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Biomedical subjects

L Viinikka

Publications and source records attributed to L Viinikka.

At least 109 records · Page 6Linked to original sources
PubMed1986

Platelet function and coagulation in normal and preeclamptic pregnancy.

Platelet function and coagulation activity were followed prospectively throughout normal pregnancy and in puerperium in 17 healthy women. Plasma beta-thromboglobulin reflecting platelet activation increased progressively during pregnancy. This was not accompanied by any changes in platelet count or lifespan nor in serum or plasma thromboxane B2 levels. The levels of both factor VIII:C and factor VIIIR:Ag increased, the former less than the latter resulting in a rise of the FVIIIR:Ag/FVIII:C ratio. Antithrombin III (AT III), however remained unaltered. FVIIIR:Ag/FVIII:C ratio was increased both in mild (n = 7) and severe (n = 9) preeclampsia, whereas beta-thromboglobulin was increased and AT III was decreased only in severe preeclampsia. Platelet count and lifespan, plasma and serum thromboxane B2 as well as FVIII:C were normal in severe preeclampsia.

Adult↗
PubMed1986

Dietary fatty acids and platelet thromboxane production in puerperal women and their offspring.

The effects of the ratio of polyunsaturated to saturated fatty acids in the diet of puerperal women on maternal and neonatal fatty acids and thromboxane A2 synthesis were studied in 91 mother-infant pairs on the fourth to fifth day after delivery. The mothers received a diet with either a low (0.1) or a high (1.5) polyunsaturated to saturated fatty acid ratio for 4 to 5 days. The fatty acid composition in maternal and neonatal serum and in breast milk was determined in 34 mother-infant pairs from both dietary groups. The capacity of the platelets to produce thromboxane B2, a stable metabolite of thromboxane A2, was determined in another 57 mother-infant pairs. The percentage of linoleic acid was increased in maternal and neonatal sera as well as in the breast milk in the group with a high dietary polyunsaturated to saturated fatty acid ratio, whereas the content of arachidonic acid was increased only in maternal serum. This was accompanied by increased platelet thromboxane B2 production in the mothers, and maternal and neonatal thromboxane B2 synthesis correlated significantly with each other (r = 0.43, p less than 0.05). This finding may provide therapeutic possibilities in the future.

Arachidonic Acid↗
PubMed1986

Maternal ingestion of acetylsalicylic acid inhibits fetal and neonatal prostacyclin and thromboxane in humans.

Small doses of maternal acetylsalicylic acid have proved to prevent preeclampsia. To study the mechanism of this action of acetylsalicylic acid, healthy women ingested 100 mg (n = 13) or 500 mg (n = 14) of acetylsalicylic acid during labor at term. The fetal prostacyclin synthesis, as assessed by the production of 6-ketoprostaglandin F1 alpha (a metabolite of prostacyclin) by the umbilical artery, was reduced from 21.3 +/- 1.6 ng/gm/min of dry weight in the controls (n = 25, mean +/- SE) to 7.8 +/- 1.1 ng/ml/min (p less than 0.001) in infants of mothers receiving 500 mg of acetylsalicylic acid, but it was unchanged in infants with mothers receiving 100 mg of acetylsalicylic acid (19.5 +/- 2.3 ng/gm/min). Maternal ingestion of 500 mg of acetylsalicylic acid also was accompanied by reduced (p less than 0.10) urinary excretion of 6-ketoprostaglandin F1 alpha in neonates during the first 3 days of life. The fetal platelet thromboxane A2 synthesis, as assessed by the release of thromboxane B2 (a metabolite of thromboxane A2) during spontaneous clotting of the umbilical blood (63.4 +/- 4.2 pg/10(5) platelets, n = 22), was inhibited in infants born to mothers given 100 mg (14.0 +/- 3.7 pg/10(5) platelets, p less than 0.001) or 500 mg of acetylsalicylic acid (6.1 +/- 3.5 pg/10(5) platelets, p less than 0.001). The thromboxane B2 release by the umbilical artery (1.1 +/- 0.1 ng/gm/min, n = 13) also was decreased in infants of mothers receiving 500 mg of acetylsalicylic acid (0.57 +/- 0.1 ng/gm/min, n = 7, p less than 0.01). Thus a small dose of maternal acetylsalicylic acid (100 mg) inhibits only the fetoplacental thromboxane A2 but leaves prostacyclin production unaffected.

