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Biomedical subjects

J Vermylen

Publications and source records attributed to J Vermylen.

At least 235 records · Page 13Linked to original sources
PubMed1984

Blood changes and enhanced thromboxane and 6-keto prostaglandin F1 alpha production in experimental acute Plasmodium bergei infection in hamsters.

Golden hamsters inoculated intraperitoneally with Plasmodium bergei infected mouse blood regularly developed P. bergei parasitaemia. This was associated with progressive thrombocytopenia and leucocytosis as the degree of parasitaemia increased with time. When infected whole blood was stimulated with collagen, significantly enhanced thromboxane B2 (TXB2) production per platelet was seen. 6-keto prostaglandin (PG) F1 alpha formation in the same system increased from the sixth infection day onwards and correlated with the relative leukocytosis. The production of 6-keto PGF1 alpha by aorta rings was significantly higher during the 4-7th days postinoculation. The increase in thromboxane production however was much more important than that of 6-keto PGF1 alpha and it therefore is concluded that P. bergei parasitaemia in hamsters tilts the haemostatic balance towards the platelet hyperaggregability that has also been described in P. falciparum infection in man.

6-Ketoprostaglandin F1 alpha↗
PubMed1984

Serum albumin enhances the impairment of platelet aggregation with thromboxane synthase inhibition by increasing the formation of prostaglandin D2.

Dazoxiben, a thromboxane synthase inhibitor, inhibits arachidonic acid induced aggregation in platelet-rich plasma from some donors only ("responders"). We have studied the effect of dazoxiben in vitro on platelet aggregation and prostaglandin (PG) metabolism and the influence of the incubation period and of exogenously added serum albumin (SA). SA, which increases the production of anti-aggregatory PGD2 from cyclic endoperoxides, induced "non-responder" human platelets to respond. With rabbit platelets, however, that are insensitive to PGD2, exogenous SA failed to potentiate dazoxiben-induced inhibition. The ratio between PGD2 and TXB2 + PGE2 formed was crucial in determining the response of human platelets to dazoxiben: whenever this ratio was high, platelet aggregation was inhibited. SQ 22536, an adenylate cyclase inhibitor, and NO164, a PGD2 antagonist, reversed the inhibition by dazoxiben in human platelet-rich plasma, stressing the importance of a PGD2 mediated rise of cyclic AMP for the effectiveness of a thromboxane synthase inhibitor.

Adenine↗
PubMed1984

BM 13.177, a selective blocker of platelet and vessel wall thromboxane receptors, is active in man.

BM 13.177, a sulphonamide derivative, prevented platelet aggregation by thromboxane A2 in vitro and selectively inhibited contraction of isolated rabbit femoral arteries induced by two stable endoperoxide analogues. In a double-blind placebo-controlled study, oral BM 13.177 inhibited platelet aggregation induced by arachidonic acid, low dose collagen, and the two stable endoperoxide analogues, and slightly prolonged the bleeding time. Generation of thromboxane or of other prostaglandins was not affected. No side-effects were seen. BM 13.177 appears selectively and safely to block platelet and vessel wall thromboxane receptors and should be useful in elucidating the role of thromboxane A2 in disease.

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

Immunological alterations in haemophiliacs treated with lyophilized Factor VIII cryoprecipitate from volunteer donors.

We studied immune function in Belgian haemophiliacs treated with Factor VIII from volunteer donors. No patient had clinical evidence of immune deficiency. We found a decrease in T-helper cells (p less than 0.0005), in the ratio of T-helper over T-cytotoxic/suppressor cells (1.72 +/- 0.47 versus 2.24 +/- 0.82 in controls, p less than 0.005) and in lymphocyte responsiveness to mitogens (p less than 0.05). These findings could not be linked to the amount of F VIII received over the last year, the time since last F VIII administration, circulating immune complexes (54% positive patients, 7% positive controls, p less than 0.005), increased ALT levels, antibodies to cytomegalo -virus (85% of the patients, 45% of the controls, p less than 0.005), antibodies to Epstein-Barr virus, nor to the presence of HLA-DR 5 which was found in 56% of the haemophiliacs (20% of the overall Belgian population, p less than 0.005). Either F VIII induces long lasting immunological alterations unrelated to AIDS, or haemophilia is itself associated with such changes.

Acquired Immunodeficiency Syndrome↗
PubMed1984

Protective effect of vitamin E on immune triggered, granulocyte mediated endothelial injury.

