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Biomedical subjects

E Anggård

Publications and source records attributed to E Anggård.

At least 73 records · Page 4Linked 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↗
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

Methadone maintenance: plasma levels and therapeutic outcome.

Twenty-one opiate-dependent subjects were inducted into methadone maintenance treatment (MMT) in a closed metabolic ward. A daily dose of 30 mg of d, 1-methadone was given for 10 to 24 days followed by 60 mg/day for another 10 to 24 days. Analysis of plasma levels at 4-day intervals showed accumulation to a peak followed by a decrease to a lower level, indicative development of dispositional tolerance. The outcome of treatment was assessed after 21 to 43 mo (median, 33 mo). The best record of rehabilitation was obtained in subjects discharged with steady-state plasma concentrations above 200 ng/ml. Lower levels of plasma methadone were associated with higher frequency of urines containing illicit drugs and poorer psychosocial rehabilitation. This study indicates that a pharmacokinetically optimized dosage regimen would be useful in increasing the therapeutic effectiveness of MMT.

Adult↗
PubMed1978

Inhibition of prostaglandin synthesis in rat brain.

Rats were injected with one of five drugs alleged to inhibit brain prostaglandin (PG) synthesis: indomethacin, diclofenac, naproxen, aspiring and paracetamol. Animals were killed after 30 min. and the endogenous formation of PGF2alpha and PGE2 in brain homogenates was measured by mass fragmentography using deuterium labelled PGF2alpha and PGE2 as internal standards. Diclofenac, indomethacin, and naproxen inhibited dose dependently, the synthesis of PGF2alpha. The ED50 for diclofenac was 0.4 mg/kg, for indomethacin 1 mg/kg and for naproxen 2 mg/kg. In equieffective doses indomethacin had the longest duration. The time taken for the inhibition to decline to half its maximal value was 32 hrs for indomethacin and about 15 hrs for diclofenac and naproxen. Under the present conditions aspirin and paracetamol failed to produce significant reduction of PG synthesis in the rat brain homogenates in doses up to 100 mg/kg.

Acetaminophen↗
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↗
PubMed1977

Identification of prostaglandin D2 as a major prostaglandin in homogenates of rat brain.

Prostaglandin (PG) E2, D2, F2alpha and thromboxane B2 (TxB2) were determined in homogenates of rat brain by gas-chromatography--mass spectrometry. The level of PGD2 was 735 +/- 19 ng/g, of PGF2alpha 150 +/- 13 ng/g, of TxB2 112 ng/g and of PGE2 86 +/- 8 ng/g. The same relative proportions of cyclooxygenase products were found in incubates of unstimulated sliced rat brain. 14C-PGH2 was converted in high yield into PGD2 by enzyme(s) present in the soluble fraction of the homogenate. These results indicate that PGD2 is the major cyclooxygenase product in the central nervous system of the rat.

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↗
PubMed1976

Effects of stimulation and inhibition of the renal prostaglandin synthetase system on renin release in vivo and in vitro.

1. The prostaglandin precursor arachidonic acid (C20:4) increases plasma renin activity in the rabbit and rat when it is infused into the renal arteries. 2. The increase in plasma renin activity after C20:4 in rats is not changed by volume expansion. 3. The inhibitor of prostaglandin synthesis indomethacin decreases plasma renin activity in the rabbit. 4. The increase plasma in renin activity after total renal ischaemia is abolished by pretreatment with indomethacin. 5. C20:4 increases dose- and time-dependent renin release from slices of rabbit kidney cortex. 6. Indomethacin or 5,8,11,14-eicosatetraynoic acid pretreatment in vivo, and addition to the incubation medium, reduces basal as well as C20:4-stimulated renin release in vitro. 7. The stimulating effect of C20:4 on renin release is assumed to be caused directly by formation of prostaglandin endoperoxides in the kidney cortex and not by prostaglandins since in vitro a natural prostaglandin endoperoxide (PGG2) and two stable synthetic prostaglandin endoperoxide analogues (EPA I and EPA II) do increase the release of renin, but PGE2 has no effect and PGF2alpha inhibits renin release.

Animals↗
PubMed1976

Prolonged symptoms of brain dysfunction--adverse effect of levodopa.

Symptoms of brain dysfunction occurred in a 67-year-old woman with idiopathic parkinsonism on treatment with levodopa. The adverse effect reappeared in a more severe and prolonged form when she was treated one year later with levodopa in combination with the peripheral decarboxylase inhibitor Ro-4-4602. The symptoms were associated with a markedly altered level of HMPG (a noradrenaline metabolite) in the cerebrospinal fluid.

Aged↗