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Biomedical subjects

L Maes

Publications and source records attributed to L Maes.

At least 73 records · Page 4Linked to original sources
PubMed1986

Endogenic PAF-acether production by guinea pig endothelial cells in experimental arterial thrombosis.

Superfusion of PAF-acether over a branch of the mesenteric artery in the guinea pig invariably results in local endothelial injury and thrombus formation within 3-10 minutes. The thrombotic phenomena do not disappear when PAF-acether superfusion is discontinued, and even when forced embolization is induced. Within a very short interval renewal of thrombosis occurs at the same site. Several data point to a mechanism involving generation and release of endogenic PAF-acether. Recents findings on PAF-acether release by cultured endothelial cells indicate that in the in vivo situation this phenomenon could well be responsible for maintaining the thrombotic status as demonstrated by ultrastructural analysis. In a later stadium polymorphonuclear leukocytes are also involved in total thromboformation.

Animals↗
PubMed1986

Thrombus induction by endogenic paf-acether and its inhibition by Ginkgo Biloba extracts in the guinea pig.

The anti-thrombotic effects of specific paf-acether antagonist BN 52021 were compared to the effects of Ginkgo Biloba extracts A, B, (A + B), and C. Local superfusion of BN 52021 over an experimentally injured arterial segment embolizes an existent paf-acether induced platelet thrombus. When applied before paf-acether, BN 52021 prevents local thromboformation in this model. Applied intravenously, BN 52021 reduces local thromboformation in a significant way. As compared to this BN 52021 standard, only Ginkgo Biloba B and the (A + B)-mixture present major thromboreductive activity.

Animals↗
PubMed1986

Endothelial injury and platelet thrombosis in mesenteric arteries of rats: a scanning electron microscopy study.

For several years, an in vivo model for the induction and on-line quantification of arterial platelet thrombosis in mesenteric arteries of a small laboratory animal species has been developed in our laboratory. In the present paper, we further document the intimal lesions and the ADP superfusion-induced local platelet thrombus as seen in the scanning electron microscope. The surface morphology of the intimal lesion, induced by electric current, shows a circular or slightly oval denuded area, affecting about 15-20 endothelial cells. The edge of this lesion is often occupied by partially disrupted and detached endothelial cells. The successive embolizations of several ADP thrombi clean this edge and augment the denuded area. The final lesion never exceeds the area of 30-40 endothelial cells. ADP-induced platelet thrombi in invariably appear as loose, sponge-like platelet aggregates, very bloodstream-lined, anchored on the denuded subendothelium. There is an excellent correlation between the in vivo light microscopic observations and the actual ultrastructure of this platelet mass.

Adenosine Diphosphate↗
PubMed1985

In vivo arterial platelet-vessel wall interaction and thrombosis: induction, on-line registration and ultrastructural control.

A technique for induction and on-line quantification of local platelet thrombi in mesenteric arteries of small laboratory animals was developed and standardized in our laboratory. In the past, this model was used to study the nature of platelet-vessel wall interaction in the living animal. The ultrastructure of the experimental intimal lesion and the vessel wall regeneration were assessed by transmission electron microscopy (TEM), both in normal and pathologic conditions. Scanning electron microscopy (SEM) now shows the ultramorphology of platelet thrombi on the experimentally injured arterial segment following topical superfusion with ADP, mepacrine or platelet-activating factor (PAF). The application of these substances, each with proper bio-activity, leads to distinct types of platelet thrombi. Mepacrine or PAF superfusion causes large thrombotic masses, as compared to control, ADP induced thrombi, and seems toxic for the endothelial cells. Mepacrine thrombi differ significantly from PAF thrombi in their platelet density, degree of platelet activation and in their relation to the endothelium that surrounds the experimental lesion. Furthermore, PAF superfusion induces a phenomenon of spontaneous regeneration of the thrombus after its forced embolization. This is probably due to some unknown bio-action of PAF in the vessel wall.

