In the developing countries of the world, few people with hemophilia receive adequate care. Nevertheless, Brazil has made significant advances in the treatment of hemophilia over the last decade. The provision of factor concentrates imported by the Government of Brazil is gradually increasing, and patients receive the concentrates for free. A national register was established as well as a coordinated program for comprehensive care. Of the 6 297 persons with hemophilia in Brazil who were registered as of January 2001, 689 of them (11.1%) were registered in the state of Rio de Janeiro. Of those 689, 664 of them were being monitored at the state's coordinating blood transfusion center, which is located in the city of Rio de Janeiro. Among those 664, factor VIII inhibitors were identified in 81 of them (12.2%). Among 653 of the Rio de Janeiro patients who were tested for transfusion-transmitted diseases, the overall prevalence found was 41.5%, with the specific rates being 13.3% for human immunodeficiency virus (HIV), 2.9% for hepatitis B virus (HBV), and 39.4% for hepatitis C virus (HCV). The state of Rio de Janeiro has adopted a comprehensive hemophilia management approach that includes medical, psychological, and social care. As a result, the quality of life of hemophilia patients has improved noticeably. For example, the rate of hospitalization among patients fell by 30% between 1998 and 2001, and there has also been a decline in the school and work activities that they have missed.
The hypothalamus, the cerebral cortex and the cerebellar cortex of the rat were labelled in vitro with 3H-noradrenaline (3H-NA) and the metabolism of the tritiated transmitter was studied during spontaneous outflow and under conditions of release elicited by exposure to 20 mM K+. In the three areas of the central nervous system of the rat 3H-NA accounted for approximately 40% of the total radioactivity in spontaneous outflow while the 3H-O-methylated deaminated fraction (3H-OMDA) and 3H-3,4-dihydroxyphenylglycol (3H-DOPEG) were the main metabolites. Exposure to the reserpine-like agent, Ro 4-1284 induced a selective increase in the spontaneous outflow of 3H-DOPEG, while the contribution of the 3H-OMDA metabolites to the release induced by Ro 4-1284 was very small. During 3H-transmitter release elicited by exposure to 20 mM K+, approximately 80% of the radioactivity was collected as unmetabolized 3H-NA, while 3H-DOPEG was the main metabolite formed under these experimental conditions. Exposure to cocaine prevented 3H-DOPEG formation from 3H-NA released by K+, indicating that 3H-DOPEG was formed after neuronal reuptake of the transmitter released by K+. After in vitro labelling with 3H-NA, the unmetabolized transmitter represented approximately 70% of the total radioactivity retained in the tissue. However, when 3H-NA was administered in vivo, by intraventricular injection, only 30% of the total radioactivity retained by the tissue was accounted for by 3H-NA, and 60% of the radioactivity corresponded to the 3H-OMDA fraction, most of which was retained as 3H-MOPEG sulfate. When the rats were pretreated with pyrogallol, free 3H-DOPEG accounted for nearly 50% of the radioactivity retained in the three areas of the central nervous system after in vivo labelling with 3H-NA. When monoamine oxidase was inhibited by pargyline and 3H-NA was administered by intraventricular injection, 3H-NMN accounted for approximately 50% of the total radioactivity retained in the three areas of the central nervous system of the rat. The results obtained are compatible with the view that formation of the deamined glycol is the first step in the metabolism of 3H-NA in the rat central nervous system. In addition, it is concluded that the determination of the levels of some NA metabolites retained in the central nervous system does not necessarily represent an accurate reflection of the degree of central noradrenergic activity or of selective metabolic pathways. Consequently, in studies on the metabolism of NA it is important to take into account not only the transmitter and its metabolites in the tissue but also in the outflow from the structures studied either under in vivo or in vitro conditions.
