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PubMed1980

[Platelet aggregation and prostaglandin turnover in man during defined linoleic acid supply with formula diets (author's transl)].

A report is given on changes of platelet aggregation and prostaglandin turnover during a cross-over experiment with six female volunteers being given a linoleic acid supply with formula diets of 0 g or 50 g daily. Collagen- and ADP-induced platelet aggregation was determined with a Borne-type aggregometer. Prostaglandin turnover was measured by analyzing the excretion of a joint derivative of prostaglandin metabolites, tetranorprostanedioic acid, in urine. With a linoleic acid supply of 50 g daily we found an increase of tetranorprostanedioic acid in urine, while platelet aggregation decreased. When the experimental subjects came from a conventional diet (linoleic acid intake 20 g daily) these changes were seen later than after a linoleic acid free formula diet. A linoleic acid-deficient formula diet caused a fall in prostaglandin turnover within 24 hr. ADP-induced platelet aggregation was unchanged after 1 week, while collagen-induced platelet aggregation was increased after 1 and 3 weeks of linoleic acid-deficient diet. These results clearly demonstrate the influence of nutrition on platelet aggregation.

Adult↗
PubMed1982

Identification of a 'urinary-type' metabolite of prostaglandin F2 alpha in the rat circulation.

During constant slow intravenous infusion of tritiated prostaglandin F2 alpha into male adult rats, a major portion of radioactivity in blood appeared as a new metabolite, identified as tetranor-15-keto-13,14-dihydroprostaglandin F2 alpha (18.8 +/- 4.2%, n = 7). The previously recognised blood metabolite, 15-keto-13,14-dihydroprostaglandin F2 alpha, was also observed (15.1 +/- 4.1%, n = 7). 15-keto-13,14-Dihydroprostaglandin F2 alpha disappeared quickly from the circulation while tetranor-15-keto-13,14-dihydroprostaglandin F2 alpha was still detected (8.6 +/- 2.8%, n = 3) 2 h after infusion was stopped. These results indicate that tetranor-15-keto-13,14-dihydroprostaglandin F2 alpha, because of its slow disappearance from the circulation, may provide a better indicator than 15-keto-13,14-dihydroprostaglandin F2 alpha of prostaglandin F2 alpha synthesis in vivo.

Animals↗
PubMed1986

Activation of protein kinase C by the action of 9,11-epithio-11,12-methano-thromboxane A2 (STA2), a stable analogue of thromboxane A2, in human platelets.

Incubation of human washed platelets with 9,11-epithio-11, 12-methano-thromboxane A2 (STA2), a stable analogue of thromboxane A2, caused the activation of protein kinase C and myosin light chain (MLC) kinase to the same extents as those induced by thrombin as judged by measuring the phosphorylation of a 40-kilodalton protein and MLC, respectively. However, STA2 stimulated much less phosphoinositide turnover than thrombin. Furthermore, the doses of STA2 necessary for protein kinase C activation and phosphoinositide turnover were higher than those necessary for MLC kinase activation, although the doses of thrombin necessary for these three reactions were nearly the same. These results suggest that protein kinase C may be activated at the Ca2+ concentrations higher than those required for MLC kinase activation by the action of STA2, presumably due to the inability of this agonist to produce diacylglycerol in an amount enough to increase the affinity of the enzyme for Ca2+.

Blood Platelets↗
PubMed1987

Influence of thromboxane receptor-antagonists on the interaction of platelets with solid-phase immobilized human collagen.