Adenosine Diphosphate↗
PubMed1985

The effect of 1-O-alkyl-2-acetyl-sn-glycero-3-phosphocholine (paf-acether) on the arterial wall.

The effect of a topical paf-acether superfusion over an injured arterial segment was assessed in the guinea-pig, using an opto-electronic in vivo thrombosis model allowing on-line quantification of small platelet thrombus dynamics. As compared to control, ADP-induced, thromboformation and behaviour, exogenous paf-acether causes a large, dense platelet thrombus, invaded and surrounded by numerous leukocytes, spreading widely over the adjoining, vacuolized, endothelium. Its embolization has to be forced with prostanoids, mepacrine, EDTA, or with a specific paf-acether antagonist (BN 52021). A few minutes after such forced embolization, a new thrombus starts growing at the same site, without renewal of the paf-acether superfusion. This phenomenon of spontaneous reappearance after forced embolization can be followed during several hours. Experiments with labelled paf-acether and the paf-acether antagonist indicate a possible endogenous paf-acether (or paf-acether-like) production triggered by superfusion with exogenous paf-acether.

Adenosine Diphosphate↗
PubMed1984

[Persistence of virus in swine stock and breeding farms following an outbreak of Aujeszky's disease].

On seven fattening farms and seven breeding farms, investigations were carried out to examine whether Aujeszky virus was capable of persisting in particular animal groups or units of the farm as a productive infection following a virologically verified outbreak. After an outbreak on fattening farms, virus persisted temporarily as newly arrived piglets became systematically infected. On the farms on which this could be accurately followed, virus persistence continued for at least 1 1/2 to 2 months. However, this cycle of infection was found to be interrupted on each farm within approximately three months after the outbreak, which resulted in a gradual return to a totally sensitive animal population, so that new outbreaks could occur. On the seven swine breeding farms, virus persistence in the farrowing house was examined by placing seronegative sentinel piglets with sows during the immediate post-partum period. Twelve sentinel piglets were placed in the various farrowing houses for a total period of sixty-seven weeks, during which time 172 sows farrowed. None of these piglets became seropositive during their stay on the breeding farms. The results of this study show that Aujeszky's disease virus did not persist on breeding farms and that the productive infection on fattening farms in only transient following an outbreak. Therefore, it is very likely that new outbreaks of the disease are due to reintroduction of Aujeszky's disease virus on the farm. Though the role of latent carrier animals cannot be totally disregarded, natural reactivation of latent virus is believed an exception rather than the general rule.

Animals↗
PubMed1984

Effect of the inhibition of platelet function on the development of the primary atherogenic lesion in rats on a fat- and cholesterol-rich diet.

The involvement of arterial smooth muscle cells in the development of atherogenic lesions following de-endothelialization and platelet-vessel wall interaction was described in detail by Ross et al. (1977). Bourgain & Six (1974) described a method for local de-endothelialization over a small area in a branch of the mesenteric artery of the male white Wistar rat. The vessel wall reaction to the endothelial cell loss was investigated in detail by Potvliege & Bourgain (1976). The reactive pattern following de-endothelialization includes both a marked hypertrophy of the smooth muscle cells, and, if induced at the site of bifurcation, is further accompanied by migration of smooth muscle cells into the subintimal layer (Potvliege & Bourgain 1980). Administration of a fat- and cholesteral-rich diet markedly increased these phenomena (Potvliege & Bourgain 1982).

Animals↗
PubMed1983

Effect of cyclooxygenase inhibition on platelet-vessel wall interaction.

Prostaglandins play an important role in the platelet-vessel wall interaction. Acetylsalicylic acid inhibits the cyclooxygenase activity within the vessel wall. Continuous superfusion with acetylsalicylic acid induces a rapid, but evanescent decrease in thromboformation. The trigger mechanism involved could be related to the ratio of cyclic endoperoxides (PGG2 and PGH2) versus prostacyclin (PGI2).

Animals↗