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Biomedical subjects

E Granström

Publications and source records attributed to E Granström.

At least 73 records · Page 4Linked to original sources
PubMed1979

Prostaglandin chemistry.

The prostaglandins and some related substances of biological importance constitute a rapidly growing family of compounds, all the members of which are oxygenated derivatives of certain polyunsaturated, essential fatty acids, such as arachidonic acid. Most cell types possess the enzyme systems necessary for the conversion of the precursor fatty acids into these compounds. The first step in the conversion leads to the production of cyclic peroxides, and this step is readily inhibited by the non-steroidal anti-inflammatory drugs. The further metabolism of the endoperoxides leads to the formation of other potent compounds: the "classical" prostaglandins, the thromboxanes, and prostacyclin.

Animals↗
PubMed1979

Prostaglandins and thromboxanes in burn injury in man.

The main urine metabolite of prostaglandin F2 alpha (5 alpha, 7 alpha-dihydroxy-11-ketotetranor-phostane-1, 16-dioic acid, PGF-metabolite) was determined by mass spectrometry (MS) and radioimmunoassay (RIA) in burned patients treated under routine conditions. The amount of the PGF-metabolite as determined by MS was 130 and 67 microgram/24 h (normal value 24 +/- 17 microgram/24 h) on days 3 and 5 respectively in one patient. In serial determinations using RIA the urine level of the PGF-metabolite was within normal values during the first days and rose to a broad peak 1-4 weeks after the injury. Thromboxane B2 (TXB2) was identified and quantitated in burn blister fluid. The amount of TXB2 was 1.7 ng/ml.

Adult↗
PubMed1978

Radioimmunoassay of prostaglandins and thromboxanes.

1. Decide on what organ or other biological material to study and select the proper compound for this study from the knowledge of precursor acid metabolism. Develop the RIA for this compound or a stable derivative thereof. 2. Whichever sample type is assayed (extracted or unextracted), the possibility of the presence of nonspecific interfering factors must be constantly kept in mind. Make dilution tests and assay for parallelism; however, do not accept parallelism as an absolute criterion of absence of nonspecific influence. 3. Use two or more completely different separation techniques for comparison when validating the RIA. 4. When evaluating the RIA, do not limit the investigation to the traditional reliability criteria: sensitivity, specificity, precision, and accuracy. The RIA may seem reliable at this stage and still give completely unrealistic values when applied to biological material. The method must be evaluated by other studies as well. 5. In the experimental design, aim at following the changes in prostaglandin levels in a series of samples instead of measuring absolute levels in single samples. 6. Make comparative studies employing different quantitative methods.

Animals↗
PubMed1977

Prostaglandin F2alpha as a mediator of pulmonary changes during platelet aggregation.

Increases in pulmonary arterial pressure, tracheal insufflation pressure, and blood levels of the prostaglandin F2alpha metabolite, 15-keto-13, 14-dihydro F2alpha, were observed after protamine chloride or thrombin-induced platelet aggregation and release reaction in dogs. These effects were largely eliminated after administration of acetylsalicylic acid, an inhibitor of prostaglandin synthesis. The platelet aggregation was not noticeably affected. It is suggested that release of prostaglandin F2alpha from platelets is an important factor for the pulmonary changes during induced platelet aggregation. The necessity of measuring metabolite levels, rather than prostaglandin F2alpha levels, in blood during in vivo conditions is demonstrated.

Airway Resistance↗
PubMed1977

Levels of prostaglandins F2 alpha and E2 and thromboxane B2 in joint fluid in rheumatoid arthritis.

Prostaglandin F2 alpha (PGF2 alpha), prostaglandin E2 (PGE2) and thromboxane B2 (TXB2) levels were determined by radioimmunoassay (RIA) in knee joint fluid in two groups of patients with classical or definite rheumatoid arthritis (RA). One group had no treatment for one week prior to the study. The second group consisted of patients who developed acute exudative arthritis despite the use of various non-steroidal anti-inflammatory drugs (NSAID). The main metabolites of PGF2 alpha in plasma and urine were measured in the untreated group. The conclusion to be drawn from this study are: 1) Treatment with NSAID effectively lowers PGF2 alpha and PGE2 and TXB2 levels in joint fluid. 2) Signs and symptoms of arthritis may persist in spite of lowered levels of PGF2 alpha and PGE2 in the joint fluid. 3) The main metabolites of PGF2 alpha in plasma and urine are above the low-normal limit in untreated patients. 4) The ratio TXB2/PG was low in untreated patients, suggesting that the thromboxane pathway is quantitatively minor in rheumatoid joint inflammation.

