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L Viinikka

Publications and source records attributed to L Viinikka.

At least 19 recordsLinked to original sources
PubMed1997

Inducible nitric oxide and prostacyclin productions are differently controlled by extracellular matrix and cell density in human vascular endothelial cells.

Both cell-matrix and cell-cell interactions are important regulators of the function of most human cells. In this study we investigated how these interactions controlled the production of vasodilators nitric oxide (NO), and prostacyclin (PGI2), in freshly isolated human umbilical vein endothelial cells (HUVECs). On the reconstituted extracellular matrix (ECM) Matrigel freshly isolated HUVECs treated with interleukin-1 beta, lipopolysaccharide, and interferon-gamma, produced more NO, but less PGI2, than on gelatin substratum. High cell density was essential for inducibility of NO production in cells plated on gelatin substratum, but not on ECM. In cells plated on gelatin substratum at low cell density, which mimicked conventional HUVEC culturing conditions, both inducible NO production and the inducible NO synthase (iNOS) mRNA levels, detected by competitive RT-PCR, were low. However, inducible PGI2 production remained high in these cells. Highest inducible NO productions were observed in HUVECs that presumably had best maintained their original differentiated phenotype. Thus our data imply that the inducible NO and PGI2 productions of freshly isolated HUVECs were differently controlled by the extracellular matrix and cell density. Our data suggest that both cell-matrix and cell-cell interactions may have a strong influence on the proinflammatory cytokine responses of human vascular endothelial cells.

Cell Communication↗
PubMed1997

Long-chain 3-hydroxyacyl-coenzyme A dehydrogenase deficiency with the G1528C mutation: clinical presentation of thirteen patients.

Long-chain 3-hydroxyacyl-coenzyme A (CoA) dehydrogenase is one of three enzyme activities of the mitochondrial trifunctional protein. We report the clinical findings of 13 patients with long-chain 3-hydroxyacyl-CoA dehydrogenase deficiency. At presentation the patients had had hypoglycemia, cardiomyopathy, muscle hypotonia, and hepatomegaly during the first 2 years of life. Seven patients had recurrent metabolic crises, and six patients had a steadily progressive course. Two patients had cholestatic liver disease, which is uncommon in beta-oxidation defects. One patient had peripheral neuropathy, and six patients had retinopathy with focal pigmentary aggregations or retinal hypopigmentation. All patients were homozygous for the common mutation G1528C. However, the enoyl-CoA hydratase and 3-ketoacyl-CoA thiolase activities of the mitochondrial trifunctional protein were variably decreased in skin fibroblasts. Dicarboxylic aciduria was detected in 9 of 10 patients, and most patients had lactic acidosis, increased serum creatine kinase activities, and low serum carnitine concentration. Neuroradiologically there was bilateral periventricular or focal cortical lesions in three patients, and brain atrophy in one. Only one patient, who has had dietary treatment for 9 years, is alive at the age of 14 years; all others died before they were 2 years of age. Recognition of the clinical features of long-chain 3-hydroxyacyl-CoA deficiency is important for the early institution of dietary management, which may alter the otherwise invariably poor prognosis.

3-Hydroxyacyl CoA Dehydrogenases↗
PubMed1997

Different effects of oral and transdermal hormonal replacement on prostacyclin and thromboxane A2.

OBJECTIVE: To elucidate the mechanism of cardiovascular protection of hormone replacement therapy (HRT) by comparing the effect of oral and transdermal HRTs on the production of antiaggregatory, vasodilatory prostacyclin, and its endogenous antagonist, thromboxane A2. METHODS: Oral estradiol (2.0 mg/d) plus norethisterone acetate (1.0 mg/d) (n = 13) or transdermal estradiol (50 micrograms/d) plus medroxyprogesterone acetate (10 mg/d) as 12-day courses at 4-week intervals (n = 13) were given to postmenopausal women. Urinary excretion of the metabolites of prostacyclin, ie, 6-ketoprostaglandinF1 alpha and 2,3-dinor-6-ketoprostaglandinF1 alpha, as well as those of thromboxane A2, ie, thromboxane B2 and 2,3-dinor-thromboxane B2, were measured by radioimmunoassays, after purification by extraction and high performance liquid chromatography, before and during the sixth and the 12th treatment cycles. RESULTS: Oral HRT stimulated excretion of thromboxane B2 from 3.4 +/- 0.7 ng/mmol creatinine to 4.5 +/- 1.5 (mean +/- standard deviation, P < .05) and that of 2,3-dinor-thromboxane B2 from 16.6 +/- 8.0 ng/mmol creatinine to 26.2 +/- 10.7 (P < .01), and thus led to the dominance of thromboxane A2. No changes in prostanoids occurred during transdermal HRT. CONCLUSIONS: The effects of various HRTs on prostanoids may significantly differ.

