Search PubMed⌕ Search

Biomedical subjects

R Eloy

Publications and source records attributed to R Eloy.

At least 55 records · Page 3Linked to original sources
PubMed1988

[In vitro study of the action of DOTA and DTPA-gadolinium complexes on platelet functions: aggregation and calcium excretion].

Interaction of 2 complexes of Gadolinium (DOTA Gd meglumin and DTPA Gd meglumin) was studied in vitro with regard to platelet function: aggregation and excretion of ATP and of ionised calcium in response to collagen (2.5 Ig/ml). Excretory functions were measured simultaneously with aggregation by bioluminescent techniques using luciferin for the measurements of ATP and aequorin for measurements of ionised calcium. Platelet aggregation and excretion functions, investigated in vitro, were moderately inhibited in the presence of gadolinium complexes. The greatest effects were seen with DTPA Gd meglumin. Complexation of extra-cellular ionised calcium by NMR products in partially responsible for the inhibition of platelet aggregation.

Adenosine Triphosphate↗
PubMed1987

Thromboresistance of bulk heparinized catheters in human.

Bulk heparinized catheters (1 mm internal diameter) containing 10% heparin ionically bound, were tested in four human volunteers. Catheters containing 0% and 10% heparin were compared in each individual using ultrasound microflow velocimetry, permeability test, sequential determinations of activated partial thromboplastin time, heparin levels and generation of Fibrinopeptide A, beta thromboglobulin and Platelet factor 4. Although the release of heparin expressed by its anti-IIa activity is of similar range in the four individuals the release of anti-Xa activity is variable and generally of greater magnitude, suggesting a privileged migration of low molecular weight components of heparin. These antiproteasic activities of heparin are sufficient to inhibit fibrin formation and blood coagulation despite their relative inability to prevent platelet activation.

Catheters, Indwelling↗
PubMed1987

Haemocompatibility and biological course of carbonaceous composites for cardiovascular devices.

A new class of carbonaceous composites has been developed for cardiovascular devices. The aim of the present study, performed in dogs, was to test the immediate blood compatibility of these materials when inserted within the vascular bed. Biocompatibility studies were performed on vascular cylinders (6 mm i.d.) and intra-atrial implants. The specimens were examined sequentially by SEM at 10, 20, 30, 180 s and 10 min after re-establishment of the blood flow. Patency of the vascular cylinders was tested during the second and third postoperative month by Doppler ultrasound investigations; specimens were examined by light and electron microscopy (scanning and transmission) at 15, 60 and 110 d following implantation. As early as 10 s after re-establishment of the blood flow platelet adhesion and a limited fibrin mesh with few erythrocytes developed on the material. Platelet aggregates were only observed on intravenous implants. Except in the case of the intravenous insert, no thrombosis developed at the contact of intra-arterial or intracardiac implants. After 15 d it was completely covered by a fibrocellular layer (3-5 cells thick) consisting of large myofibroblasts with microfilaments, newly synthesized collagen and elastin. Endothelial-like cells developed and were completed 2 mnth after implantation. However, deposits present inside and outside the fibrocytic cells of the newly developed tissue were observed corresponding to carbon peaks as indicated by wavelength dispersive X-ray microanalysis.

Animals↗
PubMed1987

Mechanical properties and biocompatibility of two polyepoxy matrices: DGEBA-DDM and DGEBA-IPD.

The aim of this paper was to study the biocompatibility and mechanical properties of materials for orthopaedic and odontologic surgical use. The products used were obtained by polycondensation of a diepoxy resin (DGEBA) with two curing agents (DDM or IPD). The materials present a slight swelling in liquid medium and their thermomechanical properties are hardly affected after 12 month implantation. The absence of molecular desorption in isotonic liquid and human serum confirms their hydrolytic stability and thus their inertia. These materials do not give rise to an intolerance reaction by neighbouring tissues during implantation time (1 d to 12 month).

Aniline Compounds↗
PubMed1987

Ultrastructural immunolocalization of elastic fibers in rat blood vessels using the protein A-gold technique.

Identification of elastic fibers at the ultrastructural level is accomplished by a post-embedding immunohistochemical technique using the protein A-colloidal gold method. Antisera against elastins from human dermis and rat aorta have been characterized by radioimmunoassay and then applied to thin sections of rat blood vessels. Two fixative solutions and two embedding media have been tested. Both antibodies bind to elastic fibers of normal arteries and veins, indicating crossreactions among organs and species. The high sensitivity of this method is demonstrated by its application to the detection of neo-elastogenesis in the intimal thickening of aortic grafts.

Animals↗
PubMed1986

[Contrast media in angiography: present and future].