Anti-Inflammatory Agents↗
PubMed1976

Radioimmunoassay for urinary metabolites of prostaglandin F2alpha.

Antibodies against the main urinary metabolite of PGF2alpha in the human, 5alpha, 7alpha-dihydroxy-11-ketotetranorprosta-1,16-dioic acid, were raised in rabbits. The compound was coupled selectively in the omega position to bovine serum albumin prior to injection. The resuling antibodies did not distinguish between tetranor compounds varying only in structure at the omega carbon, and thus the assay could be used also for other metabolites of PGF2alpha, e.g. the main urinary metabolite in the guinea pig, 5alpha,7alpha-dihydroxy-11-ketotretranorporstanoic acid. Labeled ligands for the assays were prepared either in vivo by injection of [17, 18-3H]-PGF2alpha into humans after several days treatment with indomethacin, or in vitro by incubation of [17, 18-3H]-15-keto-13, 14-dihydro-PGF2alpha with mitochondria from rat liver. The sensitivity of the assay was 10 pg or 4 pg with these two preparations, respectively. The assay was employed for a number of measurements: normal daily excretion in a number of humans; excretion of urinary metabolites during treatment with prostaglandin synthetase inhibitors in human subjects, or after intravenous injection of PGF2alpha; excretion during human pregnancy; and prostaglandin production in the guinea pig during normal estrous cycles and pregnancies and after estrogen treatment. The results of these studies were in several cases compared to similar measurements earlier performed using mass spectrometric methods, and were found to agree well. Thus, this radioimmunoassay provides a simple and accurate method for estimating prostaglandin production, particularly suitable for long-term studies and for cases where repeated blood sampling must be avoided.

Animals↗
PubMed1976

Kinetic and metabolic studies of 15-methyl-prostaglandin F2alpha administered intra-amniotically for induction of abortion.

The metabolism of tritium labeled 15-methyl-PGF2alpha, administered intra-amniotically, was studied in seven cases of mid-trimester abortion. The disappearance of the compound from the amniotic sac was a very slow process. A metabolite, dinor-15-methyl-PGF2alpha, was found in small amounts in the amniotic and kidney. Plasma levels of 15-methyl-PGF2alpha in the maternal circulation were determined.

Abortion, Induced↗
PubMed1976

A method for measuring the unstable thromboxane A2: radioimmunoassay of the derived mono-O-methyl-thromboxane B2.

A radioimmunoassay was developed for a mono-O-methyl derivative of thromboxane B2. The antibodies showed high specificity for this compound and cross reacted only 1.2% with thromboxane B2 and less than 0.1% with prostaglandins and prostaglandin metabolites. The method had a sensitivity of 7 picog. The radioimmunoassay was employed in studies where thromboxane A2 was generated in human platelets and immediately converted into mono-O-methyl thromboxane B2 by treatment of the sample with a large volume of methanol. In some of the experiments, thromboxane B2 was simultaneously measured by a separate radioimmunoassay. Using these two assays it was demonstrated that thromboxane A2 could be detected only during the earlier stages of the platelet aggregation, whereas thromboxane B2 rapidly reached a constant level. In a separate experiment, the half-life of thromboxane A2 in buffer was found to be 32.5 + 2.5 (S.D.) sec at 37 degrees C; the compound was more stable at lower temperatures. The t1/2 for thromboxane A2 was also considerably longer in plasma.

Antibody Specificity↗
PubMed1976

The release of prostaglandin F2alpha as reflected by 15-keto-13,14-dihydroprostaglandin F2alpha in the peripheral circulation during normal luteolysis in heifers.

Progesterone and the main plasma metabolite of PGF2alpha, 15-keto-13, 14-dihydro-PGF2alpha, were determined at hourly intervals in the peripheral circulation during luteolysis in two heifers. The prostaglandin release was found to occur during 2-3 days as rapid pulses with a duration of 1-5 hours prior to and during luteolysis, which was indicated by decreasing levels of progesterone.

Animals↗