Adult↗
PubMed1986

An ultrasensitive time-resolved immunofluorometric assay of human epidermal growth factor.

We have developed a sandwich-type time-resolved immunofluorometric assay (TR-IFMA) for human epidermal growth factor (hEGF) in body fluids. A two-step solid-phase technique was used. The assay utilizes a polyclonal anti-hEGF attached to the solid phase, and a monoclonal anti-hEGF labeled with Europium (III) as a tracer. The sensitivity of the assay (2.5 pg/ml) is at least 20 times better than what has been achieved by radioimmunoassay (RIA), and the measuring range is much wider: 2.5-5000 pg/ml. The feasibility of TR-IFMA was tested by assaying urine containing large amounts and amniotic fluid containing small amounts (mostly undetectable by RIA) of immunoreactive hEGF. The correlation between urine hEGF concentrations (1-100 ng/ml) measured by RIA and TR-IFMA was good: r = 0.96.

Epidermal Growth Factor↗
PubMed1986

Effects of smoking and nicotine on human prostacyclin and thromboxane production in vivo and in vitro.

We studied the effects of smoking and nicotine on the production of proaggregatory thromboxane A2 (TxA2), antiaggregatory prostacyclin (epoprostenol, PGI2), and on lipid peroxidation in vivo and in vitro. In the in vivo study, serum concentrations of thromboxane B2 (TxB2), a stable metabolite of TxA2, increased immediately after smoking three cigarettes but not after smoking the equivalent amount of tobacco in a pipe, whereas serum lipid peroxide values did not change in either group. In vitro, nicotine (2 X 10(-3) mol/liter) inhibited pulmonary TxB2 production by 70% and simultaneously stimulated the production of 6-keto-prostaglandin F1 alpha, a stable metabolite of PGI2, by 40%, which suggest that nicotine does not exert its effect at the cyclooxygenase level. During aggregation in platelet-rich plasma, TxB2 production was inhibited by 53% with 2 X 10(-3) mol/liter of nicotine, and during whole blood clotting the inhibition was 34% with 2 X 10(-4) mol/liter of nicotine. Thus the rise in cigarette smokers' serum TxB2 was probably caused by some constituent of cigarette smoke other than nicotine. The increased production of TxA2 following cigarette smoking may provide one explanation for the increased incidence of atherosclerosis and its complications in cigarette smokers.

Adult↗
PubMed1986

Increased platelet thromboxane B2 production in newborn infants of diabetic mothers.

Platelet thromboxane B2 (TxB2) production, plasma concentrations of C-peptide and pancreatic glucagon as well as blood glucose levels were measured in 12 infants of insulin-dependent diabetic mothers and eight healthy controls at the age of two hours. Platelet TxB2 production (p less than 0.05) and plasma C-peptide levels (p less than 0.02) were significantly higher and blood glucose concentrations lower (p less than 0.002) in the infants of the diabetic mothers than in the controls. The data suggest that platelets of infants of diabetic mothers produce increased amounts of proaggregatory thromboxane A2, which may contribute to the hyperaggregation in these infants.

Blood Glucose↗
PubMed1986

Dermal prostacyclin, thromboxane A2 and prostaglandin F2 alpha in climacteric women: effect of oestrogen replacement therapy.

The involvement of dermal prostanoids in menopausal flushing was studied in 8 women suffering from climacteric hot flushes and in 10 asymptomatic control subjects by inducing suction blisters on abdominal skin and assaying blister fluids for 6-keto-PGF1 alpha, a metabolite of the vasodilative prostacyclin (PGI2), thromboxane B2 (TxB2), a metabolite of the vasoconstrictive thromboxane A2 (TxA2), and 13,14-dihydro-15-keto-PGF2 alpha (M-PGF2 alpha), a metabolite of prostaglandin F2A (PGF2A). No marked differences were observed in the levels of these prostanoids in the two study groups. The women experiencing flushes then received conjugated oestrogens for 3 mth to abolish vascular instabilities. This decreased the blister fluid concentration of M-PGF2 alpha from 1720 +/- 476 pg/ml (mean +/- SE) to 1490 +/- pg/ml (P less than 0.05), but had no effect on the dermal levels of 6-keto-PGF1 alpha or TxB2. It was concluded that although certain dermal prostanoids may be affected by oestrogen treatment they are not of primary significance as regards menopausal flushing.

