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Biomedical subjects

H Bult

Publications and source records attributed to H Bult.

At least 109 records · Page 6Linked to original sources
PubMed1983

Effect of almitrine bismesylate on platelet aggregation and prostacyclin biosynthesis.

Almitrine bismesylate (1, 10 and 100 micrograms/ml) did not interfere with aggregation of rabbit blood platelets induced by arachidonic acid (100 micrograms/ml), ADP (10 microM) or collagen (10 micrograms/ml) in platelet rich plasma and did not augment the generation of prostacyclin by the rabbit aorta endothelium. Although almitrine bismesylate (2 mg/kg i.v.) increased the respiratory movements it did not stimulate prostacyclin biosynthesis in rabbits in vivo nor did it interfere with the ex vivo platelet aggregation induced by ADP or arachidonic acid and measured with the whole blood electronic aggregometer.

6-Ketoprostaglandin F1 alpha↗
PubMed1982

Contribution of complement activation to the rise in blood levels of 6-oxo-prostaglandin F1 alpha during endotoxin-induced hypotension in rabbits.

Administration of endotoxin (lipopolysaccharide W E. coli O111 B4, 0.5 mg/kg i.v.) induced about 20% activation of the complement system (measured as CH50 and C3), a biphasic hypotension, thrombocytopenia and a significant rise in blood levels of 6-oxo-PGF1 alpha. Complement depletion (CH50 and C3 less than 3%) with Cobra Venom Factor significantly reduced the initial fall in blood pressure and the rise in 6-oxo-PGF1 alpha, and abolished the second phase of hypotension and the thrombocytopenia, due to subsequent injection of endotoxin. It is concluded that activation of about 20% of the complement system by endotoxin is a prerequisite for the occurrence of thrombocytopenia and secondary hypotension, and that it is involved in the increase in blood levels of 6-oxo-PGF1 alpha. The results of histamine determinations in rabbit blood and plasma indicate that, besides products derived from prostaglandin endoperoxides, other vasoactive substances, possibly released during complement-mediated adherence aggregation of platelets, might contribute to the endotoxin-induced hypotension.

6-Ketoprostaglandin F1 alpha↗
PubMed1982

Effect of dipyridamole on the formation of 6-oxo-prostaglandin F1 alpha by the rat isolated aorta and ram seminal vesicle microsomes.

1 Dipyridamole (1 and 10 muM) enhanced the production of 6-oxo-prostaglandin F1 alpha by rat aortic tissue. 2 Dipyridamole (5 to 40 muM) did not influence the PGI2-synthetase activity in ram seminal vesicle microsomes whereas, in concentrations ranging from 100 to 200 muM, it reduced the metabolism of exogenously added arachidonic acid. The latter effect may be due to an inhibition of the cyclooxygenase.

6-Ketoprostaglandin F1 alpha↗
PubMed1981

Prostanoids and hemostasis in chickens: anti-aggregating activity of prostaglandins E1 and E2, but not of prostacyclin and prostaglandin D2.

Aggregation of chicken thrombocytes was studied in whole blood using an electronic aggregometer. Serotonin (5-hydroxytryptamine, 5HT), arachidonic acid (AA) and collagen, but not adenosinediphosphate (ADP) induced aggregation. Prostaglandin (PG) endoperoxides were essential for arachidonic acid-induced aggregation, but were not involved in 5HT-induced aggregation, as indicated by inhibitory studies with indomethacin. Similar experiments indicated that biosynthesis of endogenous PG endoperoxides contributed to the aggregation induced by low concentrations of collagen, but was of little importance when high collagen doses were employed. PGE1 and PGE2 could abolish all types of aggregation studied, whereas prostacyclin (PGI2) and PGD2 were without any anti-aggregatory activity at 1 microgram/ml. Between 1 and 100 ng/ml PGE1 and PGE2 inhibited arachidonic acid- and 5HT-induced aggregation dose-dependently. The lack of any hemostatic function of PGI2 in chickens was also indicated by the absence of biosynthesis of endogenous PGI2 in chicken aorta. PGI2 was assessed as anti-aggregating activity, released by aortic fragments stirred in rabbit platelet rich plasma. Still, the presence of chicken aorta tissue in chicken whole blood inhibited 5HT-, but not arachidonic acid-induced aggregation. This inhibition was not affected by pretreatment of the aortic fragments with indomethacin or pargyline.

