Effect of aluminum overload on the bone marrow response to recombinant human erythropoietin.
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Biomedical subjects
Publications and source records attributed to B Ehmer.
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The effects of carvedilol, a new vasodilating beta-blocking drug, were studied in experimental pigs during short-term acute myocardial ischemia. In 21 anesthetized pigs 0.01, 0.03, and 0.1 mg/kg b.w. carvedilol was studied during repeated 2-min distal LAD-occlusions and a 60-min-period of ischemia. Left ventricular volume was continuously measured by the impedance catheter method. Intravenous administration of 0.01 mg/kg carvedilol resulted in a significant decrease of heart rate (-13%), dp/dtmax (-32%), and ejection fraction (-9%), slight changes of systolic pressure (-3%), and an increase of vascular resistance (+24%), indicating a beta-blocker effect without vasodilation-while the first vasodilatory effect was found at a dose of 0.1 mg/kg. During ischemia carvedilol had no influence on the time-course or the extent of systolic bulging of the ischemic myocardium, but the ischemia-induced decrease of left ventricular ejection fraction was diminished. Both during short-term ischemia, as well as during the 60-min-ischemia-period carvedilol significantly reduced ventricular premature beats. During the 60-min-ischemia-period activation delay measured from local DC-electrograms of the ischemic myocardium, as well as the occurrence of activation block were not altered by carvedilol, as was the incidence of ventricular fibrillation (69%). We conclude that at low dosages the beta-blocking effect of carvedilol exceeds the vasodilating properties. This may also hold true in patients with cardiac failure; they are more sensitive to beta-blocking drugs. During ischemia carvedilol slightly reduces the ischemia-dependent decrease of global ventricular function and it has an antiarrhythmic effect. Therefore, it may be protective in patients with acute myocardial infarction.
Pharmacological treatment of hypertension can, cause clinically significant alterations in endocrine function and glucose homeostasis. The aim of this study was to investigate the antihypertensive efficacy and the influence on carbohydrate metabolism of carvedilol and metoprolol in non-insulin-dependent diabetics with mild to moderate hypertension. The patients received either carvedilol 25mg twice daily or metoprolol 50mg twice daily for a period of 4 weeks; if diastolic blood pressure was over 90mm Hg at this time, the dosage was doubled for the subsequent 4 weeks. 49 of 89 enrolled patients completed the trial according to the protocol and were statistically evaluated. After 4 weeks of carvedilol treatment, 23 of 25 patients (92%) showed a good response to therapy (reduction of diastolic blood pressure below 90mm Hg). Doubling of dosage in the carvedilol group did not further increase the response rate after another month of treatment. The response rate after 4 and 8 weeks of metroprolol treatment was 79 and 83%, respectively. In both treatment groups, blood glucose concentrations were maintained within narrow limits. Glycated haemoglobin A1, which provides a profile of the mean blood glucose levels present during the preceding weeks, also remained unchanged. Oral antidiabetic medication taken by the patient remained constant and no hypoglycaemia was reported. When used in therapeutic doses in non-insulin-dependent diabetics, carvedilol is thus unlikely to cause a deterioration of carbohydrate metabolism.