| Ημερομηνία | barcode | code | περιεχομενο | τιμή παραγωγός | χονδρική | λιανική |
|---|---|---|---|---|---|---|
| 05/2018 | 2802101001010 | 210100101 | OMNISCAN INJ.SOL 0,5mmol (287MG)/ML BTx1 VIAL x 10 ML | 24.53 | 25.73 | 37.80 |
| 05/2018 | 2802101001027 | 210100102 | OMNISCAN INJ.SOL 0,5mmol (287MG)/ML BTx1 VIAL x 15 ML | 24.81 | 26.03 | 38.24 |
| 05/2018 | 2802101001034 | 210100103 | OMNISCAN INJ.SOL 0,5mmol (287MG)/ML BTx1 VIAL x 20 ML | 26.42 | 27.71 | 40.70 |
| 05/2018 | 2802101001119 | 210100111 | OMNISCAN INJ.SOL 0,5mmol (287MG)/ML BTx1PF.SYR.x20ML | 27.01 | 28.33 | 41.62 |
For intravenous use in MRI to visualize lesions with abnormal vascularity (or those thought to cause abnormalities in the blood-brain barrier) in the brain (intracranial lesions), spine, and associated tissues.
Based on the behavior of protons when placed in a strong magnetic field, which is interpreted and transformed into images by magnetic resonance (MR) instruments. Paramagnetic agents have unpaired electrons that generate a magnetic field about 700 times larger than the proton's field, thus disturbing the proton's local magnetic field. When the local magnetic field around a proton is disturbed, its relaxation process is altered. MR images are based on proton density and proton relaxation dynamics. MR instruments can record 2 different relaxation processes, the T1 (spin-lattice or longitudinal relaxation time) and the T2 (spin-spin or transverse relaxation time). In magnetic resonance imaging (MRI), visualization of normal and pathological brain tissue depends in part on variations in the radiofrequency signal intensity that occur with changes in proton density, alteration of the T1, and variation in the T2. When placed in a magnetic field, gadodiamide shortens both the T1 and the T2 relaxation times in tissues where it accumulates. At clinical doses, gadodiamide primarily affects the T1 relaxation time, thus producing an increase in signal intensity. Gadodiamide does not cross the intact blood-brain barrier; therefore, it does not accumulate in normal brain tissue or in central nervous system (CNS) lesions that have not caused an abnormal blood-brain barrier (e.g., cysts, mature post-operative scars). Abnormal vascularity or disruption of the blood-brain barrier allows accumulation of gadodiamide in lesions such as neoplasms, abscesses, and subacute infarcts.
Two-compartment model with mean distribution and elimination half-lives (reported as mean ± SD) of 3.7 ± 2.7 minutes and 77.8 ± 16 minutes, respectively.
Gadodiamide is eliminated primarily in the urine.
* 200 ± 61 mL/kg
* Renal cl=1.7 mL/min/kg * Plasma cl=1.8 mL/min/kg