Search PubMed⌕ Search

Biomedical subjects

L Viinikka

Publications and source records attributed to L Viinikka.

At least 145 records · Page 8Linked to original sources
PubMed1984

Maternal thromboxane, prostacyclin, and umbilical blood flow in humans.

The stable hydration products of the vasoconstrictory and proaggregatory thromboxane A2 and vasodilatory and antiaggregatory prostacyclin, ie, thromboxane B2 and 6-keto-prostaglandin F1a, respectively, were measured with radioimmunoassays from 67 women with normal pregnancy, preeclampsia, or other pregnancy complications with the determination of the blood flow in the umbilical vein with the ultrasound method. In addition, the maternal platelets' capacity to release thromboxane B2 was studied. No relation was seen between these prostanoids and the umbilical blood flow and/or pregnancy complications. Moreover, the concentrations of the prostanoids were similar in women with high (161.1 +/- 6.8 mL/minutes/kg of fetal weight, mean +/- SE, N = 33) and low (50.5 +/- 2.1 mL/minutes/kg, N = 34) umbilical flow. If thromboxane A2 and prostacyclin regulate the umbilical circulation in the human, they exert this effect locally in the fetoplacental unit, and the changes are not reflected by the levels of their metabolites in the maternal peripheral circulation.

6-Ketoprostaglandin F1 alpha↗
PubMed1983

Relation between umbilical prostacyclin production and blood-flow in the fetus.

Umbilical blood-flow (UBF) was measured by ultrasonography in 28 pregnant women. A superfusion preparation was used to investigate the production of 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha), a breakdown product of prostacyclin (PGI2) and thromboxane B2 (TxB2), a breakdown product of TxA2, by specimens from the umbilical arteries of the infants born to these 28 mothers and those born to 36 other women in whom UBF had not been measured. UBF was significantly related to 6-keto-PGF1 alpha production. 6-keto-PGF1 alpha production was lower in infants of the 8 pre-eclamptic mothers (14.5 ng min-1 g-1) than in those of 45 healthy mothers (26.9 ng min-1 g-1). Generation of TxA2 by the umbilical artery was 15-25 times less than that of 6-keto-PGF1 alpha, and TxA2 concentrations were unrelated to UBF or the type of pregnancy. These data provide the first evidence for a direct association between blood-flow and PGI2 generation in human vasculature.

6-Ketoprostaglandin F1 alpha↗
PubMed1983

Maternal prostacyclin, thromboxane, and placental blood flow.

The vasoactive prostanoids--prostacyclin (PGI2) and thromboxane A2 (TxA2)--and their metabolites--6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) and thromboxane B2 (TxB2), respectively--have been implicated as regulators of uteroplacental blood flow in animals. To study their roles in placental blood flow in human beings, plasma or serum samples were collected for the measurement of 6-keto-PGF1 alpha and TxB2 from 42 women during late pregnancy on the same occasion, when placental intervillous blood flow (IVBF) was determined with 133Xe isotope method. The concentrations of 6-keto-PGF1 alpha in plasma or those of TxB2 in plasma or serum were not related to the IVBF. The intravenous infusion of ritodrine for 1 hour up to the dose of 200 micrograms/min increased (p less than 0.05) the plasma 6-keto-PGF1 alpha concentrations, but caused no changes in the TxB2 levels or IVBF in seven women with premature uterine contractions. We conclude that if PGI2 and TxA2 participate in the control of placental blood flow, their changes are located in the fetoplacental unit and, thus, are not reflected by the levels of their metabolites in maternal circulation, and ritodrine may stimulate PGI2 synthesis in human beings.

6-Ketoprostaglandin F1 alpha↗
PubMed1983

Differential inhibition of fetal vascular prostacyclin and platelet thromboxane synthesis by nonsteroidal anti-inflammatory drugs in humans.

