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Biomedical subjects

L Viinikka

Publications and source records attributed to L Viinikka.

At least 127 records · Page 7Linked to original sources
PubMed1985

Epidermal growth factor in human urine from birth to puberty.

The highest concentrations of epidermal growth factor (EGF) are found in urine, but the physiological role of urinary EGF is unknown. We studied human urinary EGF excretion, by measuring its concentration with a specific homologous RIA, in 265 healthy children from birth until age 16 yr. The absolute concentrations varied widely between individuals. Mean values were approximately 10 ng/ml in 1- to 30-day-old infants; 2.5-fold higher values were found in infants aged 2 to 12 months. During the second year there was a further rise to about 70 ng/ml, and urinary EGF excretion was in the same range in older subjects. The EGF/creatinine concentration ratio was less variable. The mean ratio increased 6-fold from birth to the second year of life. Thereafter, the EGF/creatinine ratio decreased gradually to one-third of the peak level at puberty. No sex difference was found.

Adolescent↗
PubMed1985

Platelet function and thrombus in diabetes.

Patients with diabetes mellitus are several fold more prone to various forms of vascular diseases than are the non-diabetic subjects. Because platelets are in the key position in thrombus formation and possibly in atherogenesis, much interest has focused on the role of platelets in the development of diabetic vascular disease. Most studies on this topic have suggested increased adhesiveness and aggregability of the platelets from diabetic patients. The increased production of von Willebrand factor may account for the enhanced adhesion. The shift of the balance between proaggregatory thromboxane A2 and antiaggregatory prostacyclin to the dominance of thromboxane A2 could explain the increased aggregability of diabetic platelets, but the data available at the moment do not allow the conclusion that such a change really exist in human in vivo. One recent work has suggested that the increased glycosylation of connective tissue proteins in diabetes would increase their aggregating potency, but also this finding needs further confirmation.

Blood Platelets↗
PubMed1985

Biochemical and clinical effects of treating the premenstrual syndrome with prostaglandin synthesis precursors.

The clinical and biochemical effects of a prostaglandin synthesis precursor (Efamol) containing linoleic acid and its metabolite, gamma-linolenic acid, were studied in 30 women with severe, incapacitating premenstrual syndrome. Efamol treatment alleviated the premenstrual symptoms in general and depression especially better than did a placebo. The capacity of platelets to release thromboxane B2 during spontaneous clotting was decreased in patients undergoing Efamol treatment (141 +/- 59 ng/ml, mean +/- SD) as compared to those undergoing placebo treatment (186 +/- 44 ng/ml, p less than 0.01) and control subjects (176 +/- 40 ng/ml, n = 25, p less than 0.05). No changes were found in plasma 6-keto-prostaglandin F1alpha or in FSH, LH, prolactin, progesterone, estradiol and testosterone. The data suggest that prostaglandins might play a role in the pathophysiology of the premenstrual syndrome.

6-Ketoprostaglandin F1 alpha↗
PubMed1985

Effect of nicotine on fetal prostacyclin and thromboxane in humans.

To study the effect of nicotine on fetal prostacyclin and thromboxane A2, specimens from the umbilical arteries of infants born to healthy nonsmoking mothers were superfused in the absence or presence of nicotine (50 to 10,000 micrograms/mL), and the releases of 6-keto-prostaglandin F1alpha (a break-down product of prostacyclin) and thromboxane B2 (a metabolite of thromboxane A2) were measured. The baseline production of 6-keto-prostaglandin F1alpha (63.9 +/- 8.8 ng/minute per gram of dry weight tissue, mean +/- SE, N = 10) or that of thromboxane B2 (1.3 +/- 0.2 ng/minute per gram, N = 10) were unaffected by nicotine. To study the effect of nicotine on thromboxane A2 synthesis by the fetal platelets, thrombin-induced platelet aggregation and consequent thromboxane A2 synthesis were allowed to occur in the whole cord blood in the absence or presence of nicotine (10 to 500 micrograms/mL). Nicotine inhibited concentration dependently platelet thromboxane A2 synthesis from the baseline level (107.3 +/- 7.1 ng/mL) by 15 to 93%. This inhibition was also seen in thromboxane A2 synthesis starting from exogenous arachidonic acid, suggesting that nicotine inhibits either cyclooxygenase and/or thromboxane A2 synthetase in the fetal platelets. Thus, nicotine is hardly responsible for maternal smoking-induced changes in fetal prostacyclin formation.

