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Biomedical subjects

H J Mest

Publications and source records attributed to H J Mest.

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

Thromboxane A2 (TXA2) formation by washed human platelets under the influence of low and high density lipoproteins from healthy donors.

Low density lipoprotein (LDL) stimulates TXA2 formation (measured as malondialdehyde) in washed human platelets with active cyclooxygenase, whereas high density lipoprotein (HDL) does not show any influence on TXA2 formation in this system. These results support the hypothesis that the proaggregatory action of a high plasma LDL concentration may be mediated by modification in the biosynthesis of eicosanoids. The mode of action of lipoproteins is discussed.

Blood Platelets↗
PubMed1986

[Effect of iloprost on aggregation behavior in kidney conditioning and changes in iloprost concentration in kidney preservation].

The conditioning of the donor by 1.0 microgram/kg X min Iloprost over 15 minutes leads to a considerable inhibition of the aggregation of thrombocytes in the domestic pig. 160% more ADP had to be added than before the application of Iloprost. When 0.5 microgram/ml Iloprost are added to the perfusion fluid and to the reperfusion fluid 0.22 microgram/ml and 0.27 microgram/ml, respectively, are to be proved in the venous efflux. Whether or not the difference is absorbed or metabolized must remain open. During the 72-hour storage of the kidney in a Euro-Collins-solution with 0.5 microgram/ml Iloprost after 24 hours a decrease of 0.34 microgram/ml, after 48 hours to 0.33 microgram/ml and after 72 hours to 0.20 microgram/ml takes place. Thus Iloprost is present in an effective concentration also after 72 hours. The decrease to one plateau rather speaks for a consumption by active metabolic effect or absorption than for a chemical decomposition.

Animals↗
PubMed1985

An improved malondialdehyde assay for estimation of thromboxane synthase activity in washed human blood platelets.

After stimulation of the washed human blood platelets by arachidonic acid (AA), the concurrent evaluations for formed malondialdehyde (MDA) measured by the common photometrical thiobarbituric acid (TBA) method, and for thromboxane B2 (TXB2) measured by gas chromatography, revealed that the formed MDA exceeded the amount of TXB2 on a molar base. However, MDA and TXB2 originating from thromboxane synthase activity should be produced in approximately equimolar amounts. By treatment of the stimulated platelet samples with stannous chloride it is possible to reduce all peroxidized products of AA which generate MDA otherwise during the TBA reaction and to estimate MDA and TXB2 in a ratio of nearly 1:1. The stannous chloride treatment does not destroy the MDA and does not influence the TBA reaction with MDA. Therefore the simple and quick TBA method can be used after stannous chloride treatment for estimation of thromboxane synthase activity in AA stimulated washed human platelets.

Arachidonic Acid↗
PubMed1984

Reduced side effects by low dose of acetylsalicylic acid (ASA) in patients with myocardial infarction; estimations of serum thromboxane B2 and PGF2 alpha.

In a secondary prevention study 867 male and female patients with myocardial infarction (MI) were divided 3 weeks after onset of MI into 4 treatment groups: I - 273 patients received additionally to their common medication 1000 mg ASA/d; II - 313 patients got 60 mg ASA/d; III - 208 patients 30 mg ASA/d resp.; IV - 73 patients received no ASA administration due to ASA contraindications. One year after onset of MI the following parameters were checked: mortality, malignant arrhythmia, exercise tolerance, gastrointestinal symptoms and hemorrhage as typical side effects of ASA, formation of thromboxane B2 and PGF2 alpha in clotting whole blood. The low dose of 30 mg ASA/d reśultes in a clear reduction of ASA side effects (6,4% of patients with symptoms) in comparison to group I (15,9% of patients with symptoms), in a tendency to decreased mortality, and in unchanged frequency of malignant arrhythmias resp. Concerning the maximum exercise tolerance no significant difference could be observed in all 4 groups investigated. Estimations of serum thromboxane B2 by radioimmunoassay and gas chromatography revealed strong inhibitions of the thromboxane formation in all patients with ASA administrations; even the low dose of 30 mg ASA/d decreased thromboxane B2 by more than 95%.

Adult↗
PubMed1984

Influence of aspirin, molsidomine, trapidil, and some trapidil derivatives on arachidonic acid induced reversible thrombocyte aggregation in the rabbit.