6-Ketoprostaglandin F1 alpha↗
PubMed1986

Vaginal and abdominal delivery increases maternal urinary 6-keto-prostaglandin F1 alpha excretion.

To study the role of the antiaggregatory and vasodilatory prostacyclin (PGI2) during human delivery, serial urine samples collected from 13 women delivered vaginally and from eight delivered abdominally were assayed for 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha, a breakdown product of PGI2) by high-performance-liquid-chromatography and radioimmunoassay. In women delivered vaginally the mean urinary 6-keto-PGF1 alpha concentration was 41.9 (SE 8.3) ng/mmol creatinine, before the onset of labour and increased progressively to a maximum of 186.5 (SE 47.6) ng/mmol creatinine 2 h after delivery irrespective of the use of oxytocin and epidural analgesia. In women delivered by caesarean section under epidural anaesthesia, the urinary 6-keto-PGF1 alpha rose from 33.4 (SE 4.2) ng/mmol creatinine to 2153 (SE 314) ng/mmol creatinine 2 h after section. In both groups the increased levels had fallen by 24 h postpartum to levels below those found before delivery. In neonatal urine 6-keto-PGF1 alpha concentrations were some 12-30 times higher than those in postpartum urine. Thus, vaginal and abdominal delivery is accompanied by significant increases in maternal PGI2 release, perhaps in the myometrium and/or intrauterine tissues. This may be of significance in the regulation of fetoplacental blood flow and in the prevention of intra- and postpartum thrombosis.

6-Ketoprostaglandin F1 alpha↗
PubMed1986

Subnormal concentrations of urinary epidermal growth factor in patients with kidney disease.

We determined the concentrations of immunoreactive epidermal growth factor (irEGF) and creatinine in urine samples from 47 adult patients with various kidney diseases and wide ranges of azotemia and proteinuria. In most of the patients, urinary irEGF concentrations (nanograms per mg creatinine) were markedly subnormal. In the entire group, urinary irEGF correlated with creatinine clearance (r = 0.79; P less than 0.001) and serum creatinine concentration (r = -0.85; P less than 0.001). In the subgroups of patients with primarily glomerular or tubulointerstitial diseases, similar correlations were found. By contrast, there was no correlation with proteinuria. We also determined the concentrations of plasma irEGF in five patients with azotemia. In four patients, the irEGF to creatinine concentration ratio was 1.9- to 8.9-fold higher in urine than in plasma, indicating that plasma irEGF was not the main source of urinary irEGF in these patients. Our data are compatible with the theory that urinary irEGF originates from nephrons per se.

Adolescent↗
PubMed1986

Renal prostacyclin and thromboxane in normotensive and preeclamptic pregnant women and their infants.

Renal synthesis of the antiaggregatory and vasodilatory prostacyclin and its endogenous antagonist thromboxane A2 may be disturbed in patients with preeclampsia. We tested this hypothesis by measuring 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha; a hydration product of prostacyclin), 2,3-dinor-6-keto-PGF1 alpha (generated from 6-keto-PGF1 alpha through beta-oxidation) and thromboxane B2 (a hydration product of thromboxane A2) in the urine of healthy pregnant and preeclamptic women. Urinary excretion of 6-keto-PGF1 alpha [19.8 +/- 10.5 pmol/mmol creatinine, (mean +/- SD)] and 2,3-dinor-6-keto-PGF1 alpha (19.2 +/- 7.5 pmol/mmol creatinine) increased during normal pregnancy, reaching a maximum (about 5-fold rise) during the last month of pregnancy. No significant changes occurred in the urinary excretion of thromboxane B2. In women with severe preeclampsia (n = 17), the excretion of both 6-keto-PGF1 alpha (37.7 +/- 29.5 pmol/mmol creatinine) and 2,3-dinor-6-keto-PGF1 alpha (54.5 +/- 56.2 pmol/mmol creatinine) was lower (P less than 0.001) than in the normotensive women during the last trimester of pregnancy (80.6 +/- 43.7 and 98.7 +/- 42.9 pmol/mmol creatinine, respectively). The neonates excreted 6-25 times more 6-keto-PGF1 alpha, 2,3-dinor-6-keto-PGF1 alpha and thromboxane B2 than did the nonpregnant women. In contrast to the adults, neonatal 6-keto-PGF1 alpha excretion was 2-3 times greater than that of 2,3-dinor-6-keto-PGF1 alpha suggesting reduced beta-oxidation in the newborns. Infants born to preeclamptic women had reduced output of 6-keto-PGF1 alpha and 2,3-dinor-6-keto-PGF1 alpha on the first day of life. Thus, renal prostacyclin synthesis is diminished in women with severe preeclampsia and their infants.