Administration, Cutaneous↗
PubMed1997

High endothelin-1 in the airways of preterm infants is associated with less severe respiratory distress during the early postnatal period.

OBJECTIVE: To study the relationship between endothelin-1 (ET-1) in the airways and respiratory distress in preterm infants. METHODS: ET-1 was determined in 60 tracheal aspirates from 11 preterm intubated infants (gestational age 28.0 +/- 2.5 weeks) during the first week of life. RESULTS: The concentration of ET-1 of the aspirates was 6 to 2760 pg/mL (median 293 pg/mL). Negative correlations existed between mean log ET-1 and mean airway pressure (R2 = .812) and fraction of inspired oxygen (R2 = .591), whereas a positive correlation was found between the arteriolar/alveolar oxygenation ratio within 3 hours of birth and mean log ET-1 on the first day (R2 = .555). CONCLUSION: The association of high ET-1 in the airways with less severe respiratory distress in the early postnatal period may be attributable to effects of ET-1 on surfactant secretion or development of airway epithelium.

Endothelin-1↗
PubMed1996

Hirudin stimulates prostacyclin but not endothelin-1 production in cultured human vascular endothelial cells.

To study the effect of hirudin on endothelial cell prostacyclin (PGI2) and endothelin-1 (ET-1) production, we cultured human umbilical vein endothelial cells (HUVECs), stimulated them with 0.00001-10 kU/l of hirudin for 12-24 hours, and measured by radioimmunoassays the concentrations of 6-ketoprostaglandinF1 alfa (6-keto, a metabolite of PGI2) and ET-1 in the incubation medium. In incubation medium containing 10% serum hirudin stimulated PGI2-production dose-dependently. The lowest stimulatory hirudin concentration was 0.001 kU/l, which increased the concentration of 6-keto by 10.8 +/- 4.4% (mean +/- S.E) (p < 0.01). The greatest stimulation rate (28.6 +/- 6.2%, p < 0.001) was obtained with the highest hirudin concentration (10 kU/l), when the culture medium contained 10% human serum. The PGI2-stimulating activity was exaggerated in the absence of serum, when 1 kU/l of hirudin increased PGI2-production by 59.7 +/- 6.2% (p < 0.001, n = 14). Stimulation of PGI2 appeared after 12 hour incubation. Hirudin had no effect on the conversion of exogenous arachidonic acid to 6-keto or on the production of ET-1. We thus conclude that hirudin stimulates PGI2-production through de novo protein synthesis. Stimulation of PGI2-production by hirudin may contribute to its antithrombotic activity, since PGI2 favours vasodilatation and attenuates platelet aggregation.

Anticoagulants↗
PubMed1996

Effect of physiological concentrations of estradiol on PGI2 and NO in endothelial cells.

OBJECTIVES: To elucidate the mechanisms by which estrogens protect against occlusive vascular disorders, we studied the effect of 17 beta-estradiol on the production of prostacyclin (PGI2) and nitric oxide (NO) in primary cultures of human umbilical vein endothelial cells (HUVECs). METHODS: To study the effect of 17 beta-estradiol on PGI2 production, HUVECs were incubated in the absence and presence of 17 beta-estradiol (0.01-10 nmol/l) encapsulated within beta-cyclodextrin for 12 h in serum-free medium. To study the effect of 17 beta-estradiol (100 nmol/l) on maximal calcium-dependent NO production, we used different approaches. First, HUVECs were incubated with 2 mumol/l calcium ionophore A23187 with or without 17 beta-estradiol (100 nmol/l) for 24 h in serum-free medium. Second, HUVECs were preincubated with or without 17 beta-estradiol (100 nmol/l) for 12 h in medium supplemented with 2% fetal calf serum, and thereafter incubated in serum-free medium with 2 mumol/l of A23187 and with 100 nmol/l of 17 beta-estradiol (cells which contained 17 beta-estradiol during the preincubation period as well as cells which did not) or without it (only cells which did not contain 17 beta-estradiol during the preincubation period) for 6 h or 24 h. RESULTS: 17 beta-Estradiol (0.1 nmol/l) increased the concentration of 6-keto-prostaglandin F1 alpha, a stable metabolite of PGI2 in the incubation medium, by 16%, and no further increase occurred with higher 17 beta-estradiol concentrations. The stimulation was prevented by tamoxifen. 17 beta-Estradiol did not affect NO production in any of our experiments measured as accumulation of nitrate and nitrite in the experimental medium. CONCLUSIONS: The stimulatory effect on PGI2 production of physiological concentrations of 17 beta-estradiol, shown now for the first time, may provide one explanation for the ability of 17 beta-estradiol to protect against occlusive vascular disorders.

