Drugs online research references
Eur Surg Res. 1992;24(5):257-64.
Sixty minutes normothermic ischemia in rat liver: the declining tissue concentration of hypoxanthine during reperfusion is not a washout phenomenon.
Karwinski W, Farstad M, Ulvik R, Sreide O.
Surgical Research Laboratory, Haukeland Hospital, University of Bergen, Norway.
A rat liver normothermic ischemia-reperfusion model was used to investigate whether hypoxanthine (HXA) that accumulated during ischemia was washed out in hepatic veins during reperfusion. Ischemia was induced in median and left lobes by clamping of the proper hepatic artery and portal branches. The effect of allopurinol (ALL) on metabolism of ATP and HXA was studied before, during and after a 60-min normothermic ischemic insult. Liver cell concentration of HXA in the group treated with ALL increased during ischemia and decreased rapidly during the first 10-min reperfusion. Recovery of ATP increased gradually during the 10-min reperfusion period and was significantly higher in the group treated by ALL compared to that of controls. Liver venous blood concentration of HXA in the ALL-treated group was 10-to 40-fold lower than that in liver tissue. The rapidly decreasing concentration of HXA in liver tissue during reperfusion and a minimal washout may indicate that HXA was used for resynthesis of ATP during reperfusion.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=1425822&dopt=Abstract
Acta Physiol Hung. 1990;76(4):319-31.
Effect of free radicals in ischaemic renal failure in the dog.
Konya L, Bencsath P, Szenasi G, Takacs L, Schaff Z, Vereckei A, Feher J.
2nd Department of Medicine, Semmelweis University Medical School, Budapest, Hungary.
After a 30-minute control period ischaemia was evoked in dogs under Nembutal (30 mg/kg, i.v.) anesthesia, by clamping the left renal artery for 45 minutes. This was followed by a 90-minute reperfusion period when diuresis, GFR, PAH clearance, sodium and potassium excretion, malondialdehyde level in the plasma of the renal vein and SOD enzyme activity of the erythrocytes in renal venous blood were determined. Besides the control group (n = 6), the following treated groups were investigated: 1. Allopurinol (n = 7) in a dose of 100 mg/kg, given orally for two days, 2. Silibinin (n = 6) in a dose of 4 mg/kg/hour, given into the renal artery, 3. MTDQ-DS (n = 6) in a dose of 150 mg/kg/hour, given intravenously. 4. SOD (n = 4) 4 mg infusion (initiated 1 minute prior reperfusion). In the first 15-minute period following reperfusion GFR was 21%, cPAH 29% and sodium and potassium excretion 67 and 42% of the values of the contralateral kidney, respectively. Renal function improved gradually during the 90 minutes of reperfusion, and the above-mentioned parameters reached 59, 57, 65 and 76% of the corresponding control data. Increase of malondialdehyde level in the venous blood of the kidney during reperfusion might have been indicative of the production of free radicals; the difference, however, was not significant statistically. The administrations did not lead to considerable change in any of the parameters investigated. No difference could be demonstrated by histological methods between the kidneys of the treated and untreated animals. The compounds studied are thought to be free radical scavengers; in the present work, however, no protective effect could be demonstrated.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=2104499&dopt=Abstract
Am J Physiol. 1987 Feb;252(2 Pt 2):H252-7.
O2 free radicals: cause of ischemia-reperfusion injury to cardiac Na+-K+-ATPase.
Kim MS, Akera T.
The role of O2 free radicals in the reduction of sarcolemmal Na+-K+-ATPase, which occurs during reperfusion of ischemic heart, was examined in isolated guinea pig heart using exogenous scavengers of O2 radicals and an inhibitor of xanthine oxidase. Ischemia and reperfusion reduced Na+-K+-ATPase activity and specific [3H]ouabain binding to the enzyme in ventricular muscle homogenates and also markedly lowered sodium pump activity estimated from ouabain-sensitive 86Rb+ uptake by ventricular muscle slices. These effects of ischemia and reperfusion were prevented to various degrees by O2-radical scavengers, such as superoxide dismutase, catalase, dimethyl-sulfoxide, histidine, or vitamin E or by the xanthine oxidase inhibitor, allopurinol. The degree of protection afforded by these agents paralleled that of reduction in enhanced lipid peroxidation of myocardial tissue as estimated from malondialdehyde production. These results strongly suggest that O2 radicals play a crucial role in the injury to sarcolemmal Na+-K+-ATPase during reperfusion of ischemic heart.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=3028176&dopt=Abstract
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