The effect of alfa-tocopherol on the cell-cell interactions at the vessel wall were studied, using an in vitro model of human umbilical vein endothelial cell cultures (HUEC). Immune triggered granulocytes (PMN) will adhere to and damage HUEC and platelets enhance this PMN mediated endothelial injury. When HUEC are cultured in the presence of vitamin E, 51Cr-leakage induced by complement stimulated PMN is significantly decreased and the enhanced cytotoxicity by platelets is completely abolished (p less than 0.001). The inhibition of PMN induced endothelial injury is directly correlated to a diminished adherence of PMN to vitamin E-cultured HUEC (p less than 0.001), which may be mediated by an increase of both basal and stimulated endogenous prostacyclin (PGI2) from alfa-tocopherol-treated HUEC (p less than 0.025). The vitamin E-effect is abolished by incubation of HUEC with the irreversible cyclo-oxygenase inhibitor, acetylsalicylic acid, but the addition of exogenous PGI2 could not reproduce the vitamin E-mediated effects. We conclude that vitamin E exerts a protective effect on immune triggered endothelial damage, partly by increasing the endogenous anti-oxidant potential, partly by modulating intrinsic endothelial prostaglandin production. The failure to reproduce vitamin E-protection by exogenously added PGI2 may suggest additional, not yet elucidated vitamin E-effects on endothelial metabolism.

Aspirin↗
PubMed1984

Wound healing following dental extractions in rabbits: effects of tranexamic acid, warfarin anti-coagulation, and socket packing.

We have investigated the importance of the coagulation and fibrinolytic systems for wound healing following dental extractions. Four front teeth were extracted in rabbits; wound healing was measured as time until complete epithelial closure. The antifibrinolytic agent tranexamic acid shortened duration of wound healing in normal rabbits. Anti-coagulation with warfarin delayed epithelial closure, which was, however, normalized by simultaneous administration of tranexamic acid, whereas complete packing of the socket with oxidized cellulose had no corrective effect. Apical packing together with tranexamic acid gave normal healing. It is concluded that the quality of the fibrin network within the dental socket determines the rate of wound healing; oxidized cellulose is not an adequate substitute for fibrin.

Alveolar Process↗
PubMed1983

Dipyridamole inhibits platelet aggregation in whole blood.

Dipyridamole possesses antithrombotic properties in the animal and in man but it does not inhibit platelet aggregation in plasma. We evaluated the effect of dipyridamole ex vivo and in vitro on platelet aggregation induced by collagen and adenosine-5'-diphosphate (ADP) in human whole blood with an impedance aggregometer. Two hundred mg dipyridamole induced a significant inhibition of both ADP- and collagen-induced aggregation in human blood samples taken 2 hr after oral drug intake. Administration of the drug for four days, 400 mg/day, further increased the antiplatelet effect. A significant negative correlation was found between collagen-induced platelet aggregation in whole blood and dipyridamole levels in plasma (p less than 0.001). A statistically significant inhibition of both collagen (p less than 0.0025) and ADP-induced (p less than 0.005) platelet aggregation was also obtained by incubating whole blood in vitro for 2 min at 37 degrees C with dipyridamole (3.9 microM). No such effects were seen in platelet-rich plasma, even after enrichment with leukocytes. Low-dose adenosine enhanced in vitro inhibition in whole blood. Our results demonstrate that dipyridamole impedes platelet aggregation in whole blood by an interaction with red blood cells, probably involving adenosine.

Adenosine↗
PubMed1983

Low prostacyclin synthetase activity of fetal rat aorta. Progressive increase after birth.

Aortae from fetal or 3 weeks old rats produced very small amounts of PGI2, prostacyclin. This production increased from 4 weeks on, reaching adult values at about ten weeks. This maturation seemed to be predominantly determined by a change in the PGI2 synthetase system, rather than in arachidonic acid availability, phospholipase or cyclo-oxygenase activity. The anti-oxidant ascorbic acid stimulated prostacyclin production more strongly in adult than in young rat aortae. This finding suggests that the lower production of PGI2 by young tissues is not due to an enhanced inhibition of prostacyclin synthetase by lipid peroxides.

6-Ketoprostaglandin F1 alpha↗
PubMed1983

Manipulation of the local thromboxane and prostacyclin balance in vivo by the antithrombotic compounds dazoxiben, acetylsalicylic acid and nafazatrom.

We have developed an experimental model for the study of local prostaglandin production by platelets and the vessel wall following stimulation 'in vivo'. A nylon thread was inserted into the external jugular vein of rabbits; its presence did not induce an occluding thrombus. Thromboxane (TXB2) values in the blood, sampled through the facial vein, immediately distal to the stimulus, rose and remained high for at least 4 hr, while 6-keto prostaglandin (PG) F1 alpha levels, after a first increase, gradually returned to normal ('exhaustion' of the endothelial cells?). No changes were observed in the contralateral jugular vein without thread. After infusion via the femoral vein of 10 mg/kg dazoxiben, a thromboxane synthetase inhibitor, local TXB2 production was completely abolished, whereas 6-keto PGF1 alpha formation no longer returned to basal values, but tended to increase. This leads to the conclusion that upon inhibition of TXB2 formation endoperoxide metabolism is reoriented 'in vivo' towards prostacyclin, and this mainly at the site where platelets are activated. Injection of 100 mg/kg lysine acetylsalicylic acid resulted in complete inhibition of TXB2 and 6-keto PGF1 alpha formation, the latter, however, slowly recovering with time. The administration of nafazatrom to the animals did not influence the local TXB2 changes, but partially prevented the decline of 6-keto PGF1 alpha with time. The antithrombotic properties of this drug thus could be related to protection of the endothelial cells from 'exhaustion'.

Animals↗