The interaction of blood platelets with surfaces coated with human type I, III, IV, and V collagen (CI, CIII, CIV, and CV) has been studied. Using scanning electron microscopy it was demonstrated that the reactivity of the collagen substrates for platelets varies widely. In contrast to CV and CIV, on surfaces coated with CI and CIII, along with spreading, the formation of thrombi-like platelet aggregates occurs. Previously, it was demonstrated that this thrombogenesis in vitro correlates well with the synthesis of platelet prostanoids, and is sensitive to inhibitors of TXA2-synthesis. Therefore, we have investigated the influence of the TXA2/PGH2 receptor-antagonists, 13-azaprostanoic acid (13-APA) and the BM 13.177 compound, on the formation of thrombi-like platelet aggregates on CI and CIII-coated surfaces. It was demonstrated that both 13-APA and BM 13.177 cause a dose-dependent inhibition of the thrombogenesis without any effect on the initiation of the thrombogenesis without any effect on the initial attachment and the spreading of platelets on collagen-coated surfaces. The obtained data suggest that (1) the formation of platelet aggregates on CI and CIII-coated surfaces is triggered by platelet prostanoids; (2) TXA2/PGH2 receptor-antagonists may be useful as antithrombotic drugs.

Blood Platelets↗
PubMedDate not supplied

Anti-aggregatory prostanoids. Part II.

The mechanism of antiplatelet potency of prostanoids and pharmacological methods that regulate their endogenous release are discussed. In addition the role of antiaggregatory prostanoids in atherosclerosis and some clinical trials with prostanoids are reviewed.

Animals↗
PubMed1980

Effects of dietary variation in linoleic acid content on the major urinary metabolites of the E prostaglandins (PGE-M) in infants.

1. EFA deficiency is associated with the impairment of prostaglandin E synthesis, which is reflected by the decrease of the urinary excretion of PGE-M. 2. Excessive administration of Intralipid results in increase of the relative concentrations of linoleic acid content in plasma, RBC, and tissues with a concomitant decrease of its higher homologue, arachidonic acid. These changes are associated with diminished PGE-M excretion similar to that seen in EFA deficiency. Further investigation is needed into the pathophysiologic consequences of EFA deficiency and the excessive administration of linoleic acid since both are associated with altered prostaglandin biosynthesis and turnover in the new-born infant, particularly among those stressed low birth weight infants whose nutritional status and management are an indication for these modes of therapy.

Dietary Fats↗
PubMed1985

Eicosanoid modulation of stress fibers in cultured bovine aortic endothelial cells.

Leukotrienes (LT) B4, LTD4, and thromboxanes (TX) are cytotoxic, and increase microvascular permeability. Because endothelial stress fibers are theorized to be part of the cytoskeletal mechanism by which microvessels maintain their barrier function, the effect of these eicosanoids on stress fibers in bovine aortic endothelial cells was tested. LTB4, LTD4, and TXB2 each decreased stress fiber numbers by 93%, 62%, and 66%, respectively, when compared to controls (P less than 0.01). In contrast, endothelial cells treated with prostacyclin (PGI2) at 10(-7) M, produced a significant increase (P greater than 0.01) in stress fiber numbers, 211% to that of controls. Azaprostanoic acid (13-APA) and FPL55712, receptor antagonists to TX and slow-reacting substance of anaphylaxis (SRS) receptors, respectively, the cyclooxygenase inhibitor ibuprofen, and the TX synthase inhibitors imidazole and ketoconazole were used to test for possible endothelial cell receptor mediation and de novo prostanoid synthesis associated with inflammatory eicosanoid-induced disassembly of stress fibers. Each pharmacologic agent inhibited the LTD4- and TXB2-induced decreases in stress fibers; LTB4-stimulated stress fiber decreases were inhibited only by pretreatment with TX synthase blockers. These data suggest that increased permeability associated with inflammatory eicosanoid metabolites may have as a common target stress fiber disassembly, and the mechanism may be receptor-mediated. That cyclooxygenase and TX synthase blockers inhibited the eicosanoid action suggests that endogenous TX synthesis may be a step in the mechanism. PGI2 enhancement of the microvascular barrier may be related to the effect of PGI2 on promoting stress fiber assembly. In summary, endothelial cell synthesized autocoids derived from arachidonic acid may help to regulate microvascular permeability by way of their action on stress fiber assembly/disassembly, and unbalanced prostanoid secretion by way of LT stimulation may result in a loss of the microvascular barrier and increased permeability.