6-Ketoprostaglandin F1 alpha↗
PubMed1986

Dynamic evaluation of prolactin secretion by successive TRH and metoclopramide stimulations.

We evaluated the clinical applicability of a 2-h test in which the prolactin (Prl) responses to thyrotrophin releasing hormone (TRH)(200 micrograms iv) and the dopamine antagonist, metoclopramide (MC; 10 mg iv) were studied successively, 1 h apart. Nine healthy women were studied with TRH-MC test and with another test in which MC alone was used or the drugs were given in opposite order. The preceding TRH injection did not affect the Prl responses to MC, nor did preceding MC affect the Prl response to TRH. With the TRH-MC test, Prl responses to TRH and MC were significantly lowered in amenorrhoea (N = 8) and hyperprolactinaemia (N = 15) regardless of whether or not treated with bromocriptine, and to MC only in oligomenorrhoea (n = 11). In normoprolactinaemic galactorrhoea (N = 7) the responses were similar as in healthy women. The ratio between Prl responses to TRH and MC was significantly higher in women with bromocriptine-treated hyperprolactinaemia (1.06 +/- 0.8, SD) than in healthy controls (0.34 +/- 0.13). The capacity of pituitary lactotrophs to secrete Prl in response TRH and MC can be evaluated with a 2-h test which has potential for investigation of pituitary Prl dynamics in gynaecological endocrine disorders, particularly in amenorrhoea and hyperprolactinaemia.

Adolescent↗
PubMed1986

Urinary neopterin index as a measure of rheumatoid activity.

The urinary neopterin index (U-NEOPT-I), expressed as micro-moles of neopterin/moles of creatinine) of 67 patients with definite or classical rheumatoid arthritis was significantly higher than that of sex- and age-matched persons or of 24 non-matched patients suffering from osteoarthrosis or arthralgia (2p less than 0.001). Furthermore, the patients with active disease had statistically significantly increased U-NEOPT-I when compared with patients with a clinically less active disease. In this study, the U-NEOPT-I value was the equal of CRP as a measure of rheumatoid activity. We suggest that neopterin might be involved in the pathogenesis of rheumatoid arthritis.

Adult↗
PubMed1986

Placental thromboxane and prostacyclin in the regulation of placental blood flow.

To study the significance of placental thromboxane A2 and prostacyclin in the regulation of placental blood flow, intervillous blood flow was measured using a 133Xenon method from 39 women zero to two days before delivery and compared it with the placental production of thromboxane A2 and prostacyclin as measured with a superfusion method postpartum. The placental production of thromboxane B2 (a metabolite of thromboxane A2; 4.5 +/- 1.3 ng/minute per gram dry weight of tissue; mean +/- SD) and that of 6-keto-prostaglandin F1 alpha (a metabolite of prostacyclin; 0.64 +/- 0.27 ng/minute per gram) did not correlate significantly with intervillous blood flow (153.1 +/- 108.0 mL/minute per 100 mL; r = -0.308 and 0.245, respectively), whereas the thromboxane B2/6-keto-prostaglandin F1 alpha ratio (8.53 +/- 4.3) was inversely related to intervillous blood flow (r = -0.419; P less than .01). In the women with intervillous blood flow below the normal mean (less than 130 mL/minute per 100 mL; N = 20) placental thromboxane B2 production (5.1 + 1.2 ng/minute per gram) was higher (P less than .005) and that of 6-keto-prostaglandin F1 alpha (0.54 +/- 0.23 ng/minute per gram) lower (P less than .02) than those in women with intervillous blood flow above 130 mL/minute per 100 mL (thromboxane B2 4.01 +/- 1.0 and 6-keto-prostaglandin F1 alpha 0.75 +/- 0.27 ng/minute per gram; N = 19). These results suggest that placental thromboxane A2 and prostacyclin may be factors in the regulation of intervillous blood flow and that their balance of production is more important than the presence of either agent alone.(ABSTRACT TRUNCATED AT 250 WORDS)