Culture Techniques↗
PubMed1996

The calcium-dependent nitric oxide production of human vascular endothelial cells in preeclampsia.

OBJECTIVE: Nitric oxide is an important vasodilator, and in this study we studied whether the calcium-dependent nitric oxide production capacity of human umbilical vein endothelial cells was affected by preeclampsia. STUDY DESIGN: Human umbilical vein endothelial cells were isolated from 11 preeclamptic and 10 normotensive pregnancies. The maximal calcium ionophore A23187-stimulated nitric oxide production capacity was measured as accumulation of nitrate and nitrite into the culture medium, and it was related to the number of viable endothelial cells by measurement of their mitochondrial dehydrogenase activity. RESULTS: The cell number-related nitric oxide production capacity was similar in preeclamptic and normotensive pregnancies. The total nitric oxide production of cells from preeclamptic pregnancies was significantly lower (p <0.001). This difference, however, was mainly caused by larger amount of viable endothelial cells recovered from normotensive pregnancies. CONCLUSION: The maximal calcium-dependent nitric oxide production capacity of individual human umbilical vein endothelial cells is not affected by preeclampsia.

Adult↗
PubMed1996

Hormone replacement therapy modifies the capacity of plasma and serum to regulate prostacyclin and endothelin-1 production in human vascular endothelial cells.

OBJECTIVE: To determine if hormone replacement therapy (HRT) modifies the ability of plasma or serum to regulate the synthesis of vasodilatory prostacyclin and that of vasoconstrictive endothelin-1 by cultured human umbilical vein endothelial cells. DESIGN: Plasma and serum collected before and during the sixth treatment cycle of HRT from 13 healthy postmenopausal women were added to cultured endothelial cells. SETTING: Helsinki University Central Hospital, Department of Obstetrics and Gynecology, Helsinki, Finland. PATIENTS: Thirteen postmenopausal women (> or = 1 year since their last menstruation, FSH level > 40 mIU/mL [conversion factor to SI unit, 1.00], clear vasomotor symptoms) that suffered from incapacitating menopausal symptoms necessitating the initiation of HRT were studied. INTERVENTIONS: A combined regimen consisting of 2 mg oral E2 for 12 days followed by 2.0 mg oral E2 + 1.0 mg norethisterone acetate for 10 days and 1.0 mg E2 for 6 days. MAIN OUTCOME MEASURES: The releases of prostacyclin, as assessed by its metabolite 6-keto-prostaglandin F1 alpha, and that of endothelin-1 by cultured human umbilical vein endothelial cells in the presence of 10% plasma or 10% serum collected from the study subjects. RESULTS: Hormone replacement therapy enhanced the ability of plasma to stimulate prostacyclin production by 21% +/- 6% (mean +/- SEM) during the E2 + norethisterone acetate phase and tended to do so also during the E2-only phase (11% +/- 10%) but caused no change in endothelin-1 release. In contrast, HRT decreased the ability of serum to stimulate prostacyclin production by 12% +/- 5% during the E2-only phase and increased that of endothelin-1 by 8% +/- 4% during the E2 + norethisterone acetate phase. CONCLUSION: Because plasma flushes endothelial cells in vivo, our data on the HRT-induced stimulation of the capacity of plasma to enhance the production of vasoprotective prostacyclin without a concomitant change in endothelin-1 release in cultured human umbilical vein endothelial cells may provide one new explanation for the cardiovascular protection of HRT.

Blood Physiological Phenomena↗
PubMed1996

High bone density in hyperandrogenic women: effect of gonadotropin-releasing hormone agonist alone or in conjunction with estrogen-progestin replacement.