Actin Cytoskeleton↗
PubMed1979

The identification of 5beta,7alpha-dihydroxy-11-oxotetranor-prostane-1,16-dioic acid as a urinary metabolite of prostaglandin F2alpha in the rat.

5beta,7alpha-Dihydroxy-11-oxotetranor-prostane-1,16-dioic acid has been identified by gas chromatography-mass spectrometry as a urinary metabolite of [9beta-3H]prostaglandin F2alpha in the rat. This tetranor prostaglandin F derivative, which is the 5beta epimer of the major urinary metabolite of prostaglandin F2alpha, accounted for at least 2% of the total dose. Absence from the metabolite of tritium label at the C-5 position indicated the existence of a minor, previously unknown metabolic pathway by which prostaglandin Falpha derivatives may be converted by oxido-reduction into prostaglandins of Fbeta stereochemistry.

Animals↗
PubMed1989

Role of prostanoids in cerebrovascular responses during seizures in piglets.

We examined the role of prostanoids to bicuculline-induced seizures in newborn pigs. Using the closed cranial window method and radioimmunoassay for prostanoids, we found that pial arterioles dilated during seizures; this dilation was associated with increased cortical periarachnoid cerebrospinal fluid (CSF) levels of prostaglandin E2, 6-ketoprostaglandin F1 alpha, prostaglandin F2 alpha, and thromboxane B2. Using radioactive microspheres, we found cerebral blood flow (CBF) increased dramatically during seizures in piglets. To examine the effects of pharmacological blockade of cyclooxygenase, we determined CBF in piglets pretreated with indomethacin (5 mg/kg) and in a corresponding group of piglets made hypothermic to be sure preseizure CBF values were similar. In the hypothermic group, CBF increased during seizure, but the increase in CBF during seizure in the indomethacin group was reduced dramatically in all brain areas. We conclude that 1) bicuculline-induced seizures result in pial arteriolar dilation and increased CBF; 2) CSF levels of prostanoids increase during seizures; and 3) pretreatment with indomethacin severely blunts increases in CBF during seizures.

Animals↗
PubMed2003

Influence of dietary linoleic acid intake with different fat intakes on arachidonic acid concentrations in plasma and platelet lipids and eicosanoid biosynthesis in female volunteers.

BACKGROUND/AIM: N-6 fatty acids are considered to promote diseases prevalent in industrialized countries and characterized by an increased eicosanoid biosynthesis from arachidonic acid (AA). We investigated the impact of the linoleic acid (LA) intake on AA levels in humans. METHODS: Six healthy female volunteers (age range 23-34 years) were given liquid formula diets (LFD) devoid of AA for 6 weeks, providing a constant intake of zero energy% (LFD 0: protein 15%, carbohydrates 85%) or 20 energy% (LFD 20: protein 15%, carbohydrates 55%, fat 30%) LA, for 3 weeks each. Fatty acids of plasma cholesteryl esters and platelet lipids were determined each week, and the prostaglandin biosynthesis was measured in 24-hour urine samples. RESULTS: LFD 0 increased (+31% of initial value) and LFD 20 lowered (-30% of initial value) the percentage of AA in plasma cholesteryl esters and platelet lipids. Moreover, absence of dietary AA lowered the percentages of AA in plasma (-31% week 0 vs. week 6) and platelet (-11%) lipids, indicating a low transformation of LA. LFD 0 reduced urinary metabolite levels of prostaglandins D, E, and F in 24-hour urine samples (-48%, p < 0.001) within 24 h, but did not significantly affect platelet aggregation (-10%) and thromboxane formation (-25%). LFD 20 significantly lowered platelet aggregation (-25%) and thromboxane formation (-43%). The prostaglandin metabolite levels increased during the first 10 days, declined thereafter, and were lower than the preexperimental values at the end of the 3-week period. CONCLUSIONS: The results show that dietary LA does not increase the AA levels in plasma or platelet lipids and does not persistently contribute to prostaglandin biosynthesis which is increased by AA intake with Western diets.