To study the synthesis of proaggregatory, vasoconstricting thromboxane A2 (TxA2) by human fetal platelets we evaluated the formation of its stable metabolite thromboxane B2 (TxB2) during thrombin-induced spontaneous clotting of blood from the umbilical vein of 13 healthy infants. We further compared the effects of acetylsalicylic acid, indomethacin, naproxen sodium and diclofenac sodium on platelet TxA2 production in response to thrombin-induced aggregation during spontaneous clotting, and on prostacyclin (PGI2) production by umbilical arteries in a superfusion system by measuring the 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) concentration in the superfusate. For every drug four concentrations covering the clinically significant range were studied. The basal production of TxB2 by fetal platelets (181.5 +/- 22.5 ng/ml, mean +/- SEM) was comparable with that of adults (216.1 +/- 11.5 ng/ml). The concentrations of the drugs needed for 50% inhibition of TxB2 generation were 19.0 mumol/l for acetyl-salicylic acid, 0.09 mumol/l for indomethacin, 0.06 mumol/l for diclofenac sodium and 4.2 mumol/l for naproxen sodium. The basal production of 6-keto-PGF1 alpha by umbilical arteries was 24.5 +/- 3.2 ng/min/g. The concentrations of the drugs needed for 50% inhibition of 6-keto-PGF1 alpha production were 360.0 mumol/l for acetylsalicylic acid, 4.0 mumol/l for indomethacin, 2.3 mumol/l for diclofenac sodium and 15.0 mumol/l for naproxen sodium. Thus fetal platelet cyclo-oxygenase was 4-44 times more sensitive to these prostaglandin synthesis inhibitors than umbilical artery cyclo-oxygenase.

Anti-Inflammatory Agents↗
PubMed1983

Prostacyclin and thromboxane in ovarian cancer: effect of cytostatics and prostaglandin synthesis inhibitors.

The production of the antiaggregatory prostacyclin (PG1(2) ) and proaggregatory thromboxane A2 (TxA2) were studied in 19 patients with residual ovarian cancer. The plasma 6-keto-PGF1 alpha (a metabolite of PG1(2) ) in cancer patients (146.7 +/- 14.7 pg/ml, mean +/- SE) was higher (P less than 0.02) than that in the controls (85.3 +/- 9.2 pg/ml, n = 17). Also the releases of TxB2 (a metabolite of TxA2) during spontaneous clotting of the blood samples were greater (P less than 0.05) in the patients (253.4 +/- 30.1 ng/ml) than controls (183.2 +/- 19.8 ng/ml). The combined administration of doxorubicin, cyclophosphamide and cis-platinum temporarily decreased the plasma 6-keto-PGF1 alpha levels but caused no changes in TxB2 generation. Prostaglandin synthesis inhibitors (acetylsalicyclic acid or indomethacin) during cytostatic infusion did not prevent the occurrence of the acute side effects of cytostatics, but they inhibited the TxB2 generation. Thus our data suggest that residual ovarian cancer is accompanied by increased production of PG1(2) and TxA2, and that prostaglandins have no role in the acute side effects of cancer chemotherapy.

6-Ketoprostaglandin F1 alpha↗
PubMed1983

Prostacyclin and thromboxane in diabetic children.

Plasma concentrations of a stable metabolite of prostacyclin, 6-keto-prostaglandin Fla (6-keto-PGF1a), and the ability of platelets to generate thromboxane B2 (TxB2), a metabolite of thromboxane A2, during spontaneous clotting of the blood were measured in 40 diabetic children and 16 healthy controls. The diabetics' platelets generated TxB2 to a lesser extent than those of controls, whereas no difference was seen in plasma 6-keto-PGF1a concentration. The balance and duration of diabetes were not related to TxB2 or 6-Keto-PGF1a. The results do not support the theory that an absolute or relative prostacyclin deficiency could trigger the onset of diabetic vascular complications.

6-Ketoprostaglandin F1 alpha↗
PubMed1983

Effect of prolonged treatment with acetylsalicylic acid and dipyridamole on platelet thromboxane A2 production in atherosclerotic subjects.

We evaluated the effect of four weeks treatment with 90 mg and 1500 mg of acetylsalicylic acid (ASA), 990 mg of ASA together with 225 mg of dipyridamole and 225 mg of dipyridamole daily on the production of thromboxane A2 (TxA2) by platelets of atherosclerotic subjects. All doses of ASA studied inhibited 99% or more of TxA2 production from the third day to the end of the treatment, whereas dipyridamole did not have any effect. After the treatment, TxA2 production recovered in two weeks. Our results argue against the clinical relevance of the recent suggestions that salicylate accumulating during prolonged treatment with ASA could reduce the effect of the parent drug on the synthesis of TxA2 by platelets. Our data also dispute the inhibition of TxA2 synthesis as an antithrombotic mechanism of dipyridamole.

Aged↗
PubMed1983

Comparison between antifibrinolytic and antiprostaglandin treatment in the reduction of increased menstrual blood loss in women with intrauterine contraceptive devices.