For testing antiaggregatory activity of substances in vivo we used transient decrease of circulating platelet number in rabbit blood after rapid i. v. injection of arachidonic acid (AA) as sign of increased thrombocyte aggregates within the tissues. We tested aspirin, molsidomine, trapidil, and 6 trapidil derivatives. Antiaggregatory effects of aspirin, molsidomine, and trapidil confirm former reports and reliability of the used model. 4 trapidil derivatives were effective in doses lower than trapidil itself.

Animals↗
PubMed1984

Influence of trapidil derivatives on arachidonic acid- and prostaglandin endoperoxide analogue- induced platelet aggregation and thromboxane A2 formation.

Five selected trapidil derivatives (12456, 12460, 12463, 12464, 12465) inhibited the arachidonic acid(AA)- and prostaglandin endoperoxide analogue(U-46619)- induced platelet aggregation as well as the AA- induced thromboxane A2(TXA2) formation. These effects of the derivatives were generally more markedly expressed than those of trapidil.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1984

Influence of a cod liver oil diet in diabetics type I on fatty acid patterns and platelet aggregation.

The influence of an eicosapentaenoic acid rich diet containing only 6,8 g cod liver oil daily for 2 weeks in 20 type I diabetics on fatty acid pattern in serum, platelet aggregation and thiobarbituric acid-reactive substances in serum were studied. There were increases in eicosapentaenoic acid portions in triglycerides, cholesterol esters and phospholipids of serum. This was associated with an inhibition of the platelet hyperaggregation, whereas platelet hyporeactivity is shifted to normal. Hyperreactivity of platelets from diabetics may be caused by enhanced TXA2 formation in comparison to healthy humans (1). On the other hand, diets rich in eicosapentaenoic acid inhibit platelet aggregation in healthy Volunteers (2,3). Therefore we investigated the dietary effect of relatively low doses of cod liver oil in diabetics type I on the eicosapentaenoic acid/arachidonic acid balance.

Adult↗
PubMed1984

Estimation of thromboxane B2 in the clotting human whole blood by gas chromatography.

In recent years, the interest within platelet reactions has been focused increasingly on thromboxane (TX) A2 formation. Thrombin formed in clotting blood stimulates platelets in their natural environment to produce TXA2. For estimation of TXB2 - the hydrolysis product of TXA2 - in serum of human blood clotted in vitro we used an internal standardization with 2,3,-dinor-TXB2 and the electron capture gas chromatography of the methoxime pentafluorobenzyl ester trimethylsilyl ether derivatives. The reliability of method was characterized by means of coefficients of variation at different stages of assay. Influences of various venous blood sampling and incubation conditions, and of addition of exogenous thrombin to native or citrated blood were investigated.

Blood Coagulation↗
PubMed1983

The influence of linseed oil diet on fatty acid pattern in phospholipids and thromboxane formation in platelets in man.

Ten healthy volunteers daily received 30 ml linseed oil for 4 weeks in addition to the "normal" diet. The influence of linseed oil diet on the fatty acid pattern of plasma phospholipids and thromboxane formation in platelets was investigated. The fatty acid pattern was analysed by gas liquid chromatography. The alpha-linolenic, eicosapentaenoic and docosahexaenoic acids were increased (p less than 0.01), whereas linoleic and arachidonic acids were decreased (p less than 0.05) after 4 weeks of the linseed oil diet. The thromboxane formation of platelets were unchanged. Additionally the influence of HDL and LDL on PGI2 biosynthesis in pig aortic microsomes (PAM) was investigated. HDL taken from serum before and after 3 weeks of linseed oil diet and LDL taken after 3 weeks of diet stimulated the PGI2 formation in PAM, whereas LDL taken from serum before the diet period inhibited the PGI2 formation in PAM.

6-Ketoprostaglandin F1 alpha↗
PubMed1983

The antiarrhythmic effect of PGE2 on premature ventricular beats (PVBs) in man.