Adult↗
PubMed1991

Endogenous vasoconstrictor prostanoids: role in serotonin and vasopressin-induced coronary vasoconstriction.

A vasoconstrictor-induced prostacyclin (PGI2) production in a perfused rat heart was found, suggesting a mitigating role of PGI2 on coronary vasoconstriction. Treatment of the heart with cyclooxygenase inhibitors (aspirin or indomethacin) decreased PGI2 production by more than 90% and paradoxically reduced the vasoconstriction response. The attenuating effect of cyclooxygenase blockade suggested that endogenous prostanoids contribute to serotonin-, vasopressin- or U46619-induced vasoconstriction. Two prostaglandin (PG) H2/thromboxane A2 (TXA2) receptor antagonists, i.e., 13-azaprostanoic acid (13-APA) and SQ 29,548 were used to investigate putative endogenous vasoconstrictor prostanoids on the exogenously induced vasoconstriction. Retrogradely perfused (5-6 ml/min) rat hearts were rendered guiescent, yet responsive to stimuli, by local injection of lidocaine to the atrioventricular node. Changes in coronary vascular resistance (i.e., perfusion pressure at constant flow) were monitored and the cardiac effluent was collected for analysis of 6-keto PGF1 alpha (the stable metabolite of PGI2) as well as PGF2 alpha by radioimmunoassay. Three vasoconstrictors, i.e., serotonin, vasopressin and the TXA2/PGH2 analog U46619, as well as authentic PGD2, PGE2 and PGF2 alpha were infused. PGD2, PGE2 and PGF2 alpha exerted a dose-related coronary vasoconstriction, as did U46619, serotonin and vasopressin. Treatment with 13-APA (100 microM) or SQ 29,548 (100 nM) almost abolished U46619-induced vasoconstriction. The addition of PGH2/TXA2 receptor antagonists also significantly reduced the pressor effect of exogenously administered PGs, serotonin and vasopressin, with the exception that SQ 29,548 did not significantly antagonize PGE2-induced vasoconstriction.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1985

Prostaglandin formation and platelet aggregation during fasting and linoleic acid intake.

Prostaglandin formation, estimated by the determination of tetranorprostanedioic acid (TNPDA) in the urine, and platelet aggregation were investigated in seven healthy volunteers each day during fasting, and in three of them additionally during intake of carbohydrates (328kcal/day) or safflor oil (328 kcal, 20 g linoleic acid). Monitoring TNPDA in 8-h fractions of the urine showed a reduction during the night (23.00-07.00) by 70% on the average. During Days 1 and 2 of fasting the amount of TNPDA in 24-h urine was the same as under a conventional diet. On Day 3, TNPDA decreased in all experimental subjects to 162 micrograms/day on the average and was not changed by carbohydrate intake. A linoleic acid intake of 20 g/day increased TNPDA in 24-h urine to pre-experimental levels measured under free diet. Platelet aggregation did not change during the experiment. No relationship between prostaglandin formation and lipolysis in man was found.

Adult↗
PubMed1986

Enteropooling in piglets induced by soya-peptone mediated via an increased biosynthesis of prostanoids.

The enteropooling activity of soya-peptone was studied in germfree piglets. The enteropooling activity was restricted to the proximal part of the jejunum and was found to be blocked by aspirin. The hypothesis that soya-peptone acts via an increased biosynthesis/release of prostanoids was further studied using guinea-pig lung parenchyma. In this tissue soya-peptone induces the release of TXB2, which was inhibited by indomethacin (3 microM). The involvement of cholinergic, histaminergic and serotonergic pathways in the soya-peptone-mediated response was excluded, using antagonists. The conclusion was reached that soya-peptone can stimulate/modulate the biosynthesis of cyclic eicosanoids and that it exerts its enteropooling activity via the same mechanism in the jejunum of piglets.

Animal Feed↗