Drugs online research references
Am J Dis Child. 1981 Mar;135(3):239-43.
Furosemide use in premature infants and appearance of patent ductus arteriosus.
Green TP, Thompson TR, Johnson D, Lock JE.
Furosemide is a known stimulant of the renal release of prostaglandin E2, a potent dilator of the ductus arteriosus. A possible relationship between furosemide use in infants with respiratory distress syndrome (RDS) and the incidence of patent ductus arteriosus (PDA) was investigated using two different retrospective analyses. The amount of furosemide administered prior to the day a murmur was heard in the infants with PDA was higher than the amount given to patients without PDA during the same period. In a historical analysis of patients treated for RDS in the years 1970 through 1979, furosemide use and fluid intake appeared to be independent factors contributing to the incidence of PDA. The proposed relationship between furosemide use and the occurrence of PDA in patients with RDS warrants further study.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7211779&dopt=Abstract
Drugs. 1993;46 Suppl 1:257-62.
Renal effects of nimesulide in furosemide-treated subjects.
Steinhauslin F, Munafo A, Buclin T, Macciocchi A, Biollaz J.
Departement de Medecine Interne, Centre Hospitalier Universitaire Vaudois, Lausanne, Switzerland.
In clinical settings where effective plasma volume is decreased, nonsteroidal anti-inflammatory drugs (NSAIDs) may induce acute renal failure. We have evaluated the effects of single and repeated doses of nimesulide on renal haemodynamics and electrolyte excretion in 8 healthy volunteers during a prolonged course of furosemide (frusemide). Under these study conditions, renal prostaglandin synthesis is expected to be elevated, with renal function being dependent upon increased levels of prostaglandins. Nimesulide induced an acute but transient decrease in indices of renal haemodynamics. Furosemide-induced increases in plasma renin activity and aldosterone levels were blunted, and urinary excretion of prostaglandin E2 was markedly reduced by nimesulide. The magnitude and time course of the natriuretic, kaliuretic and diuretic effects of furosemide were attenuated by nimesulide. Although the transient nature of the observed renal haemodynamic changes suggests that the risk of developing acute renal failure is small, the rise should be taken into account in patients with renal dysfunction. Sodium and potassium retention, and the blunting of the diuretic-induced electrolyte excretion, could be of clinical relevance. Nimesulide appears, therefore, to share the prostaglandin-dependent renal effects of other NSAIDs.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7506186&dopt=Abstract
J Membr Biol. 1995 May;145(2):129-41.
Cellular chloride depletion inhibits cAMP-activated electrogenic chloride fluxes in HT29-18-C1 cells.
Fine DM, Lo CF, Aguillar L, Blackmon DL, Montrose MH.
Department of Medicine, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.
Cyclic AMP-activated chloride fluxes have been analyzed in HT29-18-C1 cells (a clonal cell line derived from a human colon carcinoma) using measurements of cell volume (electronic cell sizing), cell chloride content (chloride titrator) and intracellular chloride activity (6-methoxy-N-(3-sulfopropyl)quinolinium; SPQ). HT29-18-C1 was shown to mediate polarized chloride transport. In unstimulated cells, the apical membrane was impermeable to chloride and net chloride flux was mediated by basolateral furosemide-sensitive transport. Forskolin (10 microM) increased furosemide-insensitive chloride permeability of the apical membrane, and decreased steady-state intracellular chloride concentration approximately 9%. Cellular chloride depletion (substitution of medium chloride by nitrate or gluconate), caused greater than fourfold reduction in cellular chloride concentration. When chloride-depleted cells were returned to normal medium, cells regained chloride and osmolytes via bumetanide-sensitive transport, but forskolin did not stimulate bumetanide-insensitive chloride uptake. The inhibition of cAMP-activated chloride reuptake was not explained by limiting cation conductance, cell shrinkage, choice of substitute anion, or decreased generation of cAMP in chloride-depleted cells. When cells with normal chloride content were depolarized (135 mM medium potassium + 10 microM valinomycin), cAMP activated electrogenic chloride uptake permselective for Cl- approximately Br- > NO3- > I-. The electrogenic transport pathway was inhibited in chloride-depleted cells. Results suggest that chloride depletion limits activation of electrogenic chloride flux.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=7563015&dopt=Abstract
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