PubMed Health⌕ Search

Biomedical subjects

E Oliw

Publications and source records attributed to E Oliw.

29 records · Page 2Linked to original sources
PubMed1979

Different effects of furosemide on urinary excretion of prostaglandin E2 and F2 alpha in rabbits.

The effect of a constant infusion of furosemide (130 micrograms/min i.v. for 60 min, n = 8) was studied on urinary excretion of water, electrolytes and immunoreactive prostaglandin E2 (iPGE2) and iPGF2alpha in chloralose-urethane anesthetized rabbits. During the furosemide infusion sodium and water excretion increased ten-fold and the excretion of potassium and iPGE2 two to three times. The excretion of iPGF2alpha (0.06 +/- 0.03 micrograms/min/100 g kidney weight) was not significantly changed during the furosemide infusion but increased markedly after the infusion and reached a maximum (1.0 +/- 0.6 microgram/min/100 g) 30 to 45 min later, while the small increase in iPGE2 excretion at this time could be attributed to cross-reaction with PGF2alpha. The results indicate that PGE2 might possibly be involved directly in the action of furosemide, while PGF2alpha might participate in sodium and water conserving mechanisms in the rabbit kidney, activated by the drug induced diuresis.

Animals↗
PubMed1979

Efflux of cyclic AMP, prostaglandin E2 and F2 alpha and thromboxane B2 in leg lymph of rabbits after scalding injury.

Leg lymph was collected from pentobarbital anaesthetized rabbits before and after scalding injury of the paw (75 degrees C for 20 s), and the contents of cyclic AMP (cAMP), prostaglandin E2 (PGE2) and PGF2 alpha and thromboxane B2 (TXB2) in lymph were determined. After injury lymph flow increased about four times. The maximal rate of flow was found between 30 and 60 min after scalding. The efflux of cAMP and immunoreactive iPGE2, iPGF2 alpha and iTXB2 also increased. The maximum values were detected at approximately 0-30, 30-60, 30-60 and 180-240 min, respectively, after the injury. The output of cAMP, iPGE2 and iPGF2 alpha and iTXB2 in lymph of the contralateral non-scalded paw remained low throughout the experiments. When rabbits were injected with indomethacin (2.5 mg/kg) or diclofenac sodium (2.5 mg/kg) immediately after the scalding injury, the efflux of cAMP, iPGE2 and iPGF2 alpha were low. Lymph flow was markedly reduced after treatment with diclofenac sodium; treatment with indomethacin did not significantly affect lymph flow. The results suggest a prostaglandin-dependent formation of cAMP following scalding injury which may be related to the initial responses to scalding.

Animals↗
PubMed1978

Indomethacin and diclofenac sodium increase sodium and water excretion after extracellular volume expansion in the rabbit.

The renal effects of an acute extracellular fluid volume expansion (50 ml Ringer/kg body weight/60 min) were studied in aldosterone-treated (100 microgram/kg), anesthetized rabbits with and without pretreatment with either indomethacin (3.0 mg/kg) or diclofenac sodium (3.0 mg/kg), two different inhibitors of renal prostaglandin (PG) biosynthesis. In controls (n = 7), the volume expansion increased urine flow from 1.5 +/- 0.24 to 6.1 +/- 0.5 (S.E.) ml/min/100 g kidney weight and sodium excretion from 0.15 +/- 0.03 to 0.99 +/- 0.10 mmol/min/100 g. PAH and inulin clearance increased by 42 and 58%, respectively, while plasma renin activity and urinary excretion of PGF2 alpha-like immunoreactivity were reduced (P less than 0.05). In animals pretreated with indomethacin (n = 6) or diclofenac sodium (n = 6), the diuresis and the natriuresis following volume expansion were significantly increased about two-fold over controls, whereas PAH and inulin clearance, plasma renin activity and hematocrit did not differ from controls. Both drugs were found to reduce urinary excretion of PGF2 alpha-like immunoreactivity by 75--95% througout the experiment. The results indicate that diclofenac sodium, indomethacin and extracellular volume expansion enhance sodium and water excretion partly by suppression of a PG sensitive reabsorption process in the kidney.

Animals↗
PubMed1978

In vivo inhibition of prostaglandin synthesis in rabbit kidney by non-steroidal anti-inflammatory drugs.