We studied 20 hirsute patients with high levels of serum testosterone (T), calculated free T, androstenedione, and dehydroepiandrosterone sulfate and 19 age-matched nonhirsute normoandrogenic control women. The bone mineral density (BMD) in the lumbar spine, femoral neck, and trochanter major region in hirsute patients was higher than that in the controls. BMD in the lumbar spine and proximal femur correlated positively with the body mass index and with serum T and free T in hyperandrogenic women and the whole study group, but not with serum androstenedione or dehydroepiandrosterone sulfate levels. The hirsute women were treated with a GnRH agonist (goserelin, 3.6-mg implant) for 9 months. After the first 3 months of treatment, half of the patients were randomized to receive estrogen-progestin replacement therapy (HRT), and the other half served as controls. After the first 3 months of trial, BMD was unaffected, and the urinary output of collagen pyridinoline, deoxypyridinoline cross-links, and hydroxyproline (all markers of bone resorption) were increased, but serum markers, the carboxy-terminal telopeptide of type I collagen (marker of bone resorption) and that of bone-specific alkaline phosphatase (marker of bone formation) did not change. After 9 months of goserelin treatment, the lumbar spine had lost 5.4% of its BMD (P < 0.01), but regained bone density 6 months after cessation of treatment. Addition of HRT protected the spine and trochanter major against bone loss. The changes in serum telopeptide and urinary output of pyridinoline and deoxypyridinoline after 3 months of treatment (from prestudy levels) correlated with the decrease in BMD in the femoral neck at 9 months. In conclusion, our data show that patients with ovarian androgen excess 1) have high BMD, 2) lose bone during 9 months of treatment with GnRH agonist, 3) show a decrease in bone density preceded by biochemical alterations in bone metabolism at least 6 months earlier, and 4) can have their bone loss prevented by add-back HRT.

Adult↗
PubMed1996

Nitric oxide as a challenge for the clinical chemistry laboratory.

Nitric oxide (NO) is an important intra- and intercellular mediator. Although NO can be measured using many different chemical methods, the compound is challenging for a clinical chemistry laboratory, since its half-life in vivo in humans is only a few seconds. Most of the NO is oxidized to nitrite/nitrate, and the concentrations of these anions have been used as quantitative indices of NO production. The simplest and most widely used technique is spectrophotometric measurement of nitrite using the Griess reaction. Nitrate, the main metabolite of NO in blood and urine, must be reduced to nitrite before the colour reaction. Other methods used for measuring nitrite/nitrate in human blood or urine include high-performance liquid chromatography, gas chromatography-mass spectrometry, chemiluminescence, enzymatic assay with nitrate reductase and electron paramagnetic resonance. The reported mean concentrations of nitrite in the blood of healthy adults have varied from non-existent to 4.2 mumol l-1, and those of nitrate from 19.7 to 44 mumol l-1. The technical measurement of nitrite/nitrate is obviously reliable, but there are problematic preanalytical factors. Normal daily food contains more nitrate than that formed from NO, and thus diet-derived nitrate may contribute considerably to the concentration in blood. The problem may to some extent be solved with dietary restrictions, but it is questionable whether the confounding effect of diet-derived nitrate can be totally avoided. Therefore, better methods for measuring the production of NO in vivo would be very welcome.

Adult↗
PubMed1995

Serum lipoproteins, insulin, and urinary prostanoid metabolites in normal and hypertensive pregnant women.

OBJECTIVE: To determine if hyperinsulinemia, hypertension, hypertriglyceridemia, and low levels of high-density lipoprotein (HDL) cholesterol are present in women with pregnancy-induced hypertension or preeclampsia. METHODS: Serum concentrations of insulin, uric acid, total and lipoprotein cholesterol, triglyceride, and apolipoproteins A-I and B were measured in 31 women with pregnancy-induced hypertension (eight with proteinuria) and in 21 healthy, pregnant, weight-matched controls at 30-39 weeks' gestation. The urinary excretion of the stable metabolites of prostacyclin (PGI2) (6-keto-prostaglandin [PG] F1 alpha and 2,3-dinor-6-keto-PGF1 alpha) and thromboxane A2 (TxA2) (thromboxane B2 and 2,3-dinor-thromboxane B2) was assessed in 17 women with pregnancy-induced hypertension and in eight controls. RESULTS: Women with pregnancy-induced hypertension exhibited 18% lower mean serum HDL2 cholesterol levels (0.9 versus 1.1 mmol/L, P < .05) and 65% higher mean triglyceride levels (3.3 versus 2.0 mmol/L, P < .05) compared to controls, whereas other serum lipid and apolipoprotein values did not differ significantly in the two groups. Mean serum insulin levels (13.3 versus 6.5 mU/L, P < .01) and uric acid levels (339.7 versus 231.2 mumol/L, P < .01) in patients with pregnancy-induced hypertension were significantly higher than those in the controls. Urinary output of PGI2 metabolites was reduced by 35-45% in patients with pregnancy-induced hypertension, whereas no differences were seen in the excretion of TxA2 metabolites. Serum HDL2 cholesterol concentrations correlated positively with 2,3-dinor-6-keto-PGF1 alpha excretion, and serum triglyceride concentrations correlated positively with 2,3-dinor-thromboxane B2 excretion. In addition, insulin levels correlated positively with triglyceride levels but negatively with HDL2 cholesterol concentrations. CONCLUSION: The metabolic characteristics (hypertriglyceridemia, hyperinsulinemia, hyperuricemia, low HDL2 cholesterol) in pregnancy-induced hypertension resemble the main features of the "insulin resistance syndrome." This may result in endothelial cell dysfunction as evidenced by PGI2 suppression.

