Search PubMed⌕ Search

Biomedical subjects

P Uotila

Publications and source records attributed to P Uotila.

At least 19 recordsLinked to original sources
PubMed1992

Responses of placental steroids, prostacyclin and thromboxane A2 to thermal stress during pregnancy.

The effect of heat stress on plasma prostacyclin and thromboxane A2 and serum estradiol, estriol and progesterone responses was studied in pregnant and non-pregnant women. Group I consisted of 15 healthy non-pregnant women, group II of 23 women 13-14 weeks pregnant, and group III of 23 women 36-37 weeks pregnant. Blood samples were taken before the heat stress, at the end of the stress (70 degrees C for 20 min) and 20 min and/or 45 min after the end of stress. The rectal temperature increased 0.3-0.4 degrees C. The concentration of progesterone did not change during the experiment but that of estradiol increased by 11% (P less than 0.005) in group II and by 10% (P less than 0.01) in group III after the end of the stress. Estriol increased only in group III (by 12%, P less than 0.005) after the end of the stress and the increase was higher as compared to group II (P less than 0.005). The metabolite of prostacyclin increased only in group III by 15% (P less than 0.05) during the heat stress. The metabolite of thromboxane A2 decreased in group II by 20% (P less than 0.005) at the end of the stress while there was no change in group III. The fetal heart rate reactivity remained unchanged and only few uterine contractions were recorded. The small changes found in the levels of prostanoids and placental steroids in response to heat stress do not seem to have any deleterious effects on fetal well-being. The slightly increased concentration of placental steroids may rather reflect changes in metabolism than an increase in uteroplacental blood flow.

6-Ketoprostaglandin F1 alpha↗
PubMed1988

Ritodrine infusion at term: effects on maternal and fetal prostacyclin, thromboxane and prostaglandin precursor fatty acids.

A prospective randomized study was performed to investigate the effect of a short-term ritodrine infusion on the concentrations of maternal and fetal prostaglandins and their precursor fatty acids. Mothers gave birth by an elective cesarean section at term, and either ritodrine (study group) or physiological saline (controls) was infused 2 h prior to the operation. Ritodrine decreased the levels of thromboxane A2 significantly in the mother, while the concentration of prostacyclin remained unchanged. In the umbilical arterial plasma concentrations of prostacyclin or thromboxane A2 there were no differences between ritodrine-treated and control subjects. Ritodrine had no effect on the prostaglandin precursor fatty acids and other fatty acids of plasma phospholipids of the mother or her fetus. It is concluded that ritodrine may suppress the maternal prostaglandin production, but has no effect on the levels of vasoactive prostaglandins or their precursor fatty acids in the fetus.

6-Ketoprostaglandin F1 alpha↗
PubMed1988

The absorption of acetylsalicylic acid from an enteric-coated formulation and the inhibition of thromboxane formation.

To compare conventional (CT) and enteric-coated (ECT) tablets of acetylsalicylic acid (ASA) six healthy adult subjects ingested one 0.5-g tablet of these formulations daily for fifteen days in a cross-over study. Significant amount of ASA was detected in peripheral blood of every subject after the ingestion of CT or ECT. The rate of absorption of ASA was faster and its peak plasma concentration was higher after the ingestion of CT. The formation of thromboxane B2 (TXB2) decreased during blood clotting concomitantly with the absorption of ASA from both formulations. The formation of TXB2 was equally and completely inhibited by CT and ECT as it decreased to 1% of the control value one day after the first dose. During treatment with a single daily dose of 0.5 g of CT or ECT, the serum level of TXB2 remained at this low level and returned to the control level gradually in two weeks after the last dose. The present study indicates that significant amount of unchanged ASA is absorbed also from ECT and that the formation of TXB2 is equally and completely inhibited with a 0.5-g daily dose of both formulations.

Adult↗
PubMed1987

The effect of acute hypoxia on prostaglandin release in perfused human fetal placenta.

