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Biomedical subjects

L Viinikka

Publications and source records attributed to L Viinikka.

At least 163 records · Page 9Linked to original sources
PubMed1982

The effect of prolonged treatment with sulphinpyrazone on thromboxane A2 and prostacyclin in man.

We studied the effect of 3 weeks' treatment with 4 x 200 mg of sulphinpyrazone daily (six healthy volunteers) on proaggregatory thromboxane A2 (TxA2) and antiaggregatory prostacyclin (PGI2). Platelet TxA2 production was evaluated by measuring its stable metabolite, immunoreactive thromboxane B2, from serum, and vessel wall PGI2 production by measuring its stable metabolite, immunoreactive 6-keto-prostaglandin F1 alpha in plasma. The TxA2 production (initially 209.0 +/- 27.1 ng/ml, mean +/- s.e. mean) decreased to about 30% from the second day of the treatment onwards, and it recovered in three days after the discontinuation of the treatment. PGI2 (initially 33.6 +/- 3.6 pg/ml) did not change. The shift of the balance between TxA2 and PGI2 to the dominance of antiaggregatory PGI2 during sulphinpyrazone treatment may be involved with the efficacy of the drug in the secondary prevention of myocardial infarction.

Adult↗
PubMed1982

Plasma prostacyclin from birth to adolescence.

The plasma concentration of 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha), the stable hydration product of prostacyclin, was measured by radioimmunoassay in 111 healthy children aged between 1 day and 16 years and in 21 healthy adults aged between 21 and 72 years. The 6-keto-PGF1 alpha levels in children up to age 16 years were higher than those in adults. During the first 4 days of life the plasma concentrations of 6-keto-PGF1 alpha in term infants were higher (P less than 0.05) than the respective levels in preterm infants. There was no difference between the 6-keto-PGF1 alpha levels measured simultaneously in umbilical arterial and peripheral venous plasma in 7 newborn infants. Maternal pre-eclampsia or epidural analgesia during labour, mode of delivery, birthweight, or sex of the infants were not related to the plasma 6-keto-PGF1 alpha levels on the first day of life. High levels of vasodilatory and anti-aggregatory prostacyclin during the first days of life may play a role in the postnatal adaptation of the circulation and platelet function.

6-Ketoprostaglandin F1 alpha↗
PubMed1982

Effect of amnioscopy on concentrations of prostaglandin F2 alpha, prostacyclin and thromboxane in maternal plasma.

To study whether amnioscopy causes a local release of prostaglandins (PG), the peripheral plasma concentrations of 13,14-dihydro-15-keto-PGF2 alpha (M-PGF2 alpha)(a metabolite of PGF2 alpha), 6-keto-PGF1 alpha (a metabolite of prostacyclin) and thromboxane B2 (a metabolite of thromboxane A2) were measured with radioimmunoassays in 12 women between 36 and 40 weeks of pregnancy before and after amnioscopy. The levels of M-PGF2 alpha and thromboxane B2 rose significantly between 10 and 30 min after amnioscopy but dropped to pre-amnioscopy levels within 60 min, whereas the 6-keto-PGF1 alpha concentration did not change. These findings suggest a local release of PGF2 alpha and Tx-A2 in the myometrium and/or intrauterine tissues as a consequence of amnioscopy.

6-Ketoprostaglandin F1 alpha↗
PubMed1982

Increased plasma immunoreactive 6-keto-prostaglandin F1 alpha levels in newborns with idiopathic respiratory distress syndrome.

