Drugs online research references
Exp Eye Res. 1983 Nov;37(5):409-20.
A model for transepithelial ion transport across the isolated retinal pigment epithelium of the frog.
DiMattio J, Degnan KJ, Zadunaisky JA.
The contribution of chloride ion movement and sodium and bicarbonate concentrations to the net current across the isolated choroid-retinal pigment epithelium (RPE) of the bullfrog were studied. The presence of a ouabain-sensitive Na+/K+-pump on the retinal side was confirmed and complete inhibition of this pump with Na+ removal and ouabain treatment abolished nearly all the RPE transepithelial transport and SCC suggesting that all ionic transport was dependent on sodium. It was found that apical to basal (AB) chloride flux accounted for 26 +/- 2% (mean +/- S.E.M.) of the short circuit (SCC). Results suggest that AB bicarbonate and/or basal to apical (BA) hydrogen ion net transport accounts for 38 +/- 2% of the SCC while BA sodium is presumably responsible for the remaining 34% of the SCC. Transport was inhibited by apical administration of known chloride inhibitors. Trans-RPE 36Cl flux measurements indicate that furosemide (10(-4) M) and SITS (10(-3) ) decrease the retinal-choroid flux. Results suggest that net transport of chloride and bicarbonate are independent of each other and additive. It was found that a bicarbonate-free preparation was relatively unaffected by changes in pH (5.5-8.5) indicating that pH has little, if any, effect on sodium or chloride current in this range. A model is presented which is compatible with the various data. It is suggested that along with the apical Na+/K+-ATPase pump, there exists an apical Na+/Cl- -co-transport system which is driven by the established sodium gradient. Moreover, this pump established sodium gradient is postulated to drive a Na+/HCO3- -co-transport system tentatively placed on the retinal side of the RPE.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6608452&dopt=Abstract
Mod Vet Pract. 1984 Jun;65(6):461-5.
Management of acute illness in cats.
Hause WR.
Pleural effusions can cause dyspnea and cyanosis, and are caused by cardiomyopathy, pyothorax, FIP, FeLV-related disease and trauma. Thoracentesis is used to obtain fluid samples for cytologic examination and culture. Radiographs made after thoracentesis may reveal the cause. Lymphosarcoma causes a sterile exudate containing neoplastic cells. Congestive cardiomyopathy causes a transudate or modified transudate. The sterile exudate of FIP has a proteinaceous background on cytologic examination. The exudate of pyothorax is septic. Treatment depends on the cause but generally includes thoracentesis and supportive care. Cardiomyopathy causes dyspnea, cyanosis, murmurs, gallop rhythms and other arrhythmias. Radiography reveals a globoid heart in the congestive form and a "valentine-shaped" heart in the hypertrophic form. Treatment of congestive cardiomyopathy involves use of furosemide, but is usually unrewarding. Hypertrophic cardiomyopathy is treated with propranolol. Fever may be caused by infection, immune-mediated disease, neoplasia and unknown causes. Treatment is aimed at removal of the underlying cause.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6738522&dopt=Abstract
Prostaglandins Leukot Med. 1982 Aug;9(2):211-21.
Effect of furosemide on the in vitro prostaglandin biosynthesis in human platelets.
Srivastava KC, Awasthi KK.
Effect of furosemide at various concentrations (0.05-4 mM) was examined on the in vitro biosynthesis of prostaglandins in human platelets. At lower furosemide concentrations (0.05 and 0.1 mM) no effect was observed. At 1 and 2 mM concentrations, PGE2 significantly (P less than 0.01) increased. At 3 and 4 mM concentrations PGE2 increased though not significantly probably because of the small number of samples (n=5). A decrease in PGD2 formation was noted at 1-4 mM furosemide concentrations, though significantly only at 3 mM conc. At 1 and 2 mM concentrations, TxB2 and HHT increased whereas at 3 and 4 mM concentrations these metabolites were decreased. These effects were, however, not significant. No effect was observed on endoperoxide generation at 1 and 2 mM conc. Furosemide at 1 and 2 mM concentrations inhibited ADP- and arachidonic acid induced platelet aggregation. An increased platelet formation of PGE2 in the presence of furosemide may point to the fact that this drug shows its effect mainly on the formation of PGE2 which has been found to exert a profound effect on renal blood flow and thus ameliorates some forms of hypertension.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6812095&dopt=Abstract
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