The release of prostaglandin E2 and F2 alpha, thromboxane B2 and 6-keto-prostaglandin F1 alpha was measured in isolated human placental cotyledons perfused under high- and low-oxygen conditions. Also the effect of reoxygenation on prostaglandin production was studied. During the high-oxygen period, prostaglandin E2 accounted for 44% and 6-keto-prostaglandin F1 alpha for 28% of all prostaglandin release, and the rank order of prostaglandin release was E2 greater than 6-keto-prostaglandin F1 alpha greater than thromboxane B2 greater than prostaglandin F2 alpha. Hypoxia had no significant effect on quantitative prostaglandin release, but the ratio of prostaglandin E2 to prostaglandin F2 alpha was significantly increased. After the hypoxic period during reoxygenation the release of 6-keto-prostaglandin F1 alpha was significantly decreased, as was the ratio of 6-keto-prostaglandin F1 alpha to thromboxane B2. Also the ratio of the vasodilating prostaglandins (E2, 6-keto-prostaglandin F1 alpha) to the vasoconstricting prostaglandins (thromboxane B2, prostaglandin F2 alpha) was decreased during reoxygenation period. With the constant flow rate, the perfusion pressure increased during hypoxia in six and was unchanged in three preparations. The results indicate that changes in the tissue oxygenation in the placenta affect prostaglandin release in the fetal placental circulation. This may also have circulatory consequences.

Aerobiosis↗
PubMed1987

Evening primrose oil in the treatment of atopic eczema: effect on clinical status, plasma phospholipid fatty acids and circulating blood prostaglandins.

In a double-blind trial patients with atopic eczema received either oral evening primrose oil (EPO) (n = 14) or placebo (n = 11) for 12 weeks. In the EPO group a statistically significant improvement was observed in the overall severity and grade of inflammation and in the percentage of the body surface involved by eczema as well as in dryness and itch. Patients in the placebo group showed a significant reduction in inflammation. The patients receiving EPO showed a significantly greater reduction in inflammation than those receiving placebo. Evening primrose oil caused a significant rise in the amount of dihomogammalinolenic acid in the plasma phospholipid fatty acids. Plasma levels of TXB2, 6-keto-PGF1 alpha and PGE1, and the amount of TXB2 released into serum during clotting were not altered by evening primrose oil.

6-Ketoprostaglandin F1 alpha↗
PubMed1987

The vasodilatation induced by hydroperoxy metabolites of arachidonic acid in the rat mesenteric and pulmonary circulation.

The effects of 15-hydroperoxy metabolites of arachidonic acid on vascular tone were evaluated in the perfused mesenteric preparation, the isolated perfused lung and segments of pulmonary arteries of the rat. In the mesenteric preparation, precontracted with phenylephrine, both 15-hydroperoxy-5,8,11,13-eicosatetraenoic acid (15-HPETE, ED50 1.6 nmol) and 8,15-dihydroperoxy-5,9,11,13-eicosatetraenoic acid (8,15-diHPETE, ED50 0.3 nmol) induced dose-dependent vasodilatation, whereas 5,15-diHPETE (0.2-100 nmol) had no effect. Prostacyclin (ED50 0.01 nmol) was, however, more potent than the hydroperoxides. In the rat isolated lung, precontracted with the stable thromboxane agonist U-46619, dose-dependent decrease in the perfusion pressure occurred with 15-HPETE(ED50 40 nmol), 5,15-diHPETE (ED50 30 nmol) and 8, 15-diHPETE (ED50 7 nmol) while 13-hydroperoxide of linoleic acid had no effect. Prostacyclin was 10 times more potent than 8, 15-diHPETE. The vasodilator effects were not affected by indomethacin. In both endothelium intact and denuded rat pulmonary arteries the hydroperoxides 15-HPETE, 8,15-diHPETE, and 5,15-diPETE induced dose-dependent relaxation. The hydroperoxide, 8,15-diHPETE was at least 3 times more potent than 15-HPETE or 5,15--diHPETE. The hydroperoxides had no effect on the basal tone of vessel segments and the relaxation induced by 15-HPETE was not attenuated by methylene blue (5 microM). These data indicate that 8,15-diHPETE may be a significant endothelium-independent vasodilator product of arachidonate lipoxygenation.