Serial plasma concentrations of immunoreactive 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha), the stable hydration product of prostacyclin (PGI2), were measured with radioimmunoassay during the first month of life in 25 preterm infants with idiopathic respiratory distress syndrome (IRDS) and 38 preterm controls with normal heart and lung function. The levels of 6-keto-PGF1 alpha (521 +/- 81 pg/ml, mean +/- S.E.) in the infants with IRDS were higher (P less than 0.05) than those in the controls (335 +/- 42 pg/ml) on the first day of life, but thereafter no difference was seen. The highest first day 6-keto-PGF1 alpha level (1448 pg/ml) was found in the infant who died because of severe IRDS at the age of 19 h. The plasma 6-keto-PGF1 alpha concentrations in the distressed infants correlated positively with the alveolar-arterial oxygen gradient and the need of additional oxygen, but negatively with the arterial pH. In addition, an inverse correlation between the first day concentrations of 6-keto-PGF1 alpha and the lowest arterial oxygen tension in infants needing assisted ventilation was found. The mode of delivery (Cesarean section versus vaginal delivery) the gestational age, birth weight, sex or Apgar scores of the infants were not related to the 6-keto-PGF1 alpha levels on the first day of life. Neither did maternal pre-eclampsia, diabetes mellitus, or antenatal glucocorticoid treatment have any effect on the 6-keto-PGF1 alpha concentrations in the newborns. Our data suggest that a surge of the vasodilatory and antiaggregatory PGI2 is released during the early stage of IRDS, possibly in an attempt to increase the pulmonary perfusion. Our results give further indirect evidence that hypoxia stimulates the PGI2 production. High plasma immunoreactive 6-keto-PGF1 alpha levels during the early phase of IRDS suggest an increased generation of the vasodilatory and antiaggregatory PGI2 in this syndrome. This may be an attempt to overcome the increased pulmonary vasconstriction in IRDS. When the PGI2 formation rapidly declines after the first day of life, a relative PGI2 deficiency may ensue.

6-Ketoprostaglandin F1 alpha↗
PubMed1982

Hormonal and metabolic effects of intravenous infusion of prostacyclin in healthy women.

To study the hormonal and metabolic effects of prostacyclin (PGI2), 6 healthy women were infused iv with PGI2 (1, 2, 4, and 8 ng/kg/min. each for 20 min) dissolved in glycine buffer, or with glycine buffer only. Serial blood samples collected before, during and after the infusion were assayed for FSH, LH, prolactin, growth hormone, thyrotrophin, oestradiol, progesterone, testosterone, cortisol, thyroxine, triiodothyronine, renin, aldosterone, glucose, insulin, glucagon, cholesterol, high density lipoprotein-cholesterol, triglycerides, alkaline phosphatase, alanine and aspartate aminotransferases, bilirubin, sodium, potassium, chloride, calcium, inorganic phosphorous, creatinine and uric acid. PGI2 infusions were accompanied by increased levels of prolactin, growth hormone and cortisol, probably due to the stressful side-effects during PGI2 infusion. In addition, plasma renin activity, glucagon and blood glucose increased, whereas the other variables measured did not change. These PGI2-effects should be kept in mind, when PGI2 is used in clinical practice.

Adolescent↗
PubMed1982

Prostacyclin and thromboxane in chronic uremia: effect of hemodialysis.

To study the effects of uremia and hemodialysis on the production rates of antiaggregatory prostacyclin (PGI2) and proaggregatory thromboxane A2 (TxA2), we collected serial plasma samples from eight patients with chronic uremia before, during and after hemodialysis and assayed them for 6-keto-PGF1 alpha and TxB2, the stable metabolites of PGI2 and TxA2, respectively. In addition, the capacity of the platelets to produce TxB2 during spontaneous clotting was studied by measuring the TxB2 levels in serum incubated at +37 degrees C for 60 minutes. The PGI2 production of the uremia patients before hemodialysis was less (P less than 0.001) than that of healthy volunteers. It rose significantly following heparinization and remained elevated during hemodialysis. TxB2 generation by platelets during clotting was diminished in uremia. Plasma TxB2 levels were normal before, but increased during hemodialysis. Thus, profound changes in the PGI2/TxA2-system seem to be associated with uremia and hemodialysis.

6-Ketoprostaglandin F1 alpha↗
PubMed1982

Production of prostacyclin and thromboxane during cesarean section.

