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Biomedical subjects

J Vermylen

Publications and source records attributed to J Vermylen.

At least 217 records · Page 12Linked to original sources
PubMed1986

Thrombosis and immune disorders.

The purpose of this review has been to draw the attention of clinicians towards the possibility that some of the patients they are treating for thrombosis may have an underlying immune disturbance. This could involve functional abnormalities of the complement system (as in acquired angioneurotic oedema or in paroxysmal nocturnal haemoglobinuria), or cell-mediated immunological damage to the vessel wall (as in Behcet's syndrome or Buerger's disease), or the presence of circulating antibodies (the lupus anticoagulant or antibodies to heparin). While obviously our knowledge on most aspects is still very incomplete, the awareness of the association of thrombosis with certain immune disorders should encourage further detailed studies of mechanisms and enhance our understanding of the role of blood constituents and the vessel wall in thrombogenesis.

Angioedema↗
PubMed1986

Evaluation of three methods of platelet labelling.

The study of the kinetics of labelled platelets makes sense only when the platelets preserve their viability after separation and labelling. The separation and labelling procedures described in the manual of two producers of 111In-oxinate (Amersham, Mallinckrodt) have been evaluated by in vitro aggregation tests. The method of Mallinckrodt diminished the aggregation capacities of the thrombocytes. The labelled platelets with normal in vitro aggregation response (Amersham) were tested in vivo in 11 patients who underwent peripheral bypass surgery. The platelet half-life and the platelet accumulation on bypass grafts were checked one week post-operatively. Because of the poor in vivo response of both methods (exponential half-life curve and bad graft visualization), a third method was optimized in our laboratory with good in vitro and in vivo results in 12 patients.

Blood Platelets↗
PubMed1985

Aspirin, indomethacin and dazoxiben do not affect the fibrinolytic activation induced by venous occlusion.

A cause-effect relation between the synthesis and release of prostaglandins and fibrinolytic activation has been suggested. We have reinvestigated this relation in a double-blind, placebo-controlled, cross-over study with cyclooxygenase inhibitors (aspirin and indomethacin) and a thromboxane synthase inhibitor (dazoxiben) in nine healthy volunteers. Euglobulin fibrinolytic activity (EFA) and tissue-type plasminogen activator antigen level (t-PA:Ag) were studied before and after 10 min of venous occlusion. Despite effective suppression of prostaglandin synthesis by aspirin and indomethacin and enhanced prostacyclin formation by dazoxiben, baseline EFA and t-PA:Ag levels did not significantly change within 2 hours after ingestion of the different drugs. The release of t-PA by venous occlusion was not altered by any of the drugs. Thus, our study does not support the hypothesis that prostaglandins play a significant role in the modulation of the synthesis or release of t-PA.

Aspirin↗
PubMed1985

Questions and answers on prothrombin time standardisation in oral anticoagulant control.

One of the reasons why oral anticoagulants fell into disrepute is the absence of internationally accepted standardised procedures for controlling the level of anticoagulation. This deplorable situation resulted in over- and under-coagulation and uncertainty in the therapeutic range. International conformity can now be obtained by using an International Normalised Ratio (INR) which is derived from the individual result obtained in a given plasma sample and the International Sensitivity Index (ISI) of the tissue thromboplastin reagent used. Any thromboplastin reagent can be calibrated against an international primary or secondary W. H. O. reference preparation, so as to obtain its International Sensitivity Index. The new system of reporting the level of anticoagulation was designed and can only safely be applied in patients taking oral anticoagulants.

Administration, Oral↗
PubMed1985

Thromboembolic complications and haemostatic changes in cyclosporin-treated cadaveric kidney allograft recipients.

The incidence of thromboembolic complications was compared retrospectively in 90 cadaveric kidney allograft recipients treated with cyclosporin and low-dose steroids and the same number of cadaveric kidney allograft recipients treated with azathioprine, antilymphocyte globulin, and high-dose steroids. In the cyclosporin group, 17 thromboembolic complications occurred in 13 patients: 10 pulmonary emboli, 1 renal vein thrombosis, 3 deep vein thromboses, and 3 haemorrhoidal thromboses. In the azathioprine group, the only thromboembolic complication was 1 episode of superficial thrombophlebitis. Haemostatic tests in cyclosporin-treated and azathioprine-treated patients and normal subjects (10 in each group) showed increased concentrations of factor VIII C, fibrinogen, antithrombin III, and protein C in the cyclosporin-treated patients. Adenosine-5'-diphosphate-induced platelet aggregation was also significantly enhanced in the cyclosporin group. The effect of cyclosporin on haemostasis may predispose to thromboembolic complications.

Azathioprine↗
PubMed1985

Influence of a vitamin E-deficient diet on prostacyclin production by mesometrial triangles and aortic rings from nondiabetic and diabetic pregnant rats.