Ginkgo biloba is the phytoterapic most used in popular medicine in the treatment of cerebral senescence. Red blood cells (RBC) labeled with technetium-99m (Tc-99m) is used for several evaluations in nuclear medicine. This labeling depends on a reducing agent, usually the stannous ion. Any drug, which alters the labeling of the tracer, could be expected to modify the disposition of the radiopharmaceutical. We have evaluated the influence of the Ginkgo biloba extract on the labeling of RBC and plasma proteins with Tc-99m. Blood was withdrawn and incubated with Ginkgo biloba extract (0; 0.004; 0.04; 0.4; 4; 20 and 40 mg/ml). Stannous chloride (1.2 ml/ml) was added and, then, Tc-99m was added. Plasma (P) and blood cells (RBC) were isolated, also precipitated with trichloroacetic acid and soluble (SF) and insoluble fractions (IF) separated. The analysis of the results shows that there is a decrease in the radioactivity (from 97.7 ± 0.7 to 49.5 ± 3.9%) in RBC with the drug (4 mg/ml). In the labeling process of RBC with Tc-99m, the stannous and pertechnetate ions pass though the membrane, so, we suggest that the Ginkgo biloba effect can be explained by (i) an inhibition of the transport of these ions, (ii) damage in membrane, (iii) competition with the cited ions for the same binding sites, or (iv) possible generation of reactive oxygen species that could oxidize the stannous ion.The use of medicinal plants or natural products has increased in the last decades all over the world. Ginkgo biloba is a gymnosperm considered a "living fossil" and is the phytoterapic most used in popular medicine in the treatment of cerebral senescence. Ginkgo biloba extract has important antioxidant properties due to probably to the presence of flavonoids 1,2,3 .In nuclear medicine, red blood cells (RBC) are usually labeled with technetium-99m (Tc-99m) and used as radiopharmaceutical in studies of the cardiac function, volemia and detection of gastrointestinal bleeding sites. Plasma proteins are also labeled with Tc-99m and used for evaluation of lung perfusion and location of placenta 4,5 . These labeling techniques involve the pre-tinning of the blood constituents with stannous ions, followed by exposure to Tc-99m, as sodium pertechnetate, which is reduced within of the cell and remains trapped intracellularly by the binding in the beta chain of hemoglobin 4,5,6 .It is reported that many substances can alter the labeling of blood elements with Tc-99m 7 . There are some studies about the effect of the medicinal plants (Thuya occidentalis, Nicotiana tabacum, Peumus boldus, Maytenus ilicifolia) on the labeling of RBC (6,7,8,9,10). We have studied the effect of Ginkgo biloba extract on the labeling of RBC and plasma proteins with Tc-99m.The analysis of the results (Table 1) indicates that there is a significant decrease (p<0.05) on the uptake of Tc-99m by the red blood cells with the concentrations from 0.4 up to 20 mg/ml of the extract of Ginkgo biloba. The analysis of the results also indicates that there is a significant decrease (...
The effects of cocaine, phentolamine and phenoxybenzamine on neuronal uptake of [3H]‐noradrenaline and on 3H‐transmitter and noradrenaline overflow elicited by nerve stimulation were determined in the perfused heart of the cat. During perfusion with cocaine 3.4 × 10−7m, there was a 2‐fold increase in transmitter overflow while neuronal uptake of [3H]‐noradrenaline was inhibited by 31.3 ± 2.1%. After exposure to phenoxybenzamine 8.7 × 10−7m for 20 min and washing with drug‐free solution for 165 min there was an 8‐fold increase in transmitter overflow during nerve stimulation. Under these conditions neuronal uptake of [3H]‐noradrenaline was inhibited by only 17.5 ± 5.4%. There was no significant change in transmitter overflow or in neuronal uptake of [3H]‐noradrenaline, 155 min after a 30 min exposure to phentolamine (3.2 × 10−5m). Perfusion with phentolamine (3.2 × 10−5m) before and during exposure to phenoxybenzamine (8.7 × 10−7m), prevented the increase in transmitter overflow observed after perfusion with phenoxybenzamine alone. Protection by phentolamine against the effects of phenoxybenzamine supports the view that the effects on transmitter release obtained after perfusion with phenoxybenzamine are due to the blockade of presynaptic α‐adrenoceptors which regulate transmitter release through a negative feed‐back mechanism.
No abstract
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.