Apolipoprotein A-I↗
PubMed1995

Prostacyclin and thromboxane in pregnant and nonpregnant women in response to exercise.

OBJECTIVES: To compare the effects of a 30-minute standardized submaximal exercise test on the urinary excretion of the metabolites of prostacyclin and thromboxane A2 in healthy pregnant and nonpregnant women. METHODS: Time-fixed urine samples were collected before, during, and after the exercise test from nine pregnant and six nonpregnant women, and the samples were assayed for 6-keto-prostaglandin (PG) F1 alpha and 2,3-dinor-6-keto-PGF1 alpha (prostacyclin metabolites), as well as for thromboxane B2 and 2,3-dinor-thromboxane B2 (thromboxane A2 metabolites) by high-pressure liquid chromatography and radioimmunoassay. RESULTS: Pregnancy itself was associated with a 3.6-4.3-fold rise in prostacyclin excretion, but with no significant change in thromboxane output. The exercise caused stimulation in both prostacyclin and thromboxane excretion. In response to exercise, the maximal rise in 6-keto-PGF1 alpha output was significantly larger among the pregnant subjects, but when compared with its pre-exercise excretion on a relative percentage scale, the range of rise in 6-keto-PGF1 alpha output (58-73%) was comparable in pregnant and nonpregnant subjects. Furthermore, excretion of 2,3-dinor-6-keto-PGF1 alpha rose similarly in the two study groups (68-166%) in response to exercise. The exercise caused a 2.3-fold rise in the output of thromboxane B2 excretion in both pregnant and nonpregnant women, but it stimulated (by a twofold rise) the excretion of 2,3-dinor-thromboxane B2 only in pregnant women. CONCLUSION: Physical activity may stimulate vasoactive prostacyclin and thromboxane excretion during pregnancy. Such changes may play a role in the regulation of blood flow during exercise.

6-Ketoprostaglandin F1 alpha↗
PubMed1995

Postmenopausal hormonal replacement decreases plasma levels of endothelin-1.

Hormone replacement therapy (HRT) protects against cardiovascular disorders, but the mechanisms of this action are poorly understood. We assessed the plasma levels of vasoconstrictive endothelin-1 (ET-1) in 26 healthy postmenopausal women before and during HRT. The women were randomized to receive either continuous transdermal (estradiol 50 ug/24 hrs) complemented with periodic 12 days' courses with medroxyprogesterone (10.0 mg/day)(n = 13) or continuous oral estradiol (2.0 mg/day) and continuous norethisterone acetate (1.0 mg/day)(n = 13). ET-1 was measured with specific radioimmunoassay after concentrating the sample with solid phase extraction. Pretreatment plasma ET-1 (1.28 +/- 0.36 pmol/ml, mean +/- SD) in the whole study group decreased (p < 0.01) to 1.05 +/- 0.26 pmol/ml at 6 months and to 1.10 +/- 0.32 pmol/ml at 12 months of treatment. A subgroup analysis between the two HRT regimens revealed no significant differences in the response of plasma ET-1 to HRT. These first data on HRT-induced reduction in plasma ET-1 may provide a new explanation for the cardiovascular protection by HRT.

Administration, Cutaneous↗
PubMed1995

17 beta-estradiol stimulates prostacyclin, but not endothelin-1, production in human vascular endothelial cells.

