress echocardiography is more sensitive and is better tolerated than adenosine or dipyridamole stress echocardiography. Adenosine echocardiography is more specific than dobutamine or dipyridamole echocardiography and is less likely to cause persistent symptoms.
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Modification of risk factors such as hypertension, diabetes, hypercholesterolemia, cigarette smoking and obesity are fundamental to stroke management. Antiplatelet therapy is highly effective in reducing the risk of recurrent vascular events and is recommended over oral anticoagulants for non-cardioembolic stroke. Evidence from head-to-head comparative clinical trials versus aspirin monotherapy has shown that clopidogrel and the combination of aspirin plus dipyridamole are safe and effective therapeutic options.
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Long-term dipyridamole use and new LDA use were associated with an increased risk of subarachnoid hemorrhage. Because of the limited precision of these risk estimates, however, caution is advised in their interpretation. Long-term LDA use was not associated with subarachnoid hemorrhage.
Among several nucleosides and nucleotides, which showed strong inhibition of growth of HL-60 cells, only adenosine (Ado) specifically induced typical apoptotic death of the cells, accompanying double-strand cleavage of DNA into nucleosomal size fragments, and subsequent apoptotic body formation. A marked enhancement of endogenous poly(ADP-ribosyl)ation activity in the cell was detected at a relatively early stage of cell death, whereas other nucleosides and nucleotides tested were ineffective on poly(ADP-ribosyl)ation activity, suggesting that the enzyme activation is closely related to apoptosis. The observed Ado effect was not mediated by Ado receptors, in contrast to the Ado-induced apoptotic death of thymocytes, judging from the facts that all of the receptor agonists tested did not substitute for Ado and that a receptor antagonist did not inhibit the effect of Ado. Ado transport into the cell seemed to be essential for the induction of apoptosis, since an inhibitor of Ado transport (dipyridamole) strongly suppressed apoptosis. Cytochalasin B blocked Ado-induced apoptotic body formation without affecting activation of endogenous poly(ADP-ribosyl)ation activity in the cell. Thus, the process of apoptosis in HL-60 cells induced by Ado seems to be separated into at least two steps, an initial step of DNA degradation and a following morphological change. While the adenine moiety of Ado was essential for its apoptosis-inducing activity, the sugar was replaceable, and various analogs with modified sugar were inducers of apoptosis, although they were less efficient than Ado.
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A meta-analysis was performed using Cox regression, including several subgroup analyses and following baseline risk stratification.
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Glucocorticoid (GC) therapy is widely accepted as effective treatment for many inflammatory conditions. However, the potential of GC to produce adverse effects may prompt both patients and prescribing doctors to take a critical view on these important drugs. The increasing awareness of potential side effects suggests that the improvement of the benefit:risk ratio represents both a current need and an ongoing challenge. The developing and detailed knowledge on mechanisms of GC action has resulted in exploration of numerous approaches to optimise treatments with these important drugs. Most advanced is a chronotherapeutic formulation of prednisone (termed modified- or delayed-release prednisone) that has been recently approved in many European and other countries, and very recently also in the United States. Another interesting example is the development of selective GC receptor (GR) agonists, with clinical studies being currently underway. The development of so called liposomal GC is ongoing. However, another approach, the synergistic combination of prednisolone and dipyridamole, has been recently discontinued because a phase 2b study with the treatment in patients with rheumatoid arthritis showed a statistically significant improvement in disease activity score measured in 28 joints (DAS28) compared with placebo, but not compared with prednisolone alone. Other interesting developments and promising concepts include the development of nitrosteroids, targeting the membrane-bound GR and the use of extracts of the medicinal plant Tripterygium wilfordii Hook F.
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The questionnaire was sent to 256 patients and returned by 222, of whom 12% (26/222) of patients reported persistent novel headache. Dipyridamole had no significant influence on the incidence. Stroke-attributed headache according to predefined criteria was reported in 7.2% (16/222) of patients, with tension-type-like headache in 50.0%, migraine-like in 31.3% and medication overuse in 6.25% of patients. More than half of patients experienced moderate to severe pain and had a score of 55 or above on the Headache Impact Test-6 scale.
