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Biomedical subjects

H Kindahl

Publications and source records attributed to H Kindahl.

At least 217 records · Page 12Linked to original sources
PubMed1980

Chemical instability of 15-keto-13,14-dihydro-PGE2: the reason for low assay reliability.

The spontaneous degradation of 15-keto-13,14-dihydro-PGE2 was studied under various conditions. In aqueous media, dehydration rapidly occurred, particularly at high or very low pH. The acid catalyzed dehydration product was identified as 15-keto-13,14-dihydro-PGA2. This compound was also formed at alkaline pH, however, at higher pH a bicyclic compound, 11-deoxy-13,14-dihydro-15-keto-11,16-cyclo-PGE2, was formed in addition (cf. Fig. 1). The amounts of the latter compound increased with time and with increasing pH. In samples containing albumin, 15-keto-dihydro-PGE2 was degraded even more rapidly than in buffer of the same pH. In addition to the formation of the dehydration products, a considerable part of the metabolite was bound to albumin to yield water soluble adducts. A similar binding occurred to a low molecular weight fraction of plasma. The compound that was bound was 15-keto-dihydro-PGA2, whereas both 15-keto-dihydro-PGE2 and the bicyclic product were relatively inert in this respect. Due to its chemical stability, the bicyclic degradation product, 11-deoxy-13,14-dihydro-15-keto-11,16-cyclo-PGE2, is suggested as a suitable target for measurements instead of the labile parent compound, 15-keto-dihydro-PGE2, or the reactive dehydration product, 15-keto-dihydro-PGA2.

Acids↗
PubMed1980

Prostaglandins and thromboxanes in amniotic fluid during rivanol-induced abortion and labour.

Abortion or delivery were induced by extra-amniotic instillation of Rivanol during the second trimester in twelve patients and during the third trimester in two patients with fetal death and one patient with fetal acrania. Serial sampling of amniotic fluid was performed through a transabdominal catheter and the levels of free arachidonic acid (AA), prostaglandin F2 alpha (PGF2 alpha), prostaglandin E2 (PGE2), 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) and thromboxane B2 (TXB2) were determined. The levels of AA, PGF2 alpha, PGE2, 6-keto-PGF1 alpha and TXB2 in amniotic fluid increased significantly during induction with the exception of AA in fetal death which was high and remained constant during induction. Furthermore, PGF2 alpha, 6-keto-PGF1 alpha and TXB2 were all significantly correlated to AA. These observations suggested that free AA is released during Rivanol-induction of abortion and labour giving an increased synthesis of PGF2 alpha, PGE2 prostacyclin and thromboxane A2 in the fetal membranes and the decidua but not in the fetus. This increase might be relevant for the initiation and progress of abortion and labour in these patients.

Abortion, Induced↗
PubMed1980

Interactions of prostaglandin H2 and thromboxane A2 with human serum albumin.

The present report describes the interactions of human plasma proteins with the unstable endoperoxide, prostaglandin H2 and thromboxane A2, generated by incubation of platelets with prostaglandin H2 or arachidonic acid. It was found that both compounds reacted very rapidly with plasma proteins to form covalently bound derivatives. The major reacting plasma protein was human serum albumin. Depending on conditions, 20-40% of added prostaglandin H2 and 50-80% of generated thromboxane were bound to proteins. This reaction of both prostaglandin H2 and thromboxane A2 prevents their detection by classical analytical methods. The protein binding of thromboxane was more pH-sensitive than the binding of prostaglandin H2. The reactions cause reduced levels of both endoperoxide and thromboxane B2 in suspensions of washed platelets using human serum albumin as compared to buffer. It was also shown that the half-life of prostaglandin H2 was considerably reduced in the presence of albumin.

Arachidonic Acids↗
PubMed1980

Induction of labor by oral PGE2 administration--evaluation of different dose schedules.

The efficacy and safety of different oral doses of PGE2 in tablet form were evaluated in 30 women admitted to the hospital for labor induction at or near term. The aim was to select a recommendable dose schedule based on recording of uterine contractility, clinical outcome and measurement of the resulting plasma levels of the two prostaglandin metabolites 15-keto-13, 14-dihydro-PGE2 and 15-keto-13, 14-dihydro-PGE2 alpha by gas-chromatography-mass spectrometry and by radio-immunoassay. Measurements of uterine contractility and of plasma levels of the PGE2 metabolite both showed that the preferable interval between oral doses of PGE2 tablets is one hour. Following 1.0 mg PGE2, the plasma concentration peaked after 45 to 60 minutes and had returned to approximately pretreatment levels after 120 minutes. With a two-hour interval between doses there was above all a decreased frequency of contractions in the last part of the interval. No such variation in the contractility pattern was seen when 1.0 mg PGE2 was administered every hour. When the individual dose was increased to 2.0 mg, signs of overstimulation of uterine contractility were observed. The plasma concentration of the E2 metabolite increased in accordance with the oral dose. A slow rise in the plasma concentrations of the E2 and F2 alpha metabolites was found some hours following initiation of treatment, possibly indicating an increased endogenous prostaglandin biosynthesis, probably secondary to the stimulated uterine contractility.