6-Ketoprostaglandin F1 alpha↗
PubMed1984

One milligramme of acetylsalicylic acid daily inhibits platelet thromboxane A2 production.

To seek the lowest dose of acetylsalicylic acid (ASA) capable of inhibiting platelet thromboxane A2 (TxA)2 production, 18 healthy volunteers ingested 9 mg, 3 mg or 1 mg of ASA/day for twenty days and the release of TxB2 (a metabolite of TxA2) during the spontaneous clotting of blood was measured by radioimmunoassay. In addition, the production of prostacyclin (epoprostenol, PGI2) was investigated by measuring the urinary excretion of its break-down product, 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) by radioimmunoassay. Significant inhibition of platelet TxA2 production was seen from the 15th day of treatment onwards with 1 mg of ASA (maximally 15%), from the 4th day of treatment onwards with 3 mg of ASA (maximally 40%), from the 1st day of treatment onwards with 9 mg of ASA (maximally 67%). No ASA dose changed platelet counts or urinary 6-keto-PGF1 alpha excretion. One mg of ASA daily, is the lowest dose ever shown to inhibit platelet TxA2 production.

Aspirin↗
PubMed1984

Evidence that prostacyclin deficiency is a specific feature in preeclampsia.

Much evidence has implied a deficient production of the antiaggregatory and vasodilator agent prostacyclin (PGI2) in preeclampsia and some other chronic fetoplacental insufficiency syndromes. So that we could study whether this might be due to the possible effects of the mode of delivery and maternal epidural or general anesthesia, specimens of the umbilical arteries of infants born after normal (n = 46) or complicated (n = 25) pregnancies were superfused in vitro and their production of PGI2 was determined by measuring 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha, the hydrolysis product of PGI2) by radioimmunoassay. The amounts of umbilical 6-keto-PGF1 alpha released in normal pregnancies after induced vaginal delivery (20.9 +/- 2.4 ng/gm/min dry weight of tissue, mean +/- SEM) and elective cesarean section (21.8 +/- 2.2 ng/gm/min) were smaller (p less than 0.025) than the amounts released after spontaneous onset of labor (35.0 +/- 6.2 ng/gm/min). Epidural or general anesthesia had no effect on this production. When the types of deliveries were matched, the production of 6-keto-PGF1 alpha was even less (p less than 0.05) in cases of preeclampsia (14.2 +/- 3.7 ng/gm/min; n = 9) than in the control subjects (21.3 +/- 1.6 ng/gm/min) and in cases of essential hypertension (21.6 +/- 5.2 ng/gm/min). Our data suggest that umbilical PGI2 deficiency is a specific feature of preeclampsia.

6-Ketoprostaglandin F1 alpha↗
PubMed1984

Ethanol inhibits platelet thromboxane A2 production but has no effect on lung prostacyclin synthesis in humans.

Ethanol (88-880 mmol/l) inhibited the formation of proaggregatory, vasoconstricting thromboxane A2 (TxA2) during whole blood clotting and during thrombin-induced aggregation of platelet rich plasma. This inhibition was counteracted by the addition of exogenous arachidonic acid, which suggested that ethanol suppressed the liberation of arachidonic acid, evidently by inhibiting phospholipase A2. Ethanol had no effect on the formation of prostacyclin (PGI2, epoprostenol), the endogenous antagonist of TxA2, by human lung. Thus our results suggest that ethanol may shift the balance between TxA2 and PGI2 to the dominance of antiaggregatory, vasodilating PGI2 by suppressing the release of arachidonic acid in platelets. This finding might partly explain why ethanol protects against atherosclerosis and also the increased risk of subarachnoidal haemorrhage after heavy ethanol intake.