6-Ketoprostaglandin F1 alpha↗
PubMed1985

Differential inhibition of platelet thromboxane and lung prostacyclin production by sulphinpyrazone, acetylsalicylic acid and indomethacin by human tissues in vitro.

To compare the inhibition of human platelet and lung cyclo-oxygenases by sulphinpyrazone (SP), acetylsalicylic acid (ASA) and indomethacin, we investigated their effects on platelet thromboxane A2 (TxA2) production during spontaneous clotting and on prostacyclin (PGI2) and TxA2 productions of superfused minced human lung. The synthesis of proaggregatory, vasoconstricting TxA2 and antiaggregatory, vasodilating PGI2 were evaluated by measuring the concentration of their stable metabolites thromboxane B2 (TxB2) and 6-keto-prostaglandin F1 alpha respectively, by radioimmunoassays. The basal platelet TxB2 production was 241.0 +/- 56.3 ng/ml (mean +/- SEM, n = 12). The concentrations needed for 50% inhibition of this production (IC50) were 41.3 mumol/l for sulphinpyrazone, 6.3 mumol/1 for ASA and 0.094 mumol/l for indomethacin. The lung generated 23.8 +/- 5.5 ng/g/min (mean +/- SEM, n = 6) of 6-keto-PGF1 alpha and 8.5 +/- 1.8 ng/g/min of TxB2. The IC50 values for pulmonary 6-keto-PGF1 alpha and TxB2 productions were 530.0 mumol/l for SP, 370.0 mumol/l for ASA and 50.0 mumol/l for indomethacin. Thus pulmonary cyclo-oxygenase, presumably originating from endothelial cells, was 13, 59, and 532 times more resistant to these prostaglandin synthesis inhibitors (PGI's) than platelet cyclo-oxygenase. These data suggest that there are considerable differences in the concentration ranges of various PGI's by which the PGI2/TxA2 balance can be shifted to a dominance of PGI2.

6-Ketoprostaglandin F1 alpha↗
PubMed1985

Haemostatic parameters in Cushing's syndrome.

We have studied haemostatic parameters in 12 patients with Cushing's syndrome. Three patients had prolonged bleeding times, and in all seven patients whose bleeding times were measured 3-6 months after surgical treatment the postoperative bleeding times were shorter (mean 7.5 min) than the pretreatment times (mean 12.3 min). In ADP- or adrenaline-induced aggregation the second wave was lacking in six and the degree of aggregation was borderline or subnormal in five patients. One patient had, in addition, a severe defect in collagen-induced aggregation. However, thromboxane B2 production of the platelets from both endogenous and exogenous arachidonic acid was unaffected. Factor VIII:C, RAg and Rcof activities were all elevated, and in patients with severe disease F VIIIR:Ag and F VIII:Rcof activities were markedly more elevated than F VIII:C activity. The changes in both primary haemostasis and in factor VIII activities correlated clearly with the clinical severity of the disease.

Adolescent↗
PubMed1985

Plasma six-keto-prostaglandin F1 alpha and endocrine pancreatic function in the newborn infant of the diabetic mother.

Plasma concentrations of 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha), C-peptide and pancreatic glucagon and blood glucose levels were measured in 13 infants of insulin-dependent diabetic mothers at the age of 2 h. Plasma 6-keto-PGF1 alpha levels were lower in these infants when compared to those of healthy controls at the same age (p less than 0.05). Plasma 6-keto-PGF1 alpha correlated negatively with the C-peptide levels (r = -0.57; p less than 0.05) and positively with the pancreatic glucagon concentrations (r = 0.83; p less than 0.001) in the infants of diabetic mothers. No correlation with blood glucose concentrations was found. The data suggest that hyperinsulinemia in infants of diabetic mothers is associated with a decreased vascular prostacyclin production.

6-Ketoprostaglandin F1 alpha↗