[Effect of deferoxamine on urinary excretion of iron in chronic non-hemochromatosic liver diseases].
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A new colorimetric method for the determination of urinary iron chelated with desferrioxamine B is proposed. A single reagent (ferrozine plus thioglycolic acid 1%) is utilized. Analytical range reached about 25 mg of iron/l, while the detection limit was 0.2 p.p.m. The evaluation of imprecision and inaccuracy were within acceptable limits. Moreover, there is good correlation with the atomic absorption spectrophotometric technique. This test shows good reliability.
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UNLABELLED: Acetylcholine produces coronary artery (CA) constriction in diabetic patients suggesting an impairment of endothelium-dependent dilation. To examine the mechanism of this abnormal response. 2 physiological tests, i.e. cold pressor test (CPT) and coronary flow-increase induced by 10 mg papaverine (PAP) injection in the distal left anterior descending CA (dLAD), were performed before (1) and after (2) either i.v. L-arginine (L-arg, 625 mg/min x 10 min) or i.v. desferrioxamine (DFX, 50 mg/min x 10 min) in 15 normotensive nonsmoker diabetic patients with angiographically normal CA and normal cholesterol. Dimensions of the proximal LAD (pLAD) were measured by quantitative angiography. [table: see text] Before administration of L-arg or DFX, CPT induced a decrease of pLAD diameter, and PAP injection in dLAD dit not modify pLAD diameter. In the 7 diabetic patients receiving L-arg, responses to CPT and PAP were not modified. Conversely in the 10 patients receiving DFX, pLAD dilated in response to the 2 tests. Intracoronary isosorbide dinitrate, an endothelium-independent dilator, produced similar dilation in the 2 groups (+20 +/- 8% and +16 +/- 6%, respectively). CONCLUSIONS: 1) responses of angiography normal CA to CPT and to flow increase are impaired in diabetic patients; 2) abnormal responses are not improved by L-arg suggesting that a deficit in substrate for NO synthesis is not involved; 3) DFX restores a vasodilator response to the 2 tests suggesting that inactivation of NO by superoxide radicals might be partly responsible of the impairment of CA dilatation in diabetic patients.