Drugs online research references
Neurochem Res. 1999 Oct;24(10):1301-6.
Effect of allopurinol on hypoxia-induced modification of the NMDA receptor in newborn piglets.
Marro PJ, Andersen CB, Mishra OP, Delivoria-Papadopoulos M.
Department of Pediatrics, Maine Medical Center, Portland 04102-3134, USA.
The present study tests the hypothesis that pretreatment with allopurinol, a xanthine oxidase inhibitor, will prevent modification of the NMDA receptor during cerebral hypoxia in newborn piglets. Eighteen newborn piglets were studied. Six normoxic control animals were compared to six untreated hypoxic and six allopurinol (20 mg/kg i.v.) pretreated hypoxic piglets. Cerebral hypoxia was induced by lowering the FiO2 to 0.05-0.07 for 1 hour and tissue hypoxia was confirmed biochemically by the measurement of ATP and phosphocreatine. Brain cell membrane Na+,K+-ATPase activity was determined to assess membrane function. Na+,K+-ATPase activity was decreased from control in both the untreated and treated hypoxic animals (46.0+/-1.0 vs 37.9+/-2.5 and 37.3+/-1.4 micromol Pi/mg protein/hr, respectively, p < 0.05). [3H]MK-801 binding was determined as an index of NMDA receptor modification. The receptor density (Bmax) in the untreated hypoxic group was decreased compared to normoxic control (1.09+/-0.17 vs 0.68+/-0.22 pmol/mg protein, p < 0.01). The dissociation constant (Kd) was also decreased in the untreated group (10.0+/-2.0 vs 4.9+/-1.4 nM, p < 0.01), indicating an increase in receptor affinity. However, in the allopurinol treated hypoxic group, the Bmax (1.27+/-0.09 pmol/mg protein) was similar to normoxic control and the Kd (8.1+/-1.2 nM, p < 0.05) was significantly higher than in the untreated hypoxic group. The data show that the administration of allopurinol prior to hypoxia prevents hypoxia-induced modification of the NMDA receptor-ion channel binding characteristics, despite neuronal membrane dysfunction. By preventing NMDA receptor-ion channel modification, allopurinol may produce a neuromodulatory effect during hypoxia and attenuate NMDA receptor mediated excitotoxicity.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10492526&dopt=Abstract
Clin Exp Rheumatol. 1983 Jan-Mar;1(1):63-6.
A study of platelet aggregation and adhesion in gout.
Macfarlane DG, Slade R, Hopes PA, Hartog MH.
Platelet aggregation and adhesion were measured in twelve male patients with gout. Tests were performed with the patients off all treatment for six weeks and after the serum uric had been lowered with allopurinol. Results of aggregation and adhesion tests were normal and not influenced by the uric acid level. The increased cardiovascular disease risk in gout is unlikely to be due to an increased thrombotic tendency.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6681128&dopt=Abstract
J Med. 1991;22(2):76-82.
Clinical significance of hypouricemia in hospitalized patients.
Ogino K, Hisatome I, Saitoh M, Miyamoto J, Ishiko R, Hasegawa J, Kotake H, Mashiba H.
First Department of Internal Medicine, Tottori University School of Medicine, Yonago, Japan.
Serum uric acid was measured in 586 normal subjects and 1,220 hospitalized patients. Hypouricemia was noted in 0.34% of the normal subjects and 2.54% of the hospitalized patients. Among hospitalized patients with hypouricemia, 22 were on medication, including allopurinol, anticancer drugs, antibiotics and glucocorticoids. Twenty-one patients had liver disorders and 11 of them had received transfusions. Neoplastic diseases were noted in 14 patients. Thus, hypouricemia was found to be relatively common in hospitalized patients, and seems to be caused mainly by medication, neoplastic diseases, liver disorders and transfusions.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1895016&dopt=Abstract
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