We investigated the effect of a vitamin E-deficient diet on the synthesis of prostacyclin in nondiabetic and diabetic pregnant rats. In both groups the diet reduced fetal growth and prostacyclin production by mesometrial triangles; it also increased serum lipid peroxides, which are known to inhibit prostacyclin synthesis. Independently of the diet, mesometrial triangles of diabetic rats produced more prostacyclin than those of control rats, whereas an opposite tendency was found in the aortic rings. Our model seems useful for fundamental and pharmacologic studies of the vascular pathology of pregnancy.

Animals↗
PubMed1985

Effects of thromboxane A2 on lymphocyte proliferation.

The main cyclooxygenase-dependent arachidonic acid derivatives produced by monocytes and macrophages have been shown to be thromboxane A2 and prostaglandin E2. The immunomodulatory effects of thromboxane A2 were examined using a specific thromboxane synthase inhibitor (dazoxiben), a thromboxane A2 analog (U46619), and a thromboxane A2 receptor blocker (BM13.177). Dazoxiben inhibited lymphocyte proliferation in response to mitogens (PHA and OKT3), but also reoriented cyclic endoperoxide metabolism towards the production of prostaglandin E2. Prostaglandin E2 has been shown previously to inhibit mitogen-induced lymphocyte proliferation. U46619, a stable thromboxane A2 analog, slightly enhanced lymphocyte responses to mitogens in the presence of dazoxiben and in the presence of a cyclooxygenase inhibitor (indomethacin). This occurred at concentrations of U46619 which are probably supraphysiological in view of the short half-life of natural thromboxane A2. Finally, the thromboxane A2 receptor blocker BM13.177 did not have any effect on mitogen-induced lymphocyte proliferation. It is concluded that thromboxane A2 has no or minimal modulatory effects on lymphocyte proliferative responses to mitogens and that the effect of thromboxane A2 synthase inhibition is rather due to reorientation of cyclic endoperoxide metabolism, resulting in increased prostaglandin E2 production.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗
PubMed1985

Blood loss following dental extractions in anticoagulated rabbits: effects of tranexamic acid and socket packing.

The present study demonstrates the feasibility of chronic anticoagulation in rabbits and of estimating the resulting increase in blood loss following extraction of four front teeth from labeled red cell disappearance curves. This setup proved useful for the evaluation of hemostatic techniques. Socket packing with oxidized cellulose soaked in thrombin solution or local application of cyanobutylacrylate reduced early blood loss; oral administration of tranexamic acid reduced both early and late bleeding; the combination of socket packing and oral tranexamic acid completely abolished the excessive blood loss that resulted from anticoagulation alone.

Administration, Oral↗
PubMed1985

Dental extractions in hemophilia: reflections on 10 years' experience.

During the past ten years we have witnessed a remarkable reduction in complications following dental extractions in patients with hemophilia. Thirty-six of 100 patients experienced delayed bleeding during the first half of this period; fourteen of 112 patients had a hemorrhagic problem after extraction during the second half. From a major undertaking involving hospitalization and general anesthesia, it has become a simple procedure in the outpatient office. During the entire period, no changes were made in the transfusion policy or in the oral administration of antifibrinolytic agents. Factors contributing to the favorable evolution have been the increasing experience of the oral surgeon, the improving dental status of our hemophilia patients, prophylactic measures to reduce gingival inflammation, and changes in the composition and amount of material used to pack the dental sockets.

Aminocaproic Acid↗
PubMed1985

Partial isolation and function of the prostacyclin regulating plasma factor.

Rat aortic rings stop producing prostacyclin upon prolonged washing in buffer. This 'exhaustion' is caused by inhibition of cyclo-oxygenase, since these rings still convert cyclic endoperoxides but not arachidonic acid into prostacyclin, and most probably is due to high concentrations of peroxides: it can be accelerated by H2O2 or by interrupting the glutathione cycle, while it is delayed by reduced glutathione. Incubation of exhausted rings in human plasma or in a plasma filtrate restores to some extent prostacyclin formation. This filtrate, in particular from uraemic subjects, also inhibits the H2O2 initiated oxidation of guaiacol by ram seminal vesicle microsomes or horseradish peroxidase. The prostacyclin regulating plasma factor has been partially purified and identified as a stable and very polar molecule of mol. wt. 300-400, able to reactivate prostacyclin generation by exhausted rings. We suggest that one or more low mol. wt. plasma components prolong vascular prostacyclin formation by acting as reducing cofactor for cyclo-oxygenase peroxidase. The main physiological role of this plasma activity is probably to protect the vascular prostacyclin forming system from exhaustion during persistent irritation.

6-Ketoprostaglandin F1 alpha↗
PubMed1985

Intravenous ionic contrast media cause local prostacyclin release in man.