Animals↗
PubMed1987

Relaxing effects of 15-lipoxygenase products of arachidonic acid on rat aorta.

In the presence of indomethacin, arachidonic acid relaxes precontracted rings of rat aorta only when the endothelium is intact. Arachidonate-induced, endothelium-dependent relaxation is potentiated by superoxide dismutase. In contrast, linoleic acid (LA) contracts endothelium-intact and -denuded rings. Arachidonate is metabolized in endothelial cells by both cyclo-oxygenase and 15-lipoxygenase. Therefore, we determined the vasodilatory effect of 15-lipoxygenase products. The products generated by soybean lipoxygenase (SLO) from arachidonate in the bioassay bath relax precontracted, de-endothelialized ring segments of rat aorta. This relaxation is potentiated by superoxide dismutase and is more prominent when high concentrations of SLO are used. The main metabolites recovered from the bioassay bath were 5,15-dihydroperoxyeicosatetraenoic acid and 8,15-dihydroperoxyeicosatetraenoic acid. At lower concentrations of SLO the degree of relaxation is less and the major product is 15-hydroperoxyeicosatetraenoic acid. LA is metabolized by SLO to 13-hydroperoxyoctadecadienoic acid. The relaxation induced by the incubation of LA with SLO in endothelium-denuded rings is less than that obtained with arachidonic acid. In endothelium-denuded rings that were precontracted with phenylephrine authentic 15-hydroperoxyeicosatetraenoic acid did not induce clear effect (at 40 microM 15-hydroperoxide caused relaxation, whereas at 15 microM induced small contraction) and 13-hydroperoxyoctadecadienoic acid of LA induced contraction. Neither 5,15-dihydroperoxyeicosatetraenoic acid nor 8,15-dihydroperoxyoctadecadienoic acid (1-15 microM) induced a well defined relaxation. This study indicates that arachidonic acid is metabolized by SLO to a vasodilatory compound(s) that is possibly derived from 15-hydroperoxyeicosatetraenoic acid.

Animals↗
PubMed1986

Detection of leukotrienes in the serum of asthmatic and psoriatic patients.

Purified serum samples from asthmatic and psoriatic patients and healthy controls were analysed by high-pressure liquid chromatography (HPLC) and the amounts of leukotrienes were measured from the corresponding HPLC fractions by specific radioimmunoassays. In the serum of healthy controls the amounts of leukotrienes B4, C4 and D4 were very small or negligible. Rather great amount of leukotriene B4 was, however, detected in the serum of many asthmatic and psoriatic patients. The amount of leukotriene B4 was in the serum of asthmatic patients 120 +/- 20 pmol/ml (n = 11, mean +/- SEM) and in that of psoriatic patients 100 +/- 10 pmol/ml (n = 10). The amounts of leukotrienes C4 and D4 were rather small in the serum of most patients. The amount of leukotriene C4 was, however, very high (250 pmol/ml) in the serum of a psoriatic patient. Significant amount of leukotriene D4 was also detected in the serum of this patient. The present study indicated that leukotrienes are formed during blood clotting in the leukocytes of asthmatic and psoriatic patients and that the rate of formation is so high that leukotrienes may have a role in these diseases.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗
PubMed1986

Prostaglandin levels in human renal venous blood during renal arteriography.

In view of the possible role of prostaglandins (PG) and thromboxane (TX) in the disturbances of renal function and blood flow after the injection of diatrizoate into the renal artery, we have determined the levels of PGE2, 6-keto-PGF1 alpha (a stable metabolite of prostacyclin) and TXB2 in the renal venous blood before, during and after renal arteriography in 12 patients. Radioimmunologically assayed PGE2 was the most abundant prostaglandin in renal venous blood. Lower basal levels of PGs were associated with renal adenocarcinomas or other tumours than non-tumour kidneys. The concentrations of 6-keto-PGF1 alpha and PGF2 alpha rapidly increased after diatrizoate injection and returned to the basal levels within 5 minutes. Slower elevation was noticed in the PGF2 level of 5 tumour kidneys. Renal plasma concentration of TXB2 remained unchanged throughout the study. The rapid elevation of renal venous prostacyclin and PGF2 alpha concentration after the contrast injection may reflect the enhanced intrarenal prostaglandin synthesis or may be secondary to hemodynamic changes in the kidney caused by hypertonic diatrizoate.