The effects of a fibrinolysis inhibitor (tranexamic acid, TA) and prostaglandin synthesis inhibitor (diclofenac sodium, DS) were compared in the reduction of excessive menstrual blood loss in 19 women with an intrauterine contraceptive device (IUCD). These women (mean blood loss before treatment to 135.1 +/- 18.9 SE ml, range 70-294 ml) were treated in random order with TA (1.5 g three times daily for 5 days starting on the first day of menstruation for two periods), and with DS (50 mg three times on the first day followed by 25 mg three times daily for 4 days, for two periods), or with placebo (one period) in a double-blind trial. The placebo treatment did not change menstrual blood loss (128.3 +/- 15.6 ml). The TA treatment decreased blood loss to 59.4 +/- 7.7 ml (P less than 0.001) and the DS treatment to 102.1 +/- 13.6 ml (P less than 0.01). Neither treatment abolished pelvic discomfort during menstruation or shortened its duration. Various side-effects were noted by 12 women during 19 TA treatments and by five women during six DS treatments. Thus, while TA is generally far more effective, DS gave pronounced decreases in menstrual bleeding in some women and had less frequent side-effects.

Adult↗
PubMed1983

Effect of vacuum curettage on the concentrations of plasma 6-keto-prostaglandin F1 alpha and serum thromboxane B2.

Serial plasma samples collected before and after vacuum curettage followed by methylergometrine injection in 10 women were assayed for 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha). The mean 6-keto-PGF1 alpha concentration was 97.2 (SE 8.8) pg/ml before cervical dilatation. The concentration rose to 128.2 (SE 13.5) pg/ml (P less than 0.10) immediately and to 133.3 (SE 17.8) pg/ml (P less than 0.05) 1 h after curettage and returned to the initial value within 5 h. Neither methylergometrine nor anaesthesia, nor non-gynaecological surgery, caused changes in the level of plasma 6-keto-PGF1 alpha. The capacity of the platelets to produce thromboxane A2 during spontaneous clotting of blood did not change during vacuum curettage, anaesthesia and non-gynaecological surgery, nor after methylergometrine. The evidence suggests that the pregnant myometrium and/or intrauterine tissues capable of generating prostacyclin (PGI2) in vitro may release PGI2 also in vivo.

6-Ketoprostaglandin F1 alpha↗
PubMed1983

Prostaglandins and endometriosis.

To study the production of prostacyclin (PGI2) and thromboxane A2 (TxA2) in endometriosis in vitro, samples of endometriotic tissue taken during operation from 6 women were superfused for 4.5 hours in 95% O2/5% CO2 at 37 degrees C, and the stable metabolites of PGI2 (=6-keto-PGF1 alpha), and TxA2 (=TxB2) were measured by radioimmunoassays from the superfusates. All samples studied produced 6-keto-PGF1 alpha in the range from 0.2 to 10.5 nanograms/gram of dry tissue/minute with a mean of 3.6 ng/g/min during the whole experiment. TxB2 was also released by each sample at rates between 0.2 and 11.9 ng/g/min (mean 2.6 ng/g/min). The production of these prostanoids tended to be greater in the serosal (n = 2) than in the ovarian (n = 4) endometriosis. The addition of indomethacin of 10(-5) - 10(-3) moles/l to the superfusion medium inhibited concentration-dependently the synthesis of these prostanoids. Apart from these in vitro data implying the production of PGs in endometriosis, 18 patients with pelvic endometriosis sustained no relief for their endometriotic symptoms from the treatments with three anti-prostaglandins (acetylsalicylic acid, indomethacin, tolfenamic acid) in a double-blind, placebo-controlled trial.

6-Ketoprostaglandin F1 alpha↗
PubMed1983

Prostaglandins in contact urticaria induced by benzoic acid.

To study the role played by prostaglandins (PGs) in contact urticaria, concentrations of 13,14-dihydro-15-keto-PGF2 alpha, 6-keto-PGF1 alpha, and thromboxane B2, the stable metabolites of PGF2 alpha, prostacycline and thromboxane A2 were measured by radio-immunoassay of the fluid taken from suction blisters in 11 patients. The blisters were raised on contact urticarial reactions induced by benzoic acid. The effect of peroral indomethacin on contact urticaria from benzoic acid was studied in a further 14 dermatological patients. The levels of these prostanoids in the blister fluid of urticarial skin did not differ from those derived from control blisters raised on apparently normal skin. Premedication with indomethacin, 50 mg t.i.d., completely prevented contact urticarial reactions to benzoic acid in all patients.

