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Biomedical subjects

M A Barradas

Publications and source records attributed to M A Barradas.

103 records · Page 6Linked to original sources
PubMed1983

Effect of nonesterified fatty acids on the stability of prostacyclin activity.

The half-life of the platelet antiaggregatory activity of prostacyclin (PGI2) is prolonged when PGI2 is incubated in human plasma or in fatty-acid-free human albumin solutions. This "PGI2-protective" effect is diminished when fatty acids are added to the incubate, and the diminution is proportional to the concentration of the nonesterified fatty acids added. Unsaturated fatty acids were more potent in causing this reduction than saturated acids. It is possible that nonesterified fatty acids displace PGI2 from binding sites on the albumin molecule and that they may thus alter the biologic half-life of any circulating PGI2. This observation may partly account for the well-documented association between raised serum nonesterified fatty acid levels and thrombosis/platelet activation.

Buffers↗
PubMed1983

Platelet hyperaggregability and increased alpha-adrenoceptor density in anorexia nervosa.

Plasma norepinephrine concentrations in a group of malnourished patients with anorexia nervosa were significantly (P less than 0.002) lower than those in an age- and sex-matched group of normal subjects. Platelet total alpha-adrenoceptor densities of these patients significantly (P less than 0.002) exceeded those of the controls. The increased total alpha-adrenoceptor density was due to an increase in the alpha 2-adrenoceptor receptor subtype, which mediates epinephrine-induced platelet aggregation. Accordingly, the aggregation response of the patients' platelets was significantly (P less than 0.002) enhanced after epinephrine challenge. We suggest that the starvation-induced fall in plasma norepinephrine levels is associated with the up-regulation of platelet alpha-adrenoceptors. This, in turn, accounts for exaggerated epinephrine-induced platelet aggregation in anorexic patients.

Adolescent↗
PubMedDate not supplied

The effect of ethanol on platelet function and vascular prostanoids.

The present review will discuss the effects of ethanol on platelet function and vascular prostanoids. Whenever possible we have considered human studies because there are marked species differences in platelet function and vascular prostanoid release even in the absence of ethanol. Because of the specialised nature of some parts of the text, we have included brief introductions to help readers who are not familiar with this field.

Alcoholism↗
PubMedDate not supplied

Does human placenta produce prostacyclin?

We have previously demonstrated that the human placenta possesses potent platelet anti-aggregatory activity. This activity was exhibited only when aggregation was induced by adenosine diphosphate (ADP), but not when induced by adrenaline, ristocetin or collagen. We have also shown that placental extracts degrade ADP. We therefore concluded that the placenta's anti-aggregatory activity, in vitro, was not due to prostacyclin (PGI2) but to an 'ADPase'. In view of some reports claiming that the human placenta produces PGI2, we carried out a series of experiments to establish whether human placental tissue can convert [14C]-arachidonic acid [( 14C]-AA) to 6-oxo-PGF1 alpha, the stable metabolite of PGI2. Tissue from placenta and the membranes did not show any appreciable conversion of [14C]-AA into 6-oxo-PGF1 alpha. This finding was confirmed by radioimmunoassay techniques where the placenta was shown to produce spontaneously only minimal amounts of 6-oxo-PGF1 alpha. We conclude that placental tissue and the fetal membranes do not synthesize a significant amount of PGI2, certainly not enough to account for the potent platelet anti-aggregatory activity of the placenta in vitro. Placental platelet anti-aggregatory activity in vitro, is probably due entirely to ADPase activity.

6-Ketoprostaglandin F1 alpha↗
PubMedDate not supplied

The effect of non-esterified fatty acids on vascular ADP-degrading enzyme activity.

Following our observations that non-esterified fatty acids (NEFAs) inhibit prostacyclin (PGI2) synthesis and accelerate PGI2 degradation, we have examined the possibility that NEFAs may also affect the activity of vascular ADPase, which converts the platelet pro-aggregatory adenosine diphosphate (ADP) to adenosine, an inhibitor of aggregation and a vasodilator. Incubation, in buffer solutions, of NEFAs with intact rat aortic rings significantly inhibited vascular ADPase activity. This inhibition was more marked at higher NEFA concentrations and with unsaturated fatty acids (linoleic, oleic) than with a saturated fatty acid (stearic). This NEFA-mediated inhibition of vascular ADPase activity could be prevented by the prior addition of fatty acid-free human albumin to the incubate. Similarly, the vascular rings recovered from NEFA-mediated inhibition by washing and further incubation in NEFA-free buffer. Therefore, elevated NEFA concentrations inhibit, reversibly, an enzyme system which is thought to protect the vascular endothelium. The NEFA-mediated inhibition of ADPase activity was also confirmed following incubation of rat aortic rings in human serum enriched with exogenous NEFA. These findings provide further evidence that NEFAs may contribute to the pathogenesis of vascular disease associated with diabetes mellitus and of other conditions where an elevation of serum NEFA concentrations occurs.

Adenosine Monophosphate↗
PubMedDate not supplied

Measurement of platelet volume using a channelyzer: assessment of the effect of agonists and antagonists.

Platelets undergo morphological changes prior to aggregating. This phenomenon is known as the platelet shape change (PSC) and is usually accompanied by at increase in median platelet volume (MePV). We evaluated MePV changes in human platelet rich plasma (PRP) using a high resolution pulse-height analyser ("channelyzer"). Increases in MePV were induced by the addition of low concentrations of known aggregating agents. These agonists showed different patterns in terms of potency, duration and reversibility.

Blood Platelets↗
PubMedDate not supplied

Platelet abnormalities in patients with cystic fibrosis and obligate heterozygotes.

Following our previous report that thrombocytosis and platelet hyperaggregability (as tested in platelet rich plasma) occur in patients with cystic fibrosis (CF), we have now examined whether this thrombocytosis is related to leukocytosis, and whether platelet hyperaggregability can be documented in whole blood using impedance aggregometry. Our observations show that platelet counts are related to white cell counts (r = 0.34; p = 0.001) and that therefore thrombocytosis may be part of a secondary response to bronchopulmonary infection, which is characteristic of these patients. Platelet counts were, however, not related to serum iron concentration despite the finding of varying degrees of iron deficiency in approximately 50% of patients with cystic fibrosis. Whole blood aggregometry demonstrated platelet hyperaggregability in patients with cystic fibrosis independently of platelet counts. Platelet aggregation (in platelet rich plasma and in whole blood) was normal in obligate heterozygotes, thus suggesting that platelet hyperaggregability in CF is not a consequence of abnormal genetic information.

Adult↗
PubMedDate not supplied

Effect of naftidrofuryl and aspirin on platelet aggregation in peripheral vascular disease.

Platelet aggregation in whole blood (WB) was assessed in healthy subjects and in patients with peripheral vascular disease (PVD) using a WB-free platelet counting (WB-FPC) method. Aggregation induced by stirring and platelet agonists was significantly enhanced in PVD patients. WB-FPC aggregation induced by 5-HT was diminished significantly by incubation with naftidrofuryl (NAF) in WB of PVD patients. In contrast, aspirin (acetylsalicylic acid; ASA), added in vitro, did not significantly affect 5-HT or stirring-induced WB-PFC aggregation in PVD patients. Furthermore, 5-HT-induced WB-FPC was inhibited by NAF in blood collected from PVD patients that were taking low dose aspirin. These findings suggest that NAF may be of benefit to patients with hyperaggregable platelets and elevated plasma 5-HT concentrations, factors thought to predispose to thrombotic complications.

Adult↗