The effect of cesarean section on the production of the antiaggregatory prostacyclin and proaggregatory thromboxane A2 was studied in 12 women by measuring the stable metabolites of prostacyclin and thromboxane A2, 6-ketoprostaglandin F1 alpha and thromboxane B2, respectively, from serial maternal blood samples collected before, during, and after the operation. The plasma 6-keto-prostaglandin F1 alpha concentration was similar to the initial concentrations before the start of anesthesia (mean 121.6 +/- SE 11.5 pg/ml), at the time of skin incision (148.0 +/- 21.0 pg/ml), and at delivery of the infant (136.3 +/- 11.2 pg/ml), but was elevated at the end of the operation (454.8 +/- 56.2 pg/ml) (P less than .001) and one hour later (233.1 +/- 39.5 pg/ml) (P less than .01). These increases were similar whether the patients were operated on under general (N = 6) or epidural (N = 6) anesthesia. The serum thromboxane B2 concentration did not change, indicating no influence of cesarean section on the capacity of the platelets to produce thromboxane B2 during spontaneous clotting. The increased output of prostacyclin may originate from the myometrium and/or intrauterine tissues, which are manipulated during cesarean section. The increased output may play a role in preventing thromboembolic complications during and after cesarean section.

6-Ketoprostaglandin F1 alpha↗
PubMed1981

Amniotic fluid prostacyclin and thromboxane in normal, preeclamptic, and some other complicated pregnancies.

To study the involvement of the antiaggregatory and vasodilator prostacyclin (PGI2) and proaggregatory and vasoconstrictor thromboxane A2 (TxA2) in complicated pregnancies, we measured by radioimmunoassay the stable metabolites of PGI2 and TxA2, 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) and thromboxane B2 (TxB2), respectively, in samples of amniotic fluid collected at amniocentesis from 88 women between 30 and 40 weeks' normal or complicated pregnancy. The concentrations (mean +/- SE) of 6-keto-PGF1 alpha were 171.8 +/- 9.0 pg/ml in normal pregnancies (N = 27), 134.4 +/- 9.3 pg/ml in severe preeclampsia (N = 13) (0.001 less than p less than 0.005 in comparison with normal pregnancy), 175.6 +/- 13.9 pg/ml in mild preeclampsia (N = 14) (0.01 less than p less than 0.05 in comparison with severe preeclampsia), 168.5 +/- 16.9 pg/ml in diabetic pregnancies (N = 14), 158.7 +/- 5.9 pg/ml in rhesus-immunized pregnancies (N = 10), and 178.7 +/- 13.7 pg/ml in pregnancies with intrauterine fetal growth retardation (N = 10). The corresponding TxB2 concentrations were, respectively, 35.0 +/- 5.7 pg/ml, 29.1 +/- 4.6 pg/ml, 31.3 +/- 3.1 pg/ml, 35.3 +/- 4.0 pg/ml, 31.4 +/- 5.9 pg/ml, and 39.2 +/- 3.2 pg/ml, and these levels did not differ from each other. The level of 6-keto-PGF1 alpha in amniotic fluid correlated with the pregnancy week in normal and preeclamptic pregnancies, and the levels of TxB2 in amniotic fluid in normal, preeclamptic, and rhesus-immunized pregnancies. Furthermore, these two prostanoids correlated with each other in normal pregnancy and in all complications except rhesus-immunized pregnancies. Thus, it is evident that the release of PGI2 into the amniotic fluid is decreased in severe preeclampsia.

6-Ketoprostaglandin F1 alpha↗
PubMed1981

Prostacyclin and thromboxane in diabetes.

