Search PubMed⌕ Search

Biomedical subjects

L Viinikka

Publications and source records attributed to L Viinikka.

At least 181 records · Page 10Linked to original sources
PubMed1981

Prostacyclin production increases during human parturition.

The role of prostacyclin (PGI2) in human parturition was studied by measuring the concentrations of its main metabolite, 6-keto-prostaglandin F1 alpha, before, during and after term labour in the plasma of 9 women and after delivery in umbilical artery and vein plasma. The mean level of 6-keto-PGF1 alpha rose significantly over the course of labour. The mean level was 266 pg/ml before labour, 341 pg/ml in the presence of regular contraction, 387 pg/ml at a cervical dilatation of 5 cm, 386 pg/ml at delivery, and 397 pg/ml at the expulsion of the placenta. The 6-keto-PGF1 alpha concentration dropped to below pre-labour levels of 233 pg/ml within 2 hours of delivery, and this level was maintained for the first four postpartum days. The mean levels of 6-keto-PGF1 alpha in the umbilical artery and vein plasma, 1667 and 1193 pg/ml respectively, were significantly higher than the maternal plasma levels. PGI2 is characterized by its antiaggregatory and vasodilating abilities, so that the rise in PGI2 during labour may play a role in the prevention of intrapartum thromboembolic complications in the maternal and the uteroplacental circulation.

6-Ketoprostaglandin F1 alpha↗
PubMed1981

Maternal plasma prostacyclin concentration in pre-eclampsia and other pregnancy complications.

To study the involvement of antiaggregatory and vasodilatory prostacyclin (PGI2) in various pregnancy complications, we measured the concentrations of 6-ketoprostaglandin F1 alpha, a stable hydration product of PGI2, using a specific radioimmunoassay, in plasma samples from 123 women between 22 and 41 weeks of complicated or normal pregnancy. The levels of 6-keto-PGF1 alpha (mean +/- SE) in pre-eclampsia (267.0 +/- 26.6 pg/ml, n = 22), diabetic pregnancy (266.6 +/- 19.2 pg/ml, n =21), twin pregnancy (310.7 +/- 28.2 pg/ml, n = 10), threatened premature labour (285.9 +/- 23.2 pg/ml, n = 26), placenta praevia or placental abruption (248.9 +/- 24.5 pg/ml, n = 6), hepatosis gravidarum (249.3 +/- 15.0 pg/ml, n = 3) or in pregnancies complicated by intrauterine fetal growth retardation (296.9 +/- 34.2 pg/ml, n = 14) or fetal death (267.5 +/- 20.9 pg/ml, n = 6) did not differ from each other or from the 6-keto-PGF1 alpha levels in normal pregnancy (266.4 +/- 15.0 pg/ml, n = 22). Furthermore, the 6-keto-PGF1 alpha levels bore no relation to the gestational age, maternal drug use (insulin, glucocorticoids, antihypertensive drugs) or to the sex, birth weight or condition of the newborn infant, or to the placenta weight.

6-Ketoprostaglandin F1 alpha↗
PubMed1981

Effect of various doses of acetylsalicylic acid in combination with dipyridamole on the balance between prostacyclin and thromboxane in human serum.

1 Thirty-six healthy human subjects were randomly divided into six groups which were treated with a single dose of 75 mg (1.3 mg/kg) of dipyridamole alone, or 75 mg of dipyridamole in combination with 30 mg (0.5 mg/kg), 50 mg (0.8 mg/kg), 160 mg (2.6 mg/kg) and 330 mg (5.7 mg/kg) of acetylsalicylic acid (ASA), or with placebo. 2 The concentrations of prostacyclin (PGI2) and thromboxane A2 (TxA2) metabolites, 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) and TxB2 respectively, were measured in serum with specific radioimmunoassays before and 1 and 3 h afer the ingestion of the test dose. 3 The basal concentrations of 6-keto-PGF1 alpha and TxB2 correlated significantly (r = 0.588, P less than 0.001). 4 Dipyridamole alone did not change PGI2 or TxA2 production. 5 Dipyridamole-ASA combinations with ASA doses between 0.5 and 0.8 mg/kg inhibited TxB2 production by 48 to 74% and with the ASA doses between 2.6 and 5.7 mg/kg by about 90%. None of these combinations changed PGI2 production. 6 The ratio of 6-keto-PGF1 alpha to TxB2 increased 3.5 to 6 times with ASA doses of 0.5 to 0.8 mg/kg and 21 to 29 times with doses between 2.6 to 5.7 mg/kg. 7 These results suggest that the anti-thrombotic effect of dipyridamole in vivo is not mediated through direct changes in PGI2 and/or TxA2 production.

Adult↗
PubMed1981

Cyproterone acetate in the treatment of hirsutism.