The effect of intravenous administration of ionic contrast media on local release of prostacyclin (PGI2) was investigated in man. Iodamide and ioxaglate, high- and low-osmolality contrast media, respectively, both significantly increased PGI2 levels at the site of injection. Iodamide was the most active, whereas an identical volume of isotonic saline had no effect. This study suggests that local formation of PGI2 may adequately reflect the degree of endothelial irritation that is caused by contrast media and that depends in part on their osmolality.

Contrast Media↗
PubMed1985

Platelet hypersensitivity to serotonin after prolonged ketanserin intake?

In the present study the effect of acute and short-term ketanserin administration on serotonin (5-HT)-induced aggregation was investigated in eight healthy volunteers. They received 40 mg ketanserin three times a day for 1 week. Blood samples were drawn before (A), 1.5 h after the first dose (B), 12 h after the evening dose of the 7th day (C), and 1.5 h after the morning dose of the 8th day (D). The maximal rate of aggregation (mm/min +/- SEM) was significantly decreased following the first dose (A: 47.6 +/- 6.0; B: 27.6 +/- 4.5; p less than 0.05); 12 h after the evening dose of the 7th day, the platelets aggregated more rapidly with 5-HT than before the onset of the study (C: 69.4 +/- 6.0; A vs. p less than 0.01). The last dose of ketanserin abolished this hyperresponsiveness (D: 46.1 +/- 7.58; C vs. D, p less than 0.05); however, there was no significant difference in the velocity of aggregation between the onset of the study and after the last dose. It appears that ketanserin has a double effect on platelet aggregation: an initial hyporesponsiveness to 5-HT is followed by a delayed hyperresponsiveness that is temporarily corrected by renewed ketanserin intake. In vitro dose-response curves suggested that prolonged ketanserin intake results in a higher "sensitivity" of the platelets to serotonin rather than a refractoriness of the platelets to ketanserin.

Adult↗
PubMed1985

Immunoglobulin G antibodies to lymphadenopathy-associated virus in differently treated French and Belgian hemophiliacs.

Immunoglobulin G antibodies to lymphadenopathy-associated virus have been detected in two groups of French hemophiliacs and in one group of Belgian hemophiliacs, whose mode of treatment differed. Seropositivity was more frequent (58.9%) in patients heavily transfused with blood products of French and foreign origin than in less frequently transfused persons (10.3%). The Belgian group, treated only with local products, showed the lowest frequency of seropositivity (3.4%). In healthy French controls, 1 of 330 had antibody to the virus. The results indicate transmission of lymphadenopathy-associated virus via blood-derived products.

Antibodies, Viral↗
PubMed1985

Thromboxane A2 and prostacyclin do not modulate the systemic hemodynamic response to cold in humans.

The immersion of a limb in a mixture of water and ice induces in normal humans an initial vasoconstriction mediated mainly by catecholamine release. In some studies the cold pressor test was associated with an increase in vasoconstrictor thromboxane A2 and in vasodilating prostacyclin. Dazoxiben hydrochloride, a thromboxane synthase inhibitor, has been reported to suppress cold-induced vasoconstriction. We compared in a double-blind, crossover, placebo-controlled study the effects of indomethacin (a cyclooxygenase inhibitor), dazoxiben hydrochloride, and BM13.177 (a novel thromboxane receptor antagonist) on the changes in cutaneous vascular resistance and arterial blood pressure induced by cold in 12 healthy volunteers. Cold challenge produced an increase in blood pressure and an initial decrease in finger blood flow, reflecting an increase in cutaneous vascular resistance. Neither effective suppression of thromboxane A2 generation or of the effects of thromboxane A2 on platelets by the three active treatments nor increase in prostacyclin generation after ingestion of dazoxiben hydrochloride modified the hemodynamic response to cold. In conclusion, thromboxane A2 and prostacyclin do not play a significant role in the modulation of the systemic hemodynamic response to cold. In addition, thromboxane receptor antagonism in normal humans does not influence basal blood pressure.

6-Ketoprostaglandin F1 alpha↗
PubMed1985

BM 13.177 selectively inhibits endoperoxide analogue induced vascular contractions.

Experiments were performed to evaluate the effects of BM 13.177 on vascular smooth muscle. Rabbit femoral arteries were mounted for isometric tension recording and made to contract with the endoperoxide analogues U44064 and U46619, prostaglandin F2 alpha and E2, norepinephrine, serotonin, histamine and ATP in the absence and in the presence of BM 13.177. This compound (7 X 10(-5)M) inhibited contractions to the endoperoxide analogues and did not affect or slightly potentiated contractions induced with the other agonists except for those evoked with prostaglandin F2 alpha, which tended to be slightly inhibited. In 2 out of 5 unstimulated preparations tested, BM 13.177 at 7 X 10(-6) and 7 X 10(-5)M caused small contractions. It is suggested that BM 13.177 is a selective thromboxane A2 receptor antagonist in vascular smooth muscle.

Animals↗