Adolescent↗
PubMed1982

Sulpiride improves inadequate lactation.

Twenty-eight newly delivered mothers with inadequate lactation volunteered for a placebo-controlled double-blind trial of sulpiride 50 mg thrice daily for four weeks. Treatment was allocated at random, and serum prolactin concentrations and breast-milk yields were measured before and serially during the trial. Of the 26 women who completed the trial, 14 had taken sulpiride and 12 the placebo. In the sulpiride-treatment group the mean maternal serum prolactin concentration rose from 49.0 +/- SE 3.6 micrograms/l to a maximum of 402.1 +/0 43.2 micrograms/l at two weeks; in the placebo-treated group, however, the concentration fell during the trial (from 84.7 +/- 24.0 micrograms/l to 47.8 +/- 8.6 micrograms/l). Mean breast-milk yields also increased in the sulpiride-treatment group (by an average of 212-265 ml) and fell in the women given placebo. Of the 14 infants in the sulpiride-treatment group, four did not need supplementary feeds during the trial; in the control group, however, all infants continued to require such feeds. Infants in the sulpiride-treatment group gained significantly more weight than did the controls (p less than 0.05). Three women taking sulpiride complained of mild side effects, but none occurred in the infants. These findings suggest that sulpiride is an effective treatment for inadequate lactation in the puerperium.

Clinical Trials as Topic↗
PubMed1982

Effect of acute ethanol intake on thromboxane and prostacyclin in human.

To investigate the effects of acute ethanol administration on the production of proaggregatory thromboxane A2 (TxA2) and antiaggregatory prostacyclin (PGI2), ethanol (1.5 g/kilogram body weight) was given to eight healthy nonsmoking men, and the stable metabolites thromboxane B2 (TxB2) and 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha), respectively, measured by radioimmunoassay from serial blood samples before drinking and during the ensuing 18 hours. Each subject was studied as his own control on another occasion when only an equivalent volume of water was given. Serum TxB2 level decreased (p less than 0.01) from 206 +/- 31 ng/ml (mean +/- S.E.) to 167 +/- 24 and 161 +/- 23 ng/ml (two and four hours after beginning of the drinking, respectively) concomitantly with the attainment of maximal blood ethanol concentrations (about 120 mg/100 ml), whereas no changes occurred in plasma 6-keto-PGF1 alpha concentrations. Our results may provide an explanation for known effects of ethanol on platelet aggregation. They also raise speculation whether TxA2-inhibition and the antiatherogenic effect of alcohol intake are somehow related.

Adult↗
PubMed1982

The effect of oral contraceptives on antiaggregatory prostacyclin and proaggregatory thromboxane A2 in humans.

The effect of different types of oral contraceptives on the productions of antiaggregatory prostacyclin (PGI2) and proaggregatory thromboxane A2 (TxA2) was studied by measuring the stable metabolites of these prostanoids, that is, 6-ketoprostaglandin F1 alpha (6-keto-PGF1 alpha) and thromboxane B2 (TxB2), respectively, from plasma. In addition, the capacity of the platelets to produce TxB2 during spontaneous clotting was studied by measuring the TxB2 levels from the serum incubated at +37 degrees C for 60 minutes. The material consisted of 48 women who had used estrogen-containing oral contraceptives for 2.0 +/- 1.9 years (mean +/- SD), 24 women using progestogen-only pills for 3.7 +/- 2.0 years, and 42 women of the same age using no oral contraceptives or intrauterine contraceptive device. The plasma concentrations of 6-keto-PGF1 alpha in women with combined oral contraceptives (65.5 +/- 16.1 pg/ml, mean +/- SD) was lower (p less than 0.01) than that in the control subjects (77.4 +/- 26.4 pg/ml), whereas the use of combined oral contraceptives was associated with no changes in TxB2 levels in plasma or serum, in women with progestogen-only oral contraceptives, the plasma levels of 6-keto-PGF1 alpha and TxB2 were normal, but the capacity of the platelets to release TxB2 during spontaneous clotting was decreased (113.6 +/- 77.6 ng/ml versus 179.9 +/- 81.9 ng/ml, p less than 0.05). In a prospective trial on 11 women, who started using 30 microgram of ethinyl estradiol and 150 microgram of levonorgestrel, no changes in PGI2 or TxA2 were seen during the first 3 months of usage. The decrease in antiaggregatory PGI2 during the prolonged use of estrogen-containing oral contraceptives may be associated with the increased risk of thromboembolism.