In 10 patients with premature ventricular beats (PVBs) we investigated the influence of PGE2 infusion on ventricular arrhythmias, arterial blood pressure, heart rate and systolic time intervals. An infusion of PGE2 in doses of 0.01, 0.02 and 0.04 microgram/kg/min, each for 10 min, did not change the blood pressure, heart rate and systolic time intervals. The incidence of PVBs decreased in a dose-dependent manner in 7 out of 10 patients, and in two of them PVBs were absolutely abolished. In one patient the incidence of PVBs was reduced dose independently, and in two patients at the beginning of infusion of PGE2 the incidence of PVBs was reduced, but the incidence of PVBs increased again although the infusion dose was doubled. In all patients the incidence of PVBs increased again when the infusion of PGE2 was stopped. Our findings demonstrate that PGE2 has antiarrhythmic properties in man.

Adult↗
PubMed1982

Electrically induced tachyarrhythmia and the effect of propranolol on the release of cyclic AMP and prostaglandin E by the canine left ventricle.

In anesthetized open-chest dogs, tachyarrhythmia (TA) was electrically induced by above-threshold stimuli via the right ventricle. During TA, a significant increase in the release of PGE and cAMP was observed in the canine coronary sinus blood (CSB). The efflux of cAMP corresponded with a concomitant increase in the left ventricular tissue level of this nucleotide. Pretreatment with propranolol (1.0 mg/kg i.v.) prevented the TA-induced changes in the level of PGE as well as cAMP in the CSB and in the tissue levels of cAMP. There was an increase in the activity of phosphorylase a in the myocardial tissue during TA which could be abolished by propranolol pretreatment. These results suggest possible interrelationships among catecholamines, cAMP, and PGE.

Animals↗
PubMed1982

Influence of 15-keto-metabolites and 13,14-dihydro-15-keto-metabolites of PGE2 and PGF2 alpha as well as of 6-keto-PGF1 alpha as a metabolite of PGI2 on aconitine induced cardiac arrhythmia in rats.

The 15-keto-metabolites of PGE2 and PGF2 alpha produced an antiarrhythmic effect on aconitine induced arrhythmias in rats. The ED50 values of these metabolites were approximately 2.0 micrograms/kg. The 13,14-dihydro-15-keto-metabolites of PGE2 and PGF2 alpha had no statistically significant antiarrhythmic effect. PGI2 (0.25-1.00 micrograms/kg) produced an antiarrhythmic effect between 15-54% (ED50 0.75 micrograms/kg), whereas 6-keto-PGF1 alpha, a metabolite of PGI2, showed no significant antiarrhythmic effect. The results suggest a participation of 15-keto-metabolites in the antiarrhythmic effects of PGE2 and PGF2 alpha.

Aconitine↗
PubMed1982

Influence of mental stress on plasma level of prostaglandins, thromboxane B2 and on circulating platelet aggregates in man.

In two groups of medical students (group A n=13, group B n=9, aged 23 to 28 years) we estimated the levels of PGE, PGF2 alpha, 6-keto-PGF1 alpha and thromboxane(TX)B2 by means of radioimmunoassay in the peripheral venous blood immediately before (BES) and 15-30 min after (AES) examination stress and compared these to control levels. Furthermore we determined the circulating platelet aggregates, the heart rate and blood pressure changes. Heart rate and systolic blood pressure increased in the BES period expressing a stressful situation. In BES the plasma level of PGE increased from 84 to 249 pg/ml (p less than 0.001), whereas PGF2 alpha was unchanged. The increase of PGE level seems to be an expression of the increased sympathetic nervous activity existing in the stressful situation. The level of 6-keto-PGF1 alpha, the stable metabolite of prostacyclin, behaved differently in the two groups. In group A there was a statistically significant increase (p less than 0.05), whereas in group B the 6-keto-PGF1 alpha level was unchanged. In AES the TXB2 level increased from 113 to 167 pg/ml (p less than 0.01), whereas under BES conditions the TXB2 level was not changed. Simultaneously with the increased TXB2 level the circulating platelet aggregates were increased. The increase in TXB2 level occurring only after the end of the examination may offer a possible explanation of the frequent appearance of heart attacks after stressful situations.

Adult↗
PubMed1981

Influence of electrically induced tachyarrhythmia on the release of cyclic AMP and PGE in canine coronary sinus blood and on the level of cyclic AMP in myocardial tissue.