Concentrations of the stable antiaggregatory prostacyclin metabolite 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) and of the proaggregatory thromboxane A2 metabolite thromboxane B2 were measured by radioimmunoassay in plasma from 53 diabetics. In 33 of these patients the ability of platelets to produce thromboxane B2 during spontaneous clotting was also studied. Plasma 6-keto-PGF1 alpha concentrations were higher (p less than 0.05) in the diabetics (mean 107.7 +/- SE 7.6 ng/l) than in non-diabetic controls matched for age and sex (87.5 +/- 4.7 ng/l), and diabetics with microangiography (n = 28) and higher (p less than 0.01) concentrations (124.3 +/- 10.8 ng/l) than those without microangiography (n = 25; 89.2 +/- 9.3 ng/l). Plasma thromboxane B2 concentrations were also higher (p less than 0.01) in the diabetics (mean 218.5 +/- SE 25.3 ng/l) than in the controls (127.7 +/- 9.8 ng/l), but this increase was not related to microangiography. The ability of platelets to generate thromboxane B2 did not differ between the diabetics (181.4 +/- 16.4 microgram/l) and controls (195.8 +/- 11.8 microgram/l). Platelets of diabetics with microangiopathy or taking oral hypoglycaemic agents (n = 19), however, produced decreased amounts of thromboxane B2 during clotting. Plasma concentrations of 6-keto-PGF1 alpha and thromboxane B2 were not related to concentrations of glucose, haemoglobin A1, high-density lipoprotein cholesterol, cholesterol, triglycerides, magnesium, or creatinine. These results suggest that in diabetics with microangiopathy a balance between prostacyclin and thromboxane A2 is shifted to dominance by prostacyclin.

6-Ketoprostaglandin F1 alpha↗
PubMed1981

A two-site immunofluorometric assay for human placental lactogen.

A two-site immunofluorometric assay for human placental lactogen (HPL) in serum has been developed. Samples and standards are incubated for 10 min with an excess of sheep anti-HPL serum covalently coupled to particles of magnetisable cellulose. After sedimenting the particles and adsorbed hormone on a magnet the supernates are aspirated (or decanted) to waste. An excess of purified sheep anti-HPL immunoglobulin, labelled with fluorescein, is added and, after a further 20 min, the fluorescence remaining in the supernates, after sedimenting the particles, is inversely related to the initial concentration of HPL. Results correlate closely with those of an established radioimmunoassay (r = 0.92), within- and between-assay coefficients of variation are less than 10% and, employing a 200 microliter sample volume, the assay extends from a minimum detection limit of 0.02 mg/l throughout the entire range of values encountered in pregnancy to more than 10 mg/l.

Female↗
PubMed1981

Prostacyclin, thromboxane, and prostaglandin F2 alpha in maternal plasma during breast-feeding.

In order to study the role of prostaglandin F2 alpha (PGF2 alpha) prostacyclin (PGI2), and thromboxane A2 in milk ejection, the stable metabolites of these prostanoids, i.e., 13,14-dihydro-15-keto-PGF2 alpha (M-PGF2 alpha), 6-keto-PGF1 alpha, and thromboxane B2, respectively, were measured from serial samples of plasma collected from 11 puerperal women before, during, and after breast-feeding. The plasma M-PGF2 alpha decreased significantly (p less than 0.01) from the level of 253.6 +/- 18.6 pg/ml (mean +/- SE) before suckling to 204.2 +/- 26.1 pg/ml at the end of suckling, but returned to 234.6 +/- 26.1 pg/ml 60 minutes after the end of suckling. The 6-keto-PGF1 alpha concentration also decreased (p less than 0.01) from 246.4 +/- 30.9 to 187.9 +/- 9.9 pg/ml within the first 15 minutes of suckling, whereas the thromboxane B2 levels did not change. Thus, these results suggest that PGF2 alpha and PGI2 are involved with milk ejection and lactation in human beings.

6-Ketoprostaglandin F1 alpha↗
PubMed1981

Lack of effect of ischemia and dipyridamole on prostacyclin production in arteriosclerosis obliterans.