Adult↗
PubMed1984

Increased thromboxane A2 production but normal prostacyclin by the placenta in hypertensive pregnancies.

The production of vasodilatory, antiaggregatory prostacyclin (PGI2) and vasoconstrictory, proaggregatory thromboxane A2 (TxA2) by the placenta was studied in the cases of hypertensive pregnancy complications by superfusing pieces from maternal and fetal sides of placentae of 9 pre-eclamptic, 6 hypertensive and 11 healthy women in vitro and measuring the release of 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) and thromboxane B2 (TxB2), the breakdown products of PGI2 and TxA2 respectively, from the superfusate. Both sides of the placentae from the controls produced 6-keto-PGF1 alpha (maternal side 0.5 +/- 0.1 ng/g/min dry weight of tissue, mean +/- SEM; fetal side 0.7 +/- 0.2 ng/g/min) and TxB2 (maternal side 2.5 +/- 0.4 ng/g/min; fetal side 2.7 +/- 0.5 ng/g/min) with no correlation between the two. The 6-keto-PGF1 alpha production was normal in hypertensive complications whereas the TxB2 production was increased on the fetal side of the placentae obtained from the pre-eclamptic (3.7 +/- 0.3 ng/g/min: p less than 0.05) and hypertensive women (4.1 +/- 0.4 ng/g/min; p less than 0.025). This may explain the occurrence of microthrombi and infarctions in placentae of hypertensive women.

6-Ketoprostaglandin F1 alpha↗
PubMed1984

Serum selenium and glutathione peroxidase, and plasma lipid peroxides in uterine, ovarian or vulvar cancer, and their responses to antioxidants in patients with ovarian cancer.

The concentrations of serum selenium and plasma lipid peroxides, and the activity of serum glutathione peroxidase (GSH-Px) were measured before any therapy in patients suffering from uterine, ovarian or vulvar cancer, and in association with 1-day combination cytotoxic chemotherapy of ovarian cancer following 1-week supplementation with selenium (96 micrograms/day), vitamin E (300 mg/day), selenium and vitamin E, or placebo. Patients with gynaecological cancer (N = 44) had lower serum concentration of selenium (1.15 +/- 0.04 S.E. mumol/l; P less than 0.05) and serum activity of GSH-Px (404 +/- 13 units/l, P less than 0.01) than the control subjects (N = 56; 1.25 +/- 0.03 mumol/l and 444 +/- 8 units/l, respectively). In association with cytotoxic chemotherapy selenium alone (P less than 0.05), vitamin E alone (P less than 0.05) and both of them together (P less than 0.001) decreased the plasma concentration of lipid peroxides, and the combination of selenium and vitamin E also increased the activity of serum GSH-Px (P less than 0.01). During placebo, cytotoxic chemotherapy did not affect plasma lipid peroxides but it decreased (P less than 0.001) the activity of GSH-Px. Selenium inhibited this effect. Our data suggest that antioxidative mechanisms of patients with gynaecological cancer may be defective and that treatment with selenium and vitamin E results in changes of biochemical factors related to lipid peroxidation.

Adult↗
PubMed1984

Vasoconstrictory thromboxane A2 and vasodilatory prostacyclin in climacteric women: effect of oestrogen-progestogen therapy.