Administration, Oral↗
PubMed1980

On the control of prostaglandin release during the bovine estrous cycle. Effects of cloprostenol injections.

The study comprise seven cows which were injected i.m. with 500 microgram of a synthetic prostaglandin analogue (cloprostenol) at different stages of their estrous cycles. Peripheral blood plasma levels of progesterone and the main blood plasma metabolite of prostaglandin F2 alpha, 15-keto-13,14-dihydroprostaglandin F2 alpha were determined. The injection of cloprostenol initiated luteolysis in all cases as evidenced by decreasing progesterone levels and occurrence of heat. In two animals injected on days 6 and 12, respectively, of the estrous cycle no release of endogenous prostaglandin F2 alpha was found. In animals injected on day 13 and 15 of their estrous cycles, respectively, a minor but sustained release of prostaglandin F2 alpha was found. In three animals injected on days 17, 17 and 19 of their estrous cycles, respectively, the endogenous release of prostaglandin F2 alpha had already started and no specific effect attributed to the injection of cloprostenol could be observed. It is concluded that the injection of cloprostenol initiates luteolysis with subsequent heat and ovulation. The release of endogenous prostaglandin F2 alpha occasionally seen in conjunction with the induced luteolysis is different and less pronounced as compared to the release seen during normal luteolysis in the cow.

Animals↗
PubMed1979

On the control of prostaglandin release during the bovine estrous cycle. Effects of progesterone implants.

Progesterone implants were inserted subcutaneously on day 12 of the estrous cycle in three heifers. The implants were known to release an amount of progesterone sufficient to maintain the peripheral blood plasma at a level of about 1 ng/lm. All three heifers showed luteolysis in a similar way with peaks of 15-keto-13, 14-dihydro-PGF2 alpha of normal magnitude and duration. Concomitantly, progesterone levels declined, but due to the presence of the implants, progesterone was maintained at a level of about 1 ng/ml. The release of prostaglandins, however, continued throughout the experimental period and did not cease until the implants were removed.

Animals↗
PubMed1979

Further studies on a specific platelet antibody found in Bernard-Soulier syndrome and its effects on normal platelet function.

An IgG antiplatelet antibody found in a multitransfused patient with Bernard-Soulier syndrome (BSS), reacted with a normal platelet surface antigen of 150 000 daltons which was similar to the glycoprotein missing from BSS platelets. The BSS platelet antibody (BSS-Pab) aggregated all control platelets which then released ADP and 5-HT and synthesized thromboxane. When mixed with the antibody, BSS platelets did not aggregate, did not release ADP and 5-HT and failed to synthesize thromboxane. The BSS-Pab was not inactivated by incubation with BSS platelet stroma. While the antibody did not aggregate thrombasthenic platelets, its aggregating activity was lost after incubation with their stroma. The BSS-Pab did not provoke ADP or 5-HT release or thromboxane synthesis in thrombasthenic platelets or in the platelets of a patient with platelet cyclooxygenase deficiency or in normal platelets treated with indomethacin. The aggregating, release and synthetic responses of platelets after binding of BSS-Pab to its membrane antigen (probably glycoprotein I) requires the presence of glycoprotein IIb and/or IIa and the normal metabolism of arachidonic acid.

Antibodies↗
PubMed1979

Effect of intrauterine saline infusion during the late luteal phase on the estrous cycle and luteal function of the mare.

The intrauterine infusion of 500 ml of warm sterile saline solution into mares on days 12, 13, or 14 after ovulation failed to alter the ovulatory interval, although intervals were shorter for days 12 and 13 (20.6 days) when compared with those in control mares (21.6 days). The IU fusion shortened luteal-life-span on days 12 (12.0 vs 13.8 days) and 13 (13.0 vs 14.4 days) (P is less than 0.05), but not day 14 (14.0 vs 13.5 days), when comparing the effects of IU infusion with an average of before and after base-line data. There was no effect on the interval from corpus luteum regression to ovulation, ie, the final follicular phases. The treatment average for days 12 and 13 combined was 7.7 days vs 7.3 days for controls. Also, no significant effect was observed for the duration of estrus in that the treatment average for days 12 and 13 was 5.1 days, and for controls, 6.0 days. The infusion of saline solution caused an immediate release of prostaglandin F(2alpha) within 5 minutes, with additional large releases occurring over the next 24 hours. Progestin concentrations decreased rapidly in relation to this prostaglandin release.

Animals↗
PubMed1978

Thromboxane generation by human peripheral blood polymorphonuclear leukocytes.

Human peripheral blood polymorphonuclear leukocytes were stimulated to generate thromboxane B2 in a time- and concentration-dependent fashion upon exposure to serum-treated zymosan particles. Conversion by stimulated PMN of [14C] arachidonic acid to [14C]thromboxane B2 was confirmed by thin-layer radiochromatography, radio-gas chromatography, and mass spectrometry. Generation of thromboxane B2 was independent of platelet contamination and could be inhibited by the cyclooxygenase inhibitor, indomethacin. Cells rendered incapable of ingesting particles by treatment with cytochalasin B generated comparable amounts of thromboxane B2. These results suggest that human peripheral blood polymorphonuclear leukocytes synthesize thromboxanes in response to surface stimulation independently of phagocytosis.

Humans↗