Cyproterone acetate (100 mg daily on the 5th-14th days of the normal cycle) together with ethinyl estradiol (0.05 mg daily on the 5th-25th days) was used for the treatment of hirsutism in 23 women for six months. This treatment caused a significant decrease in the severity of the hirsutism after only three months, the effect being maximal after six months. Sixty per cent of our patients reported being subjectively satisfied with the results. A relapse occurred, however, within three months of the end of the treatment in half the patients. The serum testosterone was significantly decreased after three months of treatment, but the changes in serum testosterone did not follow the changes in the clinical picture of hirsutism, suggesting that one facet in the favorable action of cyproterone acetate is an inhibition of the action of androgen on target cells. Various side effects, such as nausea, headache, loss of libido and depression, were reported very frequently, which undoubtedly limits the large scale use of this treatment, at least with the doses used in this study.

Adult↗
PubMed1981

The lack of significant change in plasma progesterone and estradiol-17 beta levels before the onset of human labor.

Maternal plasma levels of progesterone and estradiol-17 beta were measured weekly by radioimmunoassay in 15 healthy women during the last trimester of normal pregnancy. There was a large individual variation for both hormones. The mean concentrations rose slightly with advancing gestational age but the ratio of progesterone to estradiol did not change. It is apparent that the onset of spontaneous labor cannot be predicted by measuring the levels of progesterone and estradiol-17 beta in maternal peripheral plasma.

Adolescent↗
PubMed1981

Increased prostacyclin and thromboxane production in man during cardiopulmonary bypass.

To study the effect of the cardiopulmonary bypass (CPB) on the productions of antiaggregatory prostacyclin (PGI2) and proaggregatory thromboxane A2 (TxA2), we collected serial plasma samples from seven patients before, during, and after CPB and assayed them for 6-keto-PGF 1 alpha and thromboxane B2, the main metabolites of PGI2 and TxA2, respectively. The PGI2 production rose significantly (p less than 0.05) following cannulation of the large vessels and remained elevated during the CPB. After discontinuation of CPB, the PGI2 decreased progressively. The TxB2 production also rose during CPB, but later than the increase in PGI2. There was a significant correlation between 6-keto-PGF 1 alpha and TxB2 levels (r = 0.429, p less than 0.001, n = 77). Thus the deficient PGI2 production, or an imbalance between PGI2 and TxA2, does not seem to be responsible for the platelet loss during CPB. By contrast, the human body appears to be protected from platelet aggregation by a surge in endogenous PGI2 during CPB.

6-Ketoprostaglandin F1 alpha↗
PubMed1981

Effect of cytostatics on prostaglandin F2 alpha prostacyclin, and thromboxane in patients with gynecologic malignancies.

Serial measurements of 6-keto-PGF1 alpha (a stable metabolite of prostacyclin), thromboxane B2 (TxB2, a stable metabolite of thromboxane A2), and 13,14-dihydro-15-keto-PGF2 alpha (M-PGF2 alpha, a stable metabolite of prostaglandin F2 alpha) were made from plasma of 9 women with metastatic ovarian or uterine malignancies before and after the combined administration of doxorubicin, cyclophosphamide, 5-fluorouracil, and cis-platinum. Elevated basal levels of TxB2 were detected in all patients, elevated levels of 6-keto-PGF1 alpha in 5 patients and elevated levels of M-PGF2 alpha in 3 patients. The use of chemotherapy was accompanied by a significant increase of 37% (P less than .01) in the M-PGF2 alpha level on the day after treatment and by significant decreases of 30 to 40% (P less than .05) in 6-keto-PGF1 alpha and TxB2 levels, which became apparent immediately after the treatment and persisted for 3 to 5 days. Thus, malignancies may be accompanied by increased production of prostacyclin and thromboxane A2, which can be lowered by cytostatics.

Aged↗
PubMed1981

Experimental hyperprolactinemia and hypoprolactinemia and human chorionic gonadotropin during early pregnancy.

The effect of experimental hyperprolactinemia and hypoprolactinemia on human chorionic gonadotropin (hCG) concentration was studied in 34 healthy volunteers between weeks 6 and 11 of normal pregnancy. Hyperprolactinemia was induced in 12 women with 150 mg of sulpiride daily for 2 weeks; treatment led to a mean plasma prolactin (PRL) rise from 14.6 to 84.1 microgram/liter after 1 week and to 83.0 microgram/liter after 2 weeks. Hypoprolactinemia was effected in 11 women wit 5.0 to 7.5 mg of bromocriptine, daily for 2 weeks; treatment decreased the mean plasma prolactin from 19.2 to 6.0 microgram/liter after 1 week and to 5.2 microgram/liter after 2 weeks. These PRL changes were significant (P less than .001) in comparison with the plasma PRL concentrations in the 11 control women. Hyperprolactinemia induced by the sulpiride treatment was accompanied by a significant decrease in hCG concentration, whereas no difference in hCG was seen between hypoprolactinemia and control groups. This may suggest a synergistic action of hCG and PRL, or a direct effect of sulpiride on hCG, but the final mechanism and biologic importance of the phenomenon remain to be investigated.

Adult↗
PubMed1981

The clinical and endocrine evaluation of a pubertal boy with incomplete male pseudohermaphroditism type 1.