The production of vasoconstrictory thromboxane A2 (TxA2) and vasodilatory prostacyclin ( PG2 ) was studied in women suffering from climacteric vascular instabilities before and during the oestrogen-progestogen therapy. The serum concentrations of TxB2, a metabolite of TxA2, in climacteric patients were similar (170.5 +/- 25.5 ng/ml, mean +/- SE, n = 14) to those in control subjects (196.0 +/- 27.5 ng/ml n = 17) before the start of treatment, but rose to 209.3 +/- 24.5 ng/ml after 3 wk of treatment (P less than 0.01 in comparison with the pre-treatment level), to 227.2 +/- 44.1 ng/ml after 3 mth (P less than 0.05) and to 237.4 +/- 30.3 ng/ml after 6 mth (P less than 0.05). The plasma concentrations of 6-keto-prostaglandin F1a , a stable breakdown product of PG2 , were normal in climacteric (43.5 +/- 7.3 pg/ml as against 46.1 +/- pg/ml) and did not change during replacement therapy. It was concluded, firstly, that climacteric symptoms are not accompanied by changes in TxA2/ PG2 which can be detected in peripheral blood and, secondly, that the increase in the concentration of vasoconstrictory TxA2 induced by oestrogen-progestogen therapy may contribute to the disappearance of climacteric vascular instabilities.

6-Ketoprostaglandin F1 alpha↗
PubMed1984

Thromboxane B2 production by fetal and neonatal platelets: effect of idiopathic respiratory distress syndrome and birth asphyxia.

To study the production of proaggregatory thromboxane A2 (TxA2) by fetal and neonatal platelets, blood specimens were collected from umbilical cords immediately after delivery at term (n = 22), from newborn infants during the first 10 days of life (n = 85), from infants between 1 and 3 months of age (n = 14), and from healthy adults (n = 18). The blood samples were allowed to clot spontaneously at +37 degrees C for 60 min, and the concentrations of thromboxane B2 (TxB2), a stable metabolite of TxA2, in the sera were measured by radioimmunoassay and expressed as nanograms of TxB2/10(6) platelets. Platelet TxB2 generation in term infants at the age of 1 day (1.344 +/- 0.253 ng/10(6) platelets, mean +/- SE, n = 9) was higher than that in cord blood (0.634 +/- 0.042 ng/10(6) platelets, n = 22), or in infants of 1-3 months of age (0.881 +/- 0.099 ng/10(6) platelets, n = 14), or in adults (0.869 +/- 0.062 ng/10(6) platelets, n = 18). Increase in TxB2 generation following birth was seen already at the age of 1 h (1.076 +/- 0.114 ng/10(6) platelets, n = 9). TxB2 synthesis in preterm infants (1.032 +/- 0.136 ng/10(6) platelets, n = 10) did not differ from that in term infants on the 1st day of life, and idiopathic respiratory distress syndrome had no effect on it (1.029 +/- 0.079 ng/10(6) platelets, n = 19). Severe birth asphyxia was accompanied by reduced TxB2 formation (0.564 +/- 0.201 ng/10(6) platelets, n = 7).(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1984

Peritoneal fluid prostaglandins in endometriosis, tubal disorders, and unexplained infertility.

To elucidate the roles of prostaglandins in peritoneal fluid and sex steroids in patients with endometriosis (N = 29), tubal disorders (N = 15), and unexplained infertility (N = 13), assays were performed using 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) (a metabolite of prostacyclin), thromboxane B2 (a metabolite of thromboxane A2), estradiol, and progesterone. Women with normal pelvic anatomy (N = 25) served as controls. Peritoneal fluid 6-keto-PGF1 alpha concentrations in patients with endometriosis (742 +/- 104 pg/ml, mean +/- SE), tubal disorders (987 +/- 211 pg/ml), and unexplained infertility (1659 +/- 770 pg/ml) were higher than those in the control women (515 +/- 77 pg/ml). The thromboxane B2 levels in the peritoneal fluid in endometriosis (554 +/- 73 pg/ml), tubal disorders (614 +/- 107 pg/ml), and unexplained infertility (668 +/- 161 pg/ml) were higher than the levels in the control subjects (333 +/- 23 pg/ml). There was no relationship between 6-keto-PGF1 alpha/thromboxane B2 in peritoneal fluid and day of menstrual cycle. The concentrations of estradiol and progesterone were normal in all patient groups and were not related to the 6-keto-PGF1 alpha and thromboxane B2 levels. The authors suggest that these prostanoids, which may contribute to infertility, may originate mainly from the peritoneum as a result of irritation by endometriotic implants, tubal adhesions, and scarring.