6-Ketoprostaglandin F1 alpha↗
PubMed1985

Sodium salicylate does not prevent the inhibitory effect of indomethacin on thromboxane formation in human blood ex vivo.

Thromboxane formation during spontaneous blood clotting as well as plasma levels of TXB2 and 6-keto-PGF1 alpha, the stable metabolites of TXA2 and prostacyclin, were measured by radioimmunoassay two hours after oral administration of indomethacin (25 mg), sodium salicylate (250 mg) and their combination to human volunteers. Indomethacin effectively suppressed the tremendous formation of TXB2 during blood clotting whereas sodium salicylate had only a slight inhibitory effect on TXB2 synthesis. The combination of indomethacin and sodium salicylate inhibited the formation of thromboxane even slightly more effectively than indomethacin alone. Plasma TXB2 level was decreased after the combination treatment but not after administration of either of the drugs alone. Plasma 6-keto-PGF1 alpha level was not changed by any of the treatments. The present study suggests that simultaneous oral administration of sodium salicylate together with indomethacin at a combination ratio of 10 to 1 does not significantly interfere with the inhibitory effects of indomethacin on thromboxane synthesis in human blood ex vivo.

6-Ketoprostaglandin F1 alpha↗
PubMed1985

Verapamil decreases the formation of thromboxane from exogenous 14C-arachidonic acid in human platelets in vitro.

The effects of verapamil on the metabolism of exogenous 14C-arachidonic acid were studied in human platelets in vitro. 1 mM verapamil decreased the formation of TXB2 and HHT and increased that of PGE2, PGD2 and PGF2 alpha. The radioactivity at the area of 12-HPETE on the thin layer chromatography plate was also increased by 1 mM verapamil. In addition, 10 microM and 1 mM verapamil caused a slight decreasing trend in the amount of free unmetabolized arachidonic acid. The results suggest that high concentrations of verapamil may decrease the formation of the aggregatory thromboxane and increase that of anti-aggregatory compounds, i.e. PGD2 and 12-HPETE in human platelets in vitro. However, as lower concentrations of verapamil (10 and 100 microM) had no significant effect on the metabolism of exogenous arachidonic acid, the anti-platelet effects of the drug at therapeutic concentrations are more likely to be mediated via other mechanisms, possibly via the inhibition of arachidonate release from the platelet membrane phospholipids.

Arachidonic Acid↗
PubMed1985

The fatty acid composition of 12 North-European fish species.

Cardiovascular diseases among Greenland Eskimos are rare because their diet is rich in fatty fish and marine mammals. The beneficial effect of the fish diet appears to be mediated, at least in part, by the high amount of eicosapentaenoic acid in fish. We investigated the total lipid amount and fatty acid composition of 12 commonly eaten North-European fish species. Most of the detected fatty acids were unsaturated, and the content of eicosapentaenoic acid varied usually between 6 and 16%. The amount of total lipid varied between 3.5 and 216 mg/g wet tissue. The total amount of lipid in different fish species seems to be more important than the respective fatty acid composition when considering which fish should be especially beneficial in the diet. Herring, salmon, Baltic herring, turbot and trout seem to contain most abundantly eicosapentaenoic acid.

Animals↗
PubMed1985

Carbon monoxide is not responsible for the cigarette smoke-induced changes in the pulmonary metabolism of arachidonic acid and prostaglandin E2.