The exact mechanisms by which estrogens protect against occlusive vascular disorders are not known. One possibility could be an effect on vascular endothelial vasoactive compounds, such as vasodilatory prostacyclin (PGI2) and vasoconstrictory endothelin (ET-1). Here we report on the effect of 17 beta-estradiol on the synthesis of PGI2 and ET-1 in cultured human umbilical vein endothelial cells. These cells were incubated in the absence (control) and presence of 17 beta-estradiol (0.001-1 mumol/L) for 3-24 h with serum (10%) or without serum. The release of PGI2, as assessed by its metabolite 6-keto-prostaglandin F1 alpha, and that of ET-1, were assessed by RIA. 17 beta-Estradiol (0.01-0.1 mumol/L) predissolved in ethanol (final concentration, 0.01%) increased PGI2 production by 26-30% in endothelial cells incubated without serum. This increase in PGI2 production was enhanced up to 66% when 17 beta-estradiol (1 mumol/L) was encapsulated within beta-cyclodextrin. The stimulation of PGI2 production was detectable after 12 h of incubation. The 17 beta-estradiol-induced stimulation of PGI2 production was blocked in dose-dependent manner by antiestrogenic tamoxifen. 17 beta-Estradiol failed to affect the production of PGI2 if the endothelial cells were incubated with serum and had no effect on ET-1 production under any conditions. 17 beta-Estradiol-induced stimulation of vasodilatory and antiaggregatory PGI2 production without a concomitant change in vasoconstrictory ET-1 production may provide one explanation for the ability of estradiol to maintain vascular health and protect against vascular disorders.

6-Ketoprostaglandin F1 alpha↗
PubMed1994

Serum transferrin receptor and erythropoiesis in children with newly diagnosed acute lymphoblastic leukemia.

Thirty-five children with acute lymphoblastic leukemia were monitored weekly during the first 12 weeks of chemotherapy. The transferrin receptor (TfR) concentration was 2.8 +/- 0.2 mg/l (mean +/- S.E.M.) at diagnosis, decreased up to 3 weeks, and then increased reaching a maximal level at 8 weeks. The mean values for reticulocyte counts followed a similar pattern. In contrast, serum erythropoietin and ferritin levels were generally high. Those patients whose erythropoiesis was more accelerated had higher serum TfR concentrations. We conclude that among these patients the TfR level reflected the rate of erythropoiesis and was independent of the level of erythropoietin.

Child↗
PubMed1994

Erythropoiesis of very low-birth-weight infants dependent on prenatal growth rate and protein status.

This study investigated erythropoiesis in very low-birth-weight infants with special reference to the role of protein status in the regulation of erythropoiesis in 22 appropriate- and 11 small-for-gestational-age infants. Blood samples were drawn at three and six weeks of age. The serum concentrations of erythropoietin, estimated by a solid-phase enzyme immunoassay, were similar in the two groups at both study ages. The total circulating erythrocyte volume and the serum concentration of prealbumin were higher in the appropriate- than in the small-for-gestational-age infants at three and six weeks of age. The former group had a better protein status, although their protein intake was similar or lower. We conclude that erythropoiesis in very low-birth-weight infants is influenced more by protein status and prenatal growth than by serum concentration of erythropoietin.

Embryonic and Fetal Development↗
PubMed1993

Human serum, plasma, and platelets stimulate prostacyclin and endothelin-1 synthesis in human vascular endothelial cells.

Prostacyclin (PGI2), a powerful vasodilatory prostanoid, and endothelin-1 (ET-1), a potent vasoconstrictive peptide, are produced by vascular endothelial cells. We show that human serum (10%) caused a 3.2-fold stimulation both in PGI2 and ET-1 synthesis in human endothelial cells cultured from umbilical veins, and human plasma (10%) stimulated productions of both 1.6- and 1.7-fold, respectively. In addition, releasates from thrombin-activated platelets (20 x 10(9) platelets/l) caused a 1.9-fold increase in PGI2 and a 1.4-fold increase in the ET-1 synthesis. Releasates from frozen-thawed and sonicated platelets (20 x 10(9) platelets/l) caused a 3.6-fold increase in PGI2 release but did not affect ET-1 production. We thus conclude that, in normal situation, endothelial stimulating activity present in plasma perhaps plays a role in the regulation of endothelial function, whereas platelet-derived activity in serum may be important at site of thrombosis.

Blood Physiological Phenomena↗