Serum LH, FSH, prolactin, oestradiol, testosterone, 5 alpha-dihydrotestosterone, androstenedione, androsterone, progesterone, 17-hydroxyprogesterone and cortisol concentrations were measured in a pubertal boy suffering from gynaecomastia. At birth he had hypospadias, a scrotal anomaly, an abnormally small penis and unilateral cryptorchidism. At puberty, a small ejaculate volume with normal sperm concentration was recorded. Under basal conditions the serum concentrations of testosterone, oestradiol, 5 alpha-dihydrotestosterone, 17-hydroxyprogesterone and androsterone were clearly above normal, and they were not suppressed by dexamethasone as was the serum cortisol, which also showed normal diurnal variation. This suggested that the overproduction of sex steroids was of testicular origin. The serum LH was also elevated under basal conditions, while the serum FSH was in the reference range. The serum LH was not suppressed by ethinyl oestradiol administration, as the serum FSH was. The clinical observations and endocrine data are interpreted as indicating a partial failure in androgen action, responsible for the genital abnormalities observed and the deficiency in the hypothalamo-pituitary regulation of gonadotropin secretion, and are indicative of the findings described in connection with an unusual form of incomplete male pseudohermaphroditism type 1.

Adolescent↗
PubMed1980

Bromocriptine suppresses the thyrotrophin response to thyrotrophin releasing hormone during human pregnancy.

Thyrotrophin (TSH) responses to 200 microgram of intravenous thyrotrophin releasing hormone (TRH) were measured in fifteen healthy women in normal early pregnancy before and at the end of a bromocriptine treatment of 5.0-7.5 mg daily for 1-2 weeks. Bromocriptine did not change the basal levels of TSH, triiodothyronine (T3) and thyroxine (T4) during pregnancy. Before the start of bromocriptine, TRH caused a significant TSH elevation from 12.8 +/- 0.5 muu/ml (mean +/- SE) to 21.2 +/- 1.9 muu/ml after 20 min. During bromocriptine intake, TRH caused a TSH elevation from 11.9 +/- 0.4 muu/ml to only 15.5 +/- 1.1 muu/ml which is significantly less (P less than 0.001) than before bromocriptine. Similarly, the mean maximal TSH increment of 8.4 +/- 1.5 muu/ml before bromocriptine was greater (P less than 0.001) than that of 3.8 +/- 60 muu/ml during bromocriptine intake. When women were retested with TRH before and during bromocriptine after legal abortion, bromocriptine did not change the basal levels of TSH, T3 and T4 or the TSH response to TRH. Therefore, the TSH inhibition caused by bromocriptine is specifically related to the pregnancy itself, but the mechanism for this inhibition remains unknown.

Adolescent↗
PubMed1980

Does bromocriptine block thyrotropin-releasing hormone-induced prolactin release during pregnancy?

PRL responses to 200 microgram of iv TRH were measured in 16 healthy women with normal early pregnancy before and at the endo of bromocriptine treatment of 5.0--7.5 mg daily for 1--2 weeks. Before the start of bromocriptine, TRH caused a PRL elevation from 19.1 +/- 2.2 to 95.2 +/- 12.6 ng/ml (mean +/- SE) after 20 min, with a mean maximal PRL increment of 71.7 +/- 11.6 ng/ml. Bromocriptine suppressed basal plasma PRL level to 3.6 +/- 0.8 ng/ml (P less than 0.001). TRH then caused a PRL rise to 18.8 +/- 1.8 ng/ml at 20 min, with a mean maximal PRL increment of 15.7 +/- 1.8 ng/ml. The absolute PRL response was significantly smaller (P less than 0.001) during bromocriptine intake than before, whereas the mean percent increments in PRL levels after TRH administration were similar in the presence and absence of bromocriptine. Fifteen of these women were restudied with TRH stimulation 4--6 weeks after legal abortion, and the PRL responses to TRH were normal. When 7 of these women were once again treated with bromocriptine and retested with TRH, no absolute or relative PRL response to TRH emerged. These results release differs between the pregnant and nonpregnant states.

Abortion, Induced↗
PubMed1980

Sulpiride treatment during early human pregnancy: effect on the levels of prolactin, six steroids, and placental lactogen.

To study the role of PRL in the regulation of the production of 17 beta-estradiol, progesterone, testosterone, and human placental lactogen (hPL), 11 healthy women were given 150 mg sulpiride daily for 14 days, beginning between weeks 6--9 of normal gestation. Plasma PRL, estradiol, progesterone, testosterone, and hPL were measured before and 1 and 2 weeks after the start of sulpiride treatment, and the results were compared with those from 16 control women who were followed similarly but without sulpiride treatment. Sulpiride treatment induced significant (P less than 0.001) elevations of plasma PRL at 1 week [84.1 +/- 4.9 vs. 23.7 +/- 2.8 ng/ml (mean +/- SE)] and 2 weeks (83.0 +/- 4.1 vs. 31.9 +/- 4.1 ng/ml). No differences were observed in the concentrations of estradiol, progesterone, testosterone, or hPL. Two women treated with sulpiride reported mild uterine contractions, but no spontaneous abortion occurred in either group. It is evident that hyperprolactinemia or sulpiride treatment do not change the circulating concentrations of sex steroids and hPL between 6--11 of normal gestation.

Estradiol↗