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  • 1
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 15 (1988), S. 0 
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. Segments of the tail artery of the rat were cannulated at both ends and mounted in an organ bath filled with Krebs solution.2. Using an extracorporeal circuit, blood was pumped at a constant 2 ml/min from the carotid artery of anaesthetized rats to perfuse the segment of tail artery, and returned to the donor rat via the jugular vein.3. Peri-arterial electrical stimulation of the ex vivo blood perfused tail artery at 5 Hz produced vasoconstriction and an increase in perfusion pressure.4. The intravenous administration of frusemide 5 mg/kg to the donor rat resulted in an inhibition of the vasoconstrictor responses of the perfused tail artery segment. Diuresis-induced losses of volume and frusemide were prevented by a urinary bladder-venous shunt.5. Removal of the endothelium from the tail artery segment, by perfusion with dry gas for 4 min, prevented the vasoconstrictor-inhibitory effect of frusemide administration. Removal of the endothelium was confirmed histologically and by the absence of a vasodilator response to acetylcholine.6. On the basis of these and previous results it is concluded that parenteral frusemide administration releases an unidentified but non-prostanoid hormone from the kidney which produces an endothelium-dependent inhibition of sympathetic vascoconstriction.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Oxford, UK : Blackwell Publishing Ltd
    Clinical and experimental pharmacology and physiology 13 (1986), S. 0 
    ISSN: 1440-1681
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: 1. Omeprazole, a substituted benzimidazole and a potent gastric antisecretory drug has been tested for inhibition of microsomal drug oxidative function in the rat.2. A single dose of 40 mg/kg prolonged pentobarbitone sleeping times from 118 (range 73–168) min to 195 (159–222) min (P 〈 0.01), pentobarbitone half-lives from 89 (63–114) to 112 (54–146) min (P 〈 0.05) and aminopyrine breath 14CO2 half-lives from 43 (37–51) to 56 (49–79) min (P 〈 0.05). Omeprazole in doses of 20 mg/kg or less had no significant effect.3. In prolonging pentobarbitone sleeping times omeprazole 40 mg/kg and an equimolar (30 mg/kg) dose of cimetidine were approximately equipotent.4. These results contrast with studies in man in which much smaller doses of omeprazole have been shown to produce clinically significant inhibition of drug metabolism.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 329 (1985), S. 201-205 
    ISSN: 1432-1912
    Keywords: Cisplatinum ; Nephrotoxicity ; Furosemide ; Acetazolmide
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The influence of variations in sodium chloride diet, furosemide and acetazolamide on nephrotoxicity induced by cisplatinum have been investigated in the rat by measuring serum creatinine concentrations 5 days after cisplatinum (5 mg/kg, ip) administration. Sodium chloride depletion enhanced, while sodium chloride loading minimized changes in renal function. Increases in urine flow rate following a dextrose water load failed to alter the nephrotoxic response. Both furosemide and acetazolamide, given 30 min before cisplatinum, attenuated the nephrotoxic response. In contrast, neither sodium chloride loading, furosemide, nor acetazolamide influenced the change in renal function when given 30 min after cisplatinum. These observations indicate that renal damage due to cisplatinum can be modified by alterations in dietary salt and by diuretics and that the extent of ultimate renal damage is dependent on factors occurring immediately after cisplatinum administration.
    Type of Medium: Electronic Resource
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