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Serotonin constricts coronary arteries with endothelial dysfunction, a common abnormality in cardiac transplant recipients. To assess whether endothelial dysfunction is associated with myocardial blood flow (MBF) abnormalities, 24 patients were studied 1 to 12 months after transplantation. Serotonin in increasing doses (1, 10, and 20 micrograms/min for 2.5 min each) was infused into the coronary circulation. Diameters were measured by quantitative angiography. Fourteen patients (group A) had a pronounced artery constriction (diameter reduction > 40%), while in 10 other patients (group B), such a constriction was never reached. No patient had evidence of rejection and all had angiographically normal coronary arteries. MBF was measured at rest and after intravenous dipyridamole with dynamic nitrogen-13 ammonia positron emission tomography (PET). The resting MBF was higher in group A than in group B (94 +/- 12 vs 74 +/- 15 ml/min/100 g of tissue; p < 0.05). During dipyridamole, MBF was not significantly different (191 +/- 53 vs 184 +/- 64 ml/min/100 g; p = NS). Coronary flow reserve (the ratio of perfusion after dipyridamole to perfusion at rest) was significantly lower in group A than in group B (2.08 +/- 0.54 vs 2.66 +/- 0.57; p < 0.05). Thus, coronary hypersensitivity to serotonin in cardiac transplant recipients is associated with elevated resting MBF and reduced coronary flow reserve. Immune mechanisms inducing endothelial injuries and inflammation-related hyperemia may account for these abnormalities.
The effects of coronary vasodilating agents and alpha- and beta-adrenergic blocking agents on cyclical reductions of blood flow in the partially constricted coronary artery of anesthetized dogs were examined. Intravenous injections of nitroglycerin (50 microgram/Kg), SG 75 (150 microgram/Kg), papaverine (1 mg/Kg), and nicotinic acid (10 mg/Kg) eliminated both cyclical reductions of flow and ST elevation (group 1). Nifedipine (10 microgram/Kg), verapamil (500 microgram/Kg), diltiazem (500 microgram/Kg), and propranolol (500 microgram/Kg) suppressed ST elevation, but they could not eliminate cyclical reductions of flow (group 2). Dipyridamole (1 mg/Kg) and phenotolamine (500 microgram/Kg) augmented both ST elevation and cyclical reductions of flow (group 3). The results indicate that ST elevation due to cyclical reductions of coronary blood flow was eliminated by spasmolytic actions of group 1 on coronary artery, was suppressed by negative chronotropic and/or inotropic actions of group 2, and was augmented by peripheral actions of group 3.
The occurrence of fatal respiratory insufficiency following dipyridamole-thallium imaging is described. The patient, a 67-year-old man, had a history of chronic obstructive lung disease. Since patients with a history of chronic obstructive lung disease have an increased risk of developing bronchospasm after dipyridamole infusion, it is advised to be cautious in performing dipyridamole-thallium imaging in these patients. Dobutamine may be an acceptable alternative to dipyridamole in these patients.
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Because of its intrinsic quantitative properties, PET permits measurement of myocardial perfusion and metabolism in absolute terms (i.e., mL/g/min). However, quantification has been limited by errors produced in image acquisition, selection of regions of interest, and data analysis. The goal of this study was to evaluate a newly developed, novel, wavelet-based noise-reduction approach that can objectively extract biologic signals hidden within dynamic PET data.
More than half of diabetic individuals will die from a coronary event. Coronary artery disease often presents an atypical form among diabetic subjects. Silent myocardial ischaemia may be detected in 20 to 35% of diabetic patients with associated cardiovascular risk factors. When a coronarography is performed in patients with silent myocardial ischaemia, it demonstrates significant coronary stenosis in one to two thirds of patients. The prognosis of diabetic patients with silent myocardial ischaemia is associated with a higher incidence of cardiac events in the next three years, especially when silent ischaemia is associated with angiographically coronary stenosis. French guidelines jointly published in 2004 by the ALFEDIAM and the French Society of Cardiology propose the search for silent myocardial ischaemia--in diabetic patients with peripheral arteriopathy or overt nephropathy with proteinuria,--in diabetic patients with microalbuminuria and two other classical cardiovascular risk factors,--in a sedentary diabetic patient who wants to begin a physical activity,--in type I diabetic patients above 45 years or with a disease lasting for more than 15 years and in type 2 diabetic patients above 60 years or with a known disease lasting for more than 10 years, when at least two other traditional cardiovascular risk factors are present. Besides the standard annual electrocardiogram, these high risk patients should benefit first from an exercise test or when the latter is impossible, under-maximal or doubtful, from a myocardial scintigraphy combined with dipyridamole injection or from a stress echocardiography. The demonstration of a silent myocardial ischaemia should lead to a coronarography when the general status of the patient and the absence of severe comorbidities allow considering a coronary revascularisation procedure in these diabetic patients.