Cigarette smoke is known to interfere with the pulmonary metabolism of arachidonic acid and prostaglandin E2 (PGE2). We investigated the possible role of carbon monoxide in these cigarette smoke-induced alterations. 14C-Arachidonic acid (50 nmol) was infused into the pulmonary circulation of isolated perfused hamster lungs, and the radioactive metabolites in the perfusion effluent, as well as the distribution of incorporated radioactive arachidonic acid within the lung lipids, were analysed. Carbon monoxide, added into the ventilatory air, had no effect on the oxidative metabolism of arachidonic acid or on the distribution of radioactive arachidonic acid within the lung. In addition, carbon monoxide had no effect on the metabolism of PGE2 following infusion of 100 nmol of 14C-PGE2 into the rat pulmonary circulation. The present study suggests that carbon monoxide is not responsible for the cigarette smoke-induced changes in the pulmonary metabolism of arachidonic acid and PGE2.

Animals↗
PubMed1985

The effect of selenium and vitamin E deficiencies on the fate of arachidonic acid in rat isolated lungs.

The fate of exogenous 14C-arachidonic acid (14C-AA) was investigated in the isolated lungs of rats fed selenium and vitamin E deficient diet or diets supplemented with selenium and/or vitamin E. When 80 nmol of 14C-AA was infused into the pulmonary circulation most of the infused 14C-AA was found in different phospholipid and neutral lipid fractions of the perfused lungs. Only less than ten percent of the infused radioactivity was recovered in the perfusion effluent. The amount of arachidonate metabolites in the perfusion effluent was negligible, and most of the radioactivity in the perfusion effluent consisted of unmetabolized arachidonate. Selenium deficiency had no significant effect on the distribution of 14C-AA in different lung lipid fractions. However, in the lungs of vitamin E deficient rats the amount of radioactivity was slightly increased in the neutral lipid fraction, which was due to the increased amount of 14C-AA in the diacylglycerols. The amount of radioactivity was increased especially in the 1,3-diacylglycerols. The amount of radioactivity was increased especially in the 1,3-diacylglycerols. The amount of 14C-AA in the triacylglycerols and in different phospholipids was not significantly changed. The present study might indicate that selenium deficiency has no significant effect on the fate of exogenous arachidonic acid in isolated rat lungs, and that vitamin E deficiency would slightly increase the amount of arachidonic acid in the diacylglycerols.

Animals↗
PubMed1984

Prostanoids and hemodynamics in man before and during cardiopulmonary bypass.

The plasma concentration of 6-keto-PGF1 alpha, the stable degradation product of prostacyclin, was similar in the radial and pulmonary arteries and in the coronary sinus before and after the induction of the anesthesia in patients undergoing coronary artery bypass surgery. After the beginning of the mechanical ventilation and anesthesia the pulmonary vascular resistance decreased although no changes were detected in the plasma levels of 6-keto-PGF1 alpha or TXB2. During the prebypass period after the sternotomy and cannulation of the large vessels the plasma level of 6-keto-PGF1 alpha was increased similarly in the radial and pulmonary arteries and even more in the coronary sinus. During the cardiopulmonary bypass the concentration of 6-keto-PGF1 alpha remained at the increased level as compared to the values before the anesthesia. This indicates that pulmonary circulation is perhaps not the main source of prostacyclin in man. The plasma level of TXB2 was increased during the prebypass period significantly only in the coronary sinus, but during the bypass also in the radial artery. The concentration ratio of 6-keto-PGF1 alpha/TXB2 was increased significantly during the prebypass period in the radial and pulmonary arteries. At the same time the pulmonary vascular resistance was, however, returned to the preanesthesia level and was thus not decreased. The vascular resistance in the systemic circulation was increased during the prebypass period. The plasma level of 6-keto-PGF1 alpha or TXB2 in the radial and pulmonary arteries did not correlate significantly with the total vascular resistance in the systemic and pulmonary circulation, respectively. The vascular resistance in the coronary circulation did not correlate significantly with TXB2 level in the radial artery or coronary sinus. There was, however, a slight positive correlation between the blood flow and the concentration of TXB2 in the coronary sinus (r = 0.76, P less than 0.01). Coronary sinus flow did, however, not correlate with the plasma level of 6-keto-PGF1 alpha in the radial artery or coronary sinus. These results indicate that the detected plasma concentrations of prostacyclin and thromboxane A2 have no significant effects on the total vascular resistance in vivo.

6-Ketoprostaglandin F1 alpha↗