Six patients with advanced arteriosclerosis obliterans in the lower extremities were subjected to an exercise test on a tread mill with and without dipyridamole treatment. Prostacyclin (PGI2) release was measured by the concentration of its stable metabolite, 6-keto-prostaglandin F1 alpha in plasma. All the patients suffered from ischemic pain during both tests, but no changes were seen in plasma 6-keto-PGF1 alpha. Dipyridamole did not affect the physical performance. Our results suggest that atherosclerotic vessels do not increase PGI2 production in response to ischemia and that a single dose of dipyridamole does not change PGI2 production.

6-Ketoprostaglandin F1 alpha↗
PubMed1981

Maternal plasma levels of 6-keto-prostaglandin F1alpha during pregnancy and puerperium.

To study the production of antiaggregatory and vasodilatory prostacyclin (PGI2) during human pregnancy and puerperium, we measured the concentrations of 6-keto-prostaglandin F1alpha, the stable hydration product of PGI2, with specific radio-immunoassay in plasma samples from 53 women between 11 and 41 weeks of normal pregnancy, 11 puerperal women 53-60 days postpartum and 20 healthy nonpregnant control women. The levels of 6-keto-PGF1alpha did not change during the course of pregnancy, and the mean (+/- SE) levels of 6-keto-PGF1alpha during pregnancy (255.5 +/- 8.7 pg/ml) or puerperium (254.7 +/- 12.3 pg/ml) were not significantly different from the mean level of 277.7 +/- 10.6 pg/ml in the nonpregnant control women. There was no correlation between the 6-keto-PGF1alpha concentration and pregnancy week, maternal age, parity or lactation. Thus, it is evident that PGI2, as measured by its metabolite levels in maternal plasma, does not change during human gestation.

6-Ketoprostaglandin F1 alpha↗
PubMed1981

Measurement of 6-keto-prostaglandin E1 alpha in human plasma with radioimmunoassay: effect of prostacyclin infusion.

A radioimmunoassay for 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha), a stable hydration product of prostacyclin (PGI2), is described. The method utilises plasma extraction with ethyl acetate and saturation analysis. Antiserum was produced in rabbits against 6-keto-PGF1 alpha-BSA conjugate, and its cross-reactions with 22 prostaglandins and related compounds were insignificant. The mean mass of added 6-keto-PGF1 alpha required to displace zero-point binding by 50 % was 55.6 +/- 5.1 pg (mean +/- SD, N = 10). The method blank was 7.8 +/- 2.4 pg/ml (N = 10), resulting in a detection limit of 12.6 pg/ml (mean blank + 2 SD). The intra-assay variation was between 4.1 - 8.2 % at concentrations between 150.3 pg/ml and 560.7 pg/ml (N = 10). The interassay variation was 12.4 % (N = 15). The recoveries of 100 pg/ml or 200 pg/ml added to the plasma samples (N = 10) were 90.2 % and 95.4 %, respectively. The 6-keto-PGF1 alpha concentrations in healthy subjects ranged from 92.7 to 394.5 pg/ml with a mean of 182.5 pg/ml in plasma. The presence of acetylsalicylic acid or indomethacin in the collection tubes caused no changes in plasma 6-keto-PGF1 alpha concentration. Intravenous infusion of PGI2 (1-8 ng/kg/min) into 6 healthy women caused linear increases in 6-keto-PGF1 alpha concentrations in plasma. After the discontinuation of PGI2 infusion, the 6-keto-PGF1 alpha levels decreased rapidly, the half-life being approximately 30 minutes.

6-Ketoprostaglandin F1 alpha↗
PubMed1981

Maternal hormone levels during Na 872 infusion in late pregnancy.

In order to assess the effects of Na 872 infusion on maternal endocrinology during late pregnancy, we measured serum estradiol, estriol, progesterone, human placental lactogen, follicle simulating hormone, prolactin, cyclic adenosine monophosphate, cortisol and insulin before, during and after Na 872 infusion (bromhexine 2 mg/min for one hour) in ten mothers. As compared to six control mothers, no changes could be observed. This suggests that the claimed maturing effect of Na 872 on the fetal lungs is not mediated by the hormonal changes measurable in maternal blood.

Adult↗