6-Ketoprostaglandin F1 alpha↗
PubMed1982

Effects of two oral contraceptive combinations, 0.125 mg desogestrel + 0.050 mg ethinylestradiol and 0.125 mg levonorgestrel + 0.050 mg ethinylestradiol on the adrenal function of healthy female volunteers.

The effects of the oral contraceptive combinations of 0.125 mg desogestrel + 0.050 mg ethinylestradiol (EE), and of 0.125 mg levonorgestrel + 0.050 mg EE on serum cortisol and the urinary excretion of 17-oxogenic steroids and free cortisol were studied in 16 healthy females. Adrenal responsiveness was studied by the metyrapone test. Both contraceptive combinations increased (P less than 0.001) serum cortisol concentrations but the rhythmic fluctuation at different times of the day remained unchanged. The urinary excretion of 17-oxogenic steroids was lower (P less than 0.01) during treatment than before or after treatment with both contraceptive combinations. The metyrapone test showed normal adrenal responsiveness during the treatment cycles. The urinary excretion of free cortisol was unchanged when desogestrel + EE was used, but increased (P less than 0.01) during treatment with levonorgestrel + EE. However, even then, the urinary free cortisol was within the normal range of the population. All the test results of hormone determinations normalized soon after finishing the contraceptive treatments. It is suggested that the abnormalities seen were due to an increased serum binding capacity of cortisol induced by EE and not a sign of pathological changes in adrenal function. No major differences in the biological effects of the two combinations tested were seen.

17-Hydroxycorticosteroids↗
PubMed1982

The effect of age on circulating 6-keto-prostaglandin F1 alpha in humans.

The effect of age on the production of the antiaggregatory prostacyclin (PGI2) was studied by measuring 6-keto-PGF1 alpha in the plasma of 140 subjects (50 males and 90 females) between 10-90 years of age. The 6-keto-PGF1 alpha concentrations (mean +/- SD) in subjects between 10-20 years of age were higher (126 +/- 63 pg/ml, n = 24) than the levels in subjects between 21-30 years of age (88 +/- 30 pg/ml, n = 16), or in subjects between 51-70 years of age (88 +/- 30 pg/ml, n = 17), whereas in subjects between 71-90 years of age, the 6-keto-PGF1 alpha levels 100 +/- 59 pg/ml, n = 36) did not differ from those in subjects under 20 years of age. The 6-keto-PGF1 alpha levels in women over 70 years (118 +/- 66 pg/ml, n = 20) were higher (p = less than 0.05) than those in men of the same age (78 +/- 42 pg/ml, n = 16), but no other sex-related connections in 6-keto-PGF1 alpha concentrations were seen. Our data suggest that the PGI2 generation in vivo, as measured by 6-keto-PGF1 alpha levels in peripheral plasma, is higher in adolescence and elderly females than in the healthy adults.

6-Ketoprostaglandin F1 alpha↗
PubMed1982

Different results of plasma 6-keto-prostaglandin F1 alpha measurements utilizing two antisera with apparently similar specificity.

While developing a radioimmunoassay for the measurement of 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) in human plasma, we obtained two antibodies which had apparently similar cross-reactivities with 22 other prostaglandins and related compounds. However, in radioimmunoassay, use of one of the antibodies gave results which were about double the results obtained with the other. The results obtained by both antibodies correlated significantly with each other according to the equation y = 0.43x - 13.0 pg/ml, R = 0.89, n = 58 (p less than 0.001). The increments of plasma 6-keto-PGF1 alpha after an intravenous infusion of prostacyclin (PGI2) also correlated with the dose of PGI2 (R = 0.93 and 0.96, n = 24, p less than 0.001) in both cases, and the increments obtained by the use of both antibodies correlated with each other (R = 0.94, n = 24, p less than 0.001). The increments were, however, of different magnitude. These differences can be best explained by assuming different immunoreactivity of the two antibodies with metabolites of PGI2 other than 6-keto-PGF1 alpha, or with the two known stereochemical configuration of 6-keto-PGF1 alpha.

6-Ketoprostaglandin F1 alpha↗