To define dose- and time-response properties for in vivo inhibition of renal prostaglandin (PG) synthesis, aspirin, diclofenac sodium, indomethacin and d-naproxen were injected intravenously in different doses to unanaesthetized rabbits. After 30 min. the animals were killed and the post mortem accumulation of PGE2 and PGF2alpha in the renal medulla was determined by mass fragmentography. In control animals, the accumulated levels of PGE2 and PGF2alpha in the medulla were 9.2+/-2.2 (S.D.) and 1.5+/-0.6 microgram/g, respectively. Dose-dependent inhibition was demonstrated with all the drugs. The ED95 was for aspirin 15 mg/kg, for diclofenac sodium 1.5 mg/kg, for indomethacin 1.5 mg/kg and for d-naproxen 5 mg/kg. The duration of inhibition was studied by radioimmunoassay in anaesthetized rabbits by following the urinary excretion of PGF2alpha and PGE2 after an intravenous injection of solvent or test drug in doses twice the ED95. For three hours following aspirin, diclofenac sodium, indomethacin and d-naproxen, the decreases in urinary excretion of PGF2alpha ranged from 64 to 88, 87 to 95, 64 to 90 and from 40 to 77 per cent of the control, respectively, and the decreases in PGE2 excretion were of similar magnitude. Together these results indicate that diclofenac sodium might be used as a long-lasting and potent alternative to indomethacin and aspirin in experimental studies on the renal PG system in vivo.

Animals↗
PubMed1978

The influence of dietary sodium on urinary prostaglandin excretion.

The influence of dietary sodium chloride on the urinary excretion of prostaglandins (PGs) was studied in unanesthetized female rabbits housed in metabolic cages. Urinary PG levels were determined by radioimmunoassay, bioassay and gas chromatography-mass spectrometry. In the first experiment rabbits were fed at high (2.5%) and later a low (0.25%) sodium chloride diet ad libitum. A 2--5 fold increase in excretion of immunoreactive PGF2alpha (iPGF2alpha) and iPGE2 was noticed when animals were given the low salt diet. Since it could not be excluded that dietary factors other than sodium chloride contributed to the changes a second, more controlled experiment was undertaken. Rabbits were fed 30 g/kg per day of diets offering only in the content of sodium chloride, 2% and 0.37% respectively. On the high salt diet the rabbits excreted 0.1 +/- 0.04 microgram/day of PGE2 and 2.0 +/- 0.5 microgram/day of iPGF2alpha. After equilibration on the low salt diet the PGE2 excretion rate increased to 1.5 +/- 0.3 microgram/day (p less than 0.001) and that of iPGF2alpha to 3.4 +/- 0.4 microgram/day (p less than 0.01). These results thus point to an inverse relationship between renal sodium excretion and the activity of the renal prostaglandin system.

Animals↗
PubMed1977

Effect of indomethacin on the renal actions of theophylline.

The effects of theophylline ethylenediamine (15 mg/kg i.v.) on plasma renin activity (PRA), diuresis, creatinine clearance and plasma and urinary adenosine 3',5'-monophosphate (cyclic AMP) concentrations were studied in urethane-anaesthetized rabbits with and without pretreatment with indomethacin (5 mg/kg i.v.). Theophylline induced a several-fold increase in urinary sodium and water excretion, raised PRA from 76 +/- 15 TO 239 +/- 83 (S.E.M) ng/ml/h (p less than 0.05) and increased urinary cyclic AMP excretion from 0.21 +/- 0.04 to 0.50 +/- 0.08 nmol/min/kg/kidney (p less than 0.05) without any change in arterial plasma cyclic AMP concentration. The ratio between the clearance of creatinine and cyclic AMP was unchanged. After indomethacin pretreatment the theophylline-induced natriuresis was significantly reduced (p less than 0.05), while the effects of theophylline on PRA and urinary cyclic AMP excretion were unchanged. Under the present experimental conditions, indomethacin reduces renal prostaglandin biosynthesis by over 95%. our results indicate that prostaglandins might be concerned with the natriuretic effects of theophylline but not with the effect on PRA.

Animals↗
PubMed1976

Reduction by indomethacin of furosemide effects in the rabbit.

The effects of furosemide on urine flow, sodium and potassium excretion and on plasma renin activity (PRA) were studied in anesthetized rabbits with and without pretreatment with indomethacin 5 mg/kg. Furosemide caused a 10-fold increase in urine flow and in sodium excretion, and a 2-3 fold increase in PRA. Pretreatment with the prostaglandin synthesis inhibitor, indomethacin, reduced the effects of furosemide on diuresis and on electrolyte excretion by over 80% (p less than 0.01) and PRA did not increase over the initial level. The results suggest that the effects of furosemide on PRA and on urinary sodium excretion may be related to the intrarenal activation of the prostaglandin system.

Animals↗