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New therapies are being evaluated for patients with "no option" angina in whom medical therapy has failed. Nuclear techniques, like thallium scintigraphy, are used in multicenter trials to evaluate whether such therapies improve myocardial perfusion. However, the variability of test results is unknown in this patient group in a multicenter study.
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Eighteen young male Wistar rats were randomly divided into two groups of equal size. Each experimental animal was treated with the powerful vasodilating drug dipyridamole (4 mg kg-1 intraperitoneally twice daily) for a period of 6 weeks. The control animals received sham injections with saline. The rats were fixed by retrograde vascular perfusion. Seven transverse and two longitudinal sections per animal were randomly selected from the left ventricular papillary muscles for stereological investigation. Length density of capillaries (length of capillaries per unit of tissue volume), surface density of capillaries (surface area of capillaries per unit of tissue volume) and the "true" three-dimensional capillary-fiber ratio (length of capillaries per unit length of myocardial fibers) were estimated by means of the Dimroth-Watson distribution, a mathematical model of directional statistics which assumes that the capillary directions scatter around the longitudinal axis of the muscle. This model was recently introduced into the stereology of myocardial capillaries and leads to a more accurate quantitation of the capillary network than parameters used hitherto, such as the "capillary density" (number of capillary profiles per mm2 of cross sectional area) and the "capillary-fiber ratio" (number of capillary profiles per number of myofiber profiles in cross sections). After chronic dipyridamole treatment, the length density of myocardial capillaries (+5%; p less than 0.02), the surface density of capillaries (+8%, p less than 0.01) and the three-dimensional capillary-fiber ratio (+6%, p less than 0.05) were increased. It is therefore concluded that the vasodilating drug dipyridamole evokes capillary growth in the heart which may be induced by mechanical factors via the enhanced myocardial blood flow. Investigation of the frequency distribution of capillary directions in space in both groups provided evidence that the capillary growth resulted from neoformation of capillaries.
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We examined whether 201Tl myocardial scintigraphy with intravenous infusion of adenosine triphosphate (ATP) can be substituted for dipyridamole (DIP) in the diagnosis of coronary artery disease CAD).
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A combined MEDLINE and manual search was made for relevant articles from 1966 to November 1999. Standard meta-analysis techniques were used.
The proportion of patients that exhibited the primary endpoint, as assessed by the Kaplan-Meier method, was found to be significantly higher in group A than in group B (logrank test; P = 0.024). None of the patients in the two groups experienced serious adverse effects.
Twenty-five patients with untreated mild essential hypertension and normal coronary vessels and 10 control subjects underwent dipyridamole-rest Tc-99m sestamibi imaging. Myocardial blood flow (MBF) was estimated by measuring first transit counts in pulmonary artery and myocardial counts from tomograhic images. CFR was expressed as the ratio of stress to rest MBF. Coronary vascular resistances (CVR) were computed as the ratio between mean arterial pressure and MBF.
The cost-effectiveness estimates presented in this article support the NICE guidelines for the use of antiplatelets for the prevention of cardiovascular events. Based on these pharmacoeconomic data alone, aspirin should be prescribed for primary or secondary prevention among patients at high risk of cardiovascular events, dipyridamole for the secondary prevention of stroke (for a maximum of 5 years), and clopidogrel for the treatment of symptomatic cardiovascular disease or acute coronary syndrome (for a maximum of 2 years). The cost effectiveness of antiplatelets hinges on the patient's initial risk, the risk reduction associated with treatment, and the price of the treatment. Evidence suggests that the cost effectiveness of antiplatelets can be optimized by individualising the treatment decision based on patient risk and expected risk reduction.