In anaesthetized open-chest dogs tachyarrhythmia (TA) was electrically induced by above-threshold stimuli via the right ventricle. During TA a significant increase in the release of PGE and cyclic AMP of 20% and 40% of the control levels, respectively, was observed in the canine coronary sinus blood (CSB), whereas the level of PGF2 alpha remained nearly unchanged under these conditions. The efflux of cyclic AMP corresponded with a concomitant increase in the left ventricular tissue level of this nucleotide by 59% during TA. Pretreatment with the beta-adrenergic blocking agent propranolol (1.0 mg/kg i.v.) prevented the TA induced changes in the level of PGE as well as cyclic AMP in the CSB and in the tissue levels of cyclic AMP. Propranolol alone was without any effect on the efflux of cyclic AMP, but decreased significantly the efflux of PGE by 32%. There was an increase in the activity of phosphorylase a in the myocardial tissue from 10% to 20% of the total (a + b) activity of this enzyme during TA, which could be abolished by propranolol pretreatment. The results suggest possible interrelationships between catecholamines, cyclic AMP and PGE.

Adenosine Triphosphate↗
PubMed1981

Influence of cardiac rhythm disturbances and antiarrhythmic drugs on the efflux of PGE, PGF2 alpha, cyclic AMP, and cyclic GMP in canine coronary sinus blood.

In anaesthetized open-chest dogs, cardiac arrhythmias (CA) were induced by cumulative intravenous doses of aconitine or ouabain. Aconitine in a dose which did not induce CA had no influence on the PGE and PGF2 alpha effluxes into coronary sinus blood (CSB), whereas the PGE efflux into CSB increased after a subtoxic dose of ouabain. However, both PGE and PGF2 alpha effluxes were increased, when CA had developed. During aconitine induced CA, the PGE efflux was 6.5-fold and that of PGF2 alpha had increased by 80%. During ouabain induced CA, the effluxes of both PGs were about 3-fold. Propranolol and lidocaine decreased the PGF2 alpha efflux into CSB by about 50% and the PGE efflux was doubled after lidocaine and decreased after propranolol by about a third. The increased PGE efflux into CSB during CA was normalized after propranolol and quinidine if the CA was abolished or the cardiac rhythm improved. Lidocaine did not modify the increase in PGE efflux, despite the abolishment of CA. The increase in PGF2 alpha efflux was not influenced by antiarrhythmic drugs. The cyclic AMP and cyclic GMP in CSB remained unchanged during ouabain induced arrhythmias or after propranolol. The increased efflux of PGE into CSB during aconitine and ouabain induced CA and its abolishment by propranolol support the hypothesis that PGE participates in the modulation of increased sympathetic tone during CA.

Aconitine↗
PubMed1981

Is PGI2 arrhythmogenic? Investigations on ouabain induced arrhythmias in cats.

The present study investigated the effect of PGI2 on ouabain induced arrhythmias in cats. PGI2 was infused at a dose of 1.0, 2.0 and 5.0 microgram/kg . min. PGI2 in a dose of 1.0 microgram/kg . min was without any antiarrhythmic effect. Infusions of 2.0 and 5.0 microgram/kg . min PGI2 in 3 of 10 and 7 of 10 animals, respectively, converted the ouabain induced arrhythmias into a sinus rhythm. The duration of the antiarrhythmic effect after infusion of 2.0 microgram/kg . min lasted about 21 min, whereas the higher dose (5.0 microgram/kg . min) had a shorter effect (about 2 min). Under these conditions and doses the systolic blood pressure decreased between 35% and 39% and the diastolic blood pressure was reduced by about 50%. Thus PGI2 showed when used in the given dose range, an antiarrhythmic effect on ouabain induced arrhythmias in cats. The importance of dosage, methods and species is here discussed.

Animals↗
PubMed1981

Influence of linseed oil diet on the pattern of serum phospholipids in man.

We gave 11 volunteers 30 ml linseed oil daily for 4 weeks. This diet increased the amount of linolenic, eicosapentaenoic and docosahexaenoic acid in the serum phospholipids within 1 week, whereas the amount of dihomo-gamma-linolenic acid was decreased. Both effects were statistically significant. The results suggest that eicosapentaenoic acid can be synthesized from alpha-linolenic acid in human organism.

Adult↗