The review proposed here is not an raised up work. Its purpose is to summarise a lot of data concerning clinical trials and some toxicity factors about uro-angiographic contrast material (CM) used in radiology. the accent has been put on physico-chemical properties, particularly hypertonicity, of iodinated CM in clinical use; the natural history of a CM molecule after intravascular injection explains the repartition of drugs, according to time, in a bicompartmental model (interstitial and vascular) with urinary excretion; the pharmacological basis of side effects are known from a lot of experimental studies; these works allow to dissociate general (or systemic) toxicity and particular side effects for targets organs (heart, nervous system, kidney). Finally the future of CM molecules, specifically for angiography, is evoked about some research ways.

Angiography↗
PubMed1986

Adventitial resection of small artery provokes endothelial loss and intimal hyperplasia.

While adventitial resection is a part of the preparation of microvessels for operation, the procedure may provoke damage to the vessel wall. The histologic and ultrastructural endothelial lesions associated with adventitial resection, the interface of the blood vessel and the course of endothelial repair are discussed herein. The adventitia of the abdominal aorta of rats was stripped under microscopic magnification (32X) around the whole circumference of infrarenal segment of 1 centimeter in length. The rats were sequentially sacrificed. Fixation and silver staining were carried out in vivo. The specimens were collected at six, 12 and 24 hours, at seven, 15, 30 and 90 days, and at six, nine and 12 months after injury. These specimens were studied by en face light microscopy, scanning electron microscopy (SEM) and transmission electron microscopy (TEM). The results of en face light microscopy and SEM investigations showed: an initial severe trauma of the endothelial surface leading to complete de-endothelial areas as early as six hours after injury, the lesions were limited to the adventitial resected areas; at seven days the polygonal cells were recognized in silver stain preparation; at 30 days the endothelial surface was partially reconstituted but cells had large protoplasmic areas, TEM in the same time period confirm the absence of the endothelial cells up to 30 days; at 90 days the reconstitution of the endothelial layer was almost complete, and intimal hyperplasia was observed already at one month and appeared to have stabilized at six months postoperatively with three to four cell layers. These results suggest that: adventitial resection immediately provokes endothelial desquamation; endothelialization is a slow process when large areas are involved, and intimal hyperplasia may develop even on an autologous arterial segment, thus providing new insight to the etiopathogeny of vascular graft initial hyperplastic reactions.

Animals↗
PubMed1985

Immunolocalization of factor V in adult and fetal rat liver.

Immunolocalization of the factor V was performed in adult and fetal rat liver by means of an indirect peroxidase labelling. This could be done owing to the production in our laboratory of a mono-specific antiserum anti rat factor V. In all the cases (perfused and non-perfused adult liver and fetal one) the observation of the sections has revealed an intense circular or granular labelling into all the hepatocytes whatever was their localization in the hepatic lobule. Hepatic endothelial cells seemed to be negative for factor V and this aspect of our results was discussed.

Animals↗
PubMed1985

In vitro study of the inhibition of coagulation induced by different radiocontrast molecules.

The anticoagulant activity of seven intravascular radiocontrast molecules (RCM) was evaluated in different in vitro systems using citrated human plasma. Each RCM was tested in a concentration range of 5 to 50 mM. The thrombin time and the reptilase time showed a dose-dependent lengthening of fibrinoformation, the recording of fibrinoformation exhibited a significant delay of fibrin monomer generation and polymerization although the amplitude of the fibrinoformation was not decreased. The interfering effect with fibrin clot formation impairs also global coagulation tests and monospecific coagulation tests using fibrinoformation as the final step of the assay, but a possible interaction between RCM and some specific coagulation factors cannot be excluded. RCM potentiated the anti-thrombin action of heparin but the inhibition or delay of fibrinoformation is not related to an antithrombinic effect of contrast media. The thrombin amidolytic activity is not modified by RCM but the generation of FpA is delayed and decreased. The ultrastructure of the fibrin clot is not altered at the end of the polymerization.

Adult↗
PubMed1985

Long-term behavior of bovine collagen membrane used as vascular substitute. Experimental study in rats.