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Vasodilator therapy in congestive heart failure has proven an effective adjunct to conventional treatment with digitalis and diuretics. In this study dipyridamole was used in combination with isosorbide dinitrate to treat twelve patients (mean age 55 years) with idiopathic congestive cardiomyopathy. All patients were in N.Y.H.A. class III or IV and were already treated with digitalis and diuretics. This conventional therapy was not discontinued for the study. Acute studies were performed during diagnostic right and left heart catheterization. Hemodynamics were obtained at rest, after intravenous administration of 40 mg dipyridamole and after 5 mg isosorbide dinitrate sublingually. An increase in cardiac index and stroke volume index was noted, while left ventricular enddiastolic pressure and systemic vascular resistance decreased significantly. The twelve patients were then treated with 4 X 150 mg dipyridamole and 4 X 40 mg isosorbide dinitrate per day while also continuing the digitalis and diuretic treatment. They were followed up clinically for a period of 8 to 24 months. Three patients died but the other nine showed a clinical improvement (mean of 1.45 N.Y.H.A. classes). It was possible to perform a second right and left heart catheterization in four patients. Cardiac index, stroke volume index and maximum and minimum DP/dt were significantly higher, and left ventricular enddiastolic pressure was significantly lower, than before vasodilator therapy. These results suggest a sustained effect of dipyridamole and isosorbide dinitrate. The postextrasystolic modification of maximum DP/dt could be of prognostic value in congestive cardiomyopathy.(ABSTRACT TRUNCATED AT 250 WORDS)
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In 110 patients with mesangioproliferative glomerulonephritis the treatment (n = 48) with chlorambucil, warfarin, dipyridamol and prednisone (CAA) and the treatment with imuran and prednisone (CP, n = 23) are compared with the conditions of an untreated control group. The CAA-therapy is above all suited for active clinical pictures without sclerosis with short duration of the disease, even when the renal function is already restricted. The CP-therapy is suitable in non-active forms with sclerosis also in a longer duration of the disease.
Vasodilator infusion yields higher cardiac 201Tl uptake than exercise, but when given alone this results in poor heart-to-background ratios. Combining either vasodilator with exercise maintains the high cardiac uptake, but substantially improves the heart-to-background ratios to levels similar to exercise alone. Dobutamine stress produces an intermediate cardiac uptake, and heart-to-background ratios similar to the vasodilators. Therefore, optimal imaging conditions are obtained by stress which combines a vasodilator with exercise.
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This study shows that stress echo in patients with hypertension yields a satisfactory diagnostic accuracy for identifying significant epicardial CAD. Our results indicate that dobutamine might be superior to dipyridamole. The low specificity of myocardial scintigraphy probably relates to the fact that this method traces perfusion abnormalities, not necessarily caused by epicardial CAD, possibly due to microvascular disease and not causing obvious wall motion abnormalities.
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Overall, 96 patients with SCF and 79 controls were enrolled in the study. Coronary flow was quantified according to the thrombolysis in myocardial infarction (TIMI) frame count (TFC) on angiogram. Coronary diastolic peak flow velocities (DPFV) were measured with color Doppler flow mapping at baseline and after dipyridamole infusion. Coronary flow reserve was calculated as the ratio of hyperemic to baseline DPFV. The eNOS 4a/b polymorphism was detected by PCR. Patients with diabetes were excluded from the study.
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Effect of modulators on protein kinase A (PKA) activity, promastigote growth and their ability to infect peritoneal macrophages was monitored. PKA inhibitors reduced [Protein Kinase Inhibitor (PKI) - 56%; H89 - 54.5%] kemptide phosphorylation by Leishmania major promastigote lysates, while activators increased phosphorylation (8-CPT-cAMP - 88%; Sp-cAMPS-AM - 152%). Activation was specifically inhibited by PKI. Phosphodiesterase inhibitors also increased kemptide phosphorylation (dipyridamole - 171%; rolipram - 106%; and 3-isobutyl-1-methyl-xanthine - 154%). Parasite proliferation was significantly retarded (200 nM H89; 100 microM myristoylated-PKI) or completely inhibited (500 nM H89) by culturing with PKA inhibitors. Incubation with dipyridamole or Sp-cAMPS-AM also inhibited proliferation. Brief treatment (2h) with either H89, myristoylated-PKI, dipyridamole or Sp-cAMPS-AM reduced initial macrophage infection at days 1 and 2 (>40%) and on day 3 (>78% only for 100 microM myr-PKI). Characterization of leishmanial cAMP mediated signal transduction pathways will serve as the basis for the new drug design.
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This study sought to assess the diagnostic value of myocardial perfusion imaging during exercise and pharmacologic stress in patients with left bundle branch block.