Alprostadil↗
PubMed1980

Blood levels of 6-oxo-prostaglandin F 1 alpha during endotoxin-induced hypotension in rabbits.

Levels of 6-oxo-prostaglandin F1 alpha (6-oxo-PGF1 alpha), the non-enzymic degradation product of prostacyclin, were measured in arterial blood from anaesthetized rabbits, before and after intravenous (i.v.) administration of endotoxin (Lipopolysaccharine W E. coli 0111:B4, 5 mg/kg). 6-Oxo-PGF1 alpha was assessed by radioimmunoassay after extraction and separation by thin-layer chromatography. The basal concentration of 6-oxo-PGF1 alpha in blood was less than 100 mg/ml in 19 out of 20 rabbits. This indicates that the level of circulating prostacyclin is generally below 100 pg/ml. The administration of endotoxin induced a biphasic hypotension, and increased levels of 6-oxo-PGF1 alpha were found in all endotoxin-treated animals during the secondary hypotension after 60 and 120 min. Pretreatment with indomethacin (2.5 mg/kg) prevented the secondary fall in arterial blood pressure and significantly suppressed the rise in 6-oxo-PGF1 alpha. However, indomethacin failed to alter the endotoxin-induced thrombocytopenia and did not modify the endotoxin-induced platelet aggregation in vitro. It is concluded that prostacyclin contributed to the secondary hypotension which accompanied the i.v. administration of endotoxin. Thromboxane A2 seems not to be of primary importance in the endotoxin-platelet interaction.

6-Ketoprostaglandin F1 alpha↗
PubMed1979

Thromboxane A2 biosynthesis during endotoxin-induced aggregation of platelets from normal and sensitized guinea-pigs.

Endotoxin lipopolysaccharides Escherichia coli O26:B6 and E. coli O127:B8 were weak inducers of aggregation in normal guinea-pig platelet-rich plasma (PRP), even in the presence of Ca2+. Indomethacin hardly inhibited endotoxin-induced aggregation, indicating that biosynthesis of thromboxane A2 (TXA2) was of little importance. In accordance with this conclusion TXA2 was not detectable by means of bioassay during endotoxin-induced aggregation in normal guinea-pig PRP. Pretreatment of the guinea-pigs with endotoxin sensitized their PRP to endotoxin. This was due to a humoral factor with a selectively directed towards the polysaccharide moiety of endotoxin. The combination of this factor with endotoxin indued a marked biosynthesis of TXA2 and concomitant platelet aggregation.

Animals↗
PubMed1979

The role of thromboxane A2 in endotoxin-induced aggregation of guinea-pig platelets in vitro.

Large concentrations of endotoxin lipopolysaccharides (LPS) E. coli O127:B8 and E. coli O26:B6 were needed for induction of platelet aggregation in citrated platelet rich plasma (PRP) from normal guinea-pigs. When guinea-pigs were actively immunized with LPS E. coli O127:B8 their PRP became more sensitive to the aggregatory effects of this type of LPS. The increase in sensitivity was rather selective since the responses to ADP and LPS E. coli O26:B6 remained unchanged. In endotoxin-stimulated PRP from normal guinea-pigs thromboxane A2 (TXA2) was not detectable by bioassay. Thus biosynthesis of TXA2 seemed to be of little importance in endotoxin-induced platelet responses in normal citrate PRP. LPS E. coli O127:B8, but not LPS E. coli O26:B6, was a potent inducer of the biosynthesis of TXA2 in sensitized PRP. Under those conditions endotoxin-induced aggregation seemed to be dependent on the endogenous biosynthesis of TXA2 by the platelets.

Animals↗