Deferoxamine improves coronary vascular responses to sympathetic stimulation in patients with type 1 diabetes mellitus
Autor: | Alexander Drzezga, Stephan G. Nekolla, Eberhard Standl, Markus Schwaiger, Naoya Hattori, Julian Rihl, Oliver Schnell, Frank M. Bengel |
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Rok vydání: | 2002 |
Předmět: |
Male
medicine.medical_specialty Sympathetic Nervous System Endothelium medicine.medical_treatment Deferoxamine Iron Chelating Agents Sensitivity and Specificity Ammonia Reference Values Diabetes mellitus Internal medicine Coronary Circulation Physical Stimulation medicine Humans Radiology Nuclear Medicine and imaging Endothelial dysfunction Saline Type 1 diabetes Nitrogen Radioisotopes business.industry Cold pressor test Hemodynamics Reproducibility of Results General Medicine Middle Aged medicine.disease Coronary Vessels Cold Temperature medicine.anatomical_structure Endocrinology Diabetes Mellitus Type 1 Vascular resistance Cardiology Female Radiopharmaceuticals business medicine.drug Tomography Emission-Computed |
Zdroj: | European journal of nuclear medicine and molecular imaging. 29(7) |
ISSN: | 1619-7070 |
Popis: | Effects of oxygen-derived free radicals are suggested to be a potential pathogenic factor for endothelial dysfunction. In this study we sought to evaluate the effect of hydroxyl radicals on the human coronary vascular bed in type I diabetes mellitus using positron emission tomography (PET). Thirteen patients with type 1 diabetes underwent PET using nitrogen-13 ammonia at rest and during sympathetic stimulation with the cold pressor test (CPT). The rest-stress study protocol was repeated twice (on different days) using pre-stress infusion of either saline as placebo or deferoxamine, an iron chelator which inhibits generation of hydroxyl radicals. At rest, global MBF was higher in diabetics than in normal controls (78.1+/-17.5 vs 63.2+/-14.9 mg 100 g(-1) min(-1), P0.05) and myocardial vascular resistance (MVR) showed a trend towards lower values (patients, 1.28+/-0.35; controls, 1.55+/-0.32, P=NS). CPT increased MBF in all controls while 7/13 diabetics responded normally. CPT decreased MVR in 10/13 controls but in only 4/13 diabetics. There was no significant difference in the duration of diabetes, HbA1c, daily insulin dose, body mass index, or lipid profiles between patients with and patients without abnormal MBF or MVR responses. Pre-stress infusion of deferoxamine normalized MBF response in all six patients, and MVR response in six of the nine patients. Another group consisting of seven patients underwent a rest-rest protocol after infusion of deferoxamine and saline to investigate the effect of deferoxamine on resting MBF. Deferoxamine did not change the resting MBF (deferoxamine, 81+/-17 ml 100 g(-1) min(-1); saline, 75+/-19 ml 100 g(-1) min(-1), P=NS) or MVR (deferoxamine, 1.0+/-0.5 mmHg ml(-1) 100 g(-1) min(-1); saline, 1.2+/-0.6 mmHg ml(-1) 100 g(-1) min(-1), P=NS). In conclusion, inhibition of hydroxyl radical formation using deferoxamine significantly improved the responses of coronary microvasculature to sympathetic stimulation. Hydroxyl radicals may play a role in the pathogenesis of flow abnormalities in type 1 diabetes. |
Databáze: | OpenAIRE |
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