Adult↗
PubMed1984

Treatment of inadequate lactation with oral sulpiride and buccal oxytocin.

Thirty-six puerperal women with inadequate lactation were treated with 50 mg sulpiride (N = 24) or placebo (N = 12) three times a day for two weeks. These treatments were supplemented with buccal oxytocin (100 IU, 300 IU, or 400 IU) or placebo preceding each breast-feeding on the sixth and 14th and on the seventh and 13th days of oral treatment, respectively. One woman treated with sulpiride and three women treated with placebo discontinued the trial because of the lack of the effect of treatment. The concentration of prolactin in maternal serum was higher (P less than .001) during sulpiride than placebo treatment at one week (380 +/- 43 ng/ml vs 23 +/- 7 ng/ml, mean +/- SE) and two weeks of treatment (381 +/- 38 ng/ml vs 34 +/- 10 ng/ml). Also, the daily breast milk yield, as measured objectively, was greater (P less than .05) during sulpiride than placebo treatment both at one week (628 +/- 51 ml vs 440 +/- 68 ml) and two weeks of treatment (684 +/- 67 ml vs 423 +/- 60 ml). Various doses of oxytocin failed to stimulate the milk secretion in the presence or absence of sulpiride-induced hyperprolactinemia. Thus, sulpiride improved inadequate lactation, whereas exogenous oxytocin alone or together with sulpiride had no effect on lactation in these mothers whose infants were able to suckle normally.

Adult↗
PubMed1984

Lipid peroxides, prostacyclin, and thromboxane A2 in runners during acute exercise.

We studied the effect of physical activity on lipid peroxidation and on the production of antiaggregatory, vasodilatory prostacyclin (epoprostenol, PGI2) and its endogenous antagonist, thromboxane A2 (TxA2) in 10 well-trained long-distance runners before, during, and after maximal exercise on a cycle ergometer. Pre-exercise levels of lipid peroxides (2.0 +/- 0.4 mumol X l-1, means +/- SD), plasma immunoreactive 6-keto-prostaglandin F1 alpha (i 6-keto-PGF1 alpha, a metabolite of PGI2) (192.8 +/- 51.7 pmol X l), and serum immunoreactive thromboxane B2 (i TxB2, a metabolite of TxA2) (703.3 +/- 290.1 nmol X l) did not differ from those of 10 non-athletic controls. Plasma i 6-keto-PGF1 alpha was increased at the seventh minute of the exercise test, but not any more at the end of the exercise or 30 min later. Lipid peroxides or i TxB2 did not change. Our data suggest that the changes of the PGI2/TxA2-ratio induced by long-term or acute physical exercise are too small to explain the protective effect of physical fitness against coronary heart disease.

Adolescent↗
PubMed1984

An antagonist of prostaglandin synthesis in cardiovascular diseases.

Prostaglandins potently regulate platelet aggregation and vascular tone. Thus they are of great importance in the blood supply of tissue. The strategy of the attempts to prevent occlusive vascular disease have been either to decrease the amount of aggregatory, vasoconstricting prostaglandins or to increase antiaggregatory, vasodilatory prostaglandins. Acetylsalicylic acid has been mostly used in attempts to inhibit platelet TxA2-synthesis without disturbing endothelial cell PGI2-synthesis. Primary prevention trials of myocardial infarction have given results of great discrepancy whereas reinfarctions are likely in part to be inhibited by acetylsalicylic acid. In the prevention of ischaemic cerebral disease, most of the trials have indicated the beneficial effect of acetylsalicylic acid, as is the case also in the prevention of venous thrombosis. It is, however, likely that the doses of acetylsalicylic acid have not been optimal in any work, and thus better results are to be awaited. The infusion of anti-aggregatory, vasodilatory prostaglandins, mainly PGI2 or PGE1, have relieved the symptoms of ischaemia of the lower extremities, coronary heart disease and Raynaud's syndrome. The technical difficulties of these infusions, however, limit their applicability to special groups of patients.

Arterial Occlusive Diseases↗