The aim of the present study was to evaluate the sequence of the immediate and the mid/long-term organization of the blood interface of a collagenous membrane used as vascular substitute in rats. The implants were prepared from calf skin type I insoluble collagen, obtained after acidic dispersion, in absence of chemical or tanning treatment. They were used to patch an aortic defect by means of microsurgical techniques. The animals were sequentially sacrificed for immediate hemocompatibility studies at 10 s, 30 s, 10 min, 3 h, and 6 h, for long-term analyses of the organization of the blood material interface at the 7th, 15th, 45th, 60th, 90th day following the surgery and each month until 14 months after aortic replacement. The superficial immediate events at the blood patch interface demonstrated erythrocytes heavily engulfed in a thin but dense fibrin mesh both at the patch and at the adjacent aortic wall surfaces. Neither adherent platelet nor platelet aggregate were detectable on the collagen patch surface. This fibrinoerythrocytic membrane covered the patch completely at 60 s and at 3 h the deposit was limited to 5-6 erythrocyte layers as confirmed by histology. It did not further develop on the 7th day. At the blood-collagen interface there progressively developed a tissue composed of active myofibroblasts, collagen bundles, and elastic fibers. After 4 months, nests of fibroendothelial cells were present, and between 6 and 14 months surface cell differentiation, although complete on the adjacent aorta was still incomplete on the bovine collagen patch, amorphous fibers, and fibroendothelial cells coexisting. Heterologous patch debris were still present 14 months after implantation and were associated with macroscopic and ultrastructural calcification, which need further investigations concerning the exact nature and mechanism of mineralization of vascular substitutes of biological nature.

Animals↗
PubMed1985

Experimental DMNA induced hepatic necrosis: early course of haemostatic disorders in the rat.

The course of haemostasis defects was investigated in dimethylnitrosamine (DMNA) acute liver necrosis. Before 18 hr there was no evidence of disseminated intravascular coagulation (DIC) nor of abnormal fibrinolysis. At 12 hr the level of the vitamin-K-dependent factors (factors II, VII, IX and X) was reduced to 25-63% of control. Factors V and VIII:C levels decreased to about 10 and 20% by 12 hr. Factor V was the only molecule which decreased significantly by 6 hr. The rapid decrease of these proteins might be related to an early parenchymal functional impairment attested by early structural lesions observed in the endoplasmic reticulum and nucleus. The isolated decrease of factor V in the absence of any significant change in serum transaminase (SGOT and SGPT) levels is proposed, at least in the rat, as an early criterion of hepatic failure.

Alanine Transaminase↗
PubMed1985

An ultrastructural study of the contact between type I collagen assemblies and the induced human platelet aggregates.

Several type I collagen assemblies have been tested for their ability to induce platelet aggregation: a molecular solution, native and reconstituted native-type fibrils, segment long spacing aggregates (SLS) and an unordered collagen multimer. The ultrastructure of the inducer has been observed before its introduction into the platelet suspension as well as within the final aggregates. The following results have been obtained: 1) platelet aggregation was induced by the monomeric solution of collagen only after a long lag phase. While the original solution did not contain fibrillar elements, the platelet aggregates were in contact with collagen filaments showing a faint banding pattern. The results confirm that the longer lag time recorded is necessary for the collagen to polymerize and that the monomeric collagen actually does not induce platelet aggregation; 2) native and reconstituted native-type fibrils, SLS and unordered collagen multimer similarly induce platelet aggregation and were not modified during the course of this phenomenon; 3) although the general ultrastructure of the contacts between platelet and collagen assemblies were similar, a difference was noted in the extent of contact: a focal zone with native-type fibrils, numerous zones of contact with SLS and very extensive contact with unordered multimer. These results suggest that the combination of three factors are necessary to trigger platelet activation by collagen: the nature of the active sites on collagen, the density of these sites and the geometry of the collagen assembly.

Animals↗
PubMed1984

A freeze-fracture and thin section study of the interaction of blood platelets with native type I collagen fibrils.

The membranes of non-activated and activated human blood platelets have been studied with freeze-fracture and conventional electron microscopy. Aggregated platelets activated by ADP or by native collagen fibrils did not show any intramembrane particle clustering. No intramembrane modification is detectable at the contact regions with collagen fibrils. However, a local densification of the cortical cytoplasm is noted in thin sections where platelets make contact with collagen fibrils. These results suggest that either the membrane receptor for collagen is not visualized by freeze-fracturing or that, as suggested previously, the binding site on collagen may not have a specificity and affinity as high as expected from a conventional receptor-ligand interaction.

Blood Platelets↗
PubMed1983

[Venous grafts as arterial substitutes. Immediate and medium-term development].

This study, based on the authors' experiments in dogs and on data from the literature, describes the immediate and mediumterm histological development of autologous vein grafts. Dissection alone results in extensive endothelial cell desquamation, which may be aggravated by distension and preservation of the graft in an inappropriate medium. Immediately after re-establishment of the arterial blood flow the inner surface of the graft is covered by a fibrinoerythrocytic membrane. Endothelialization begins 10-15 days later but remains incomplete in dogs after 9 months; it is not limited to the suture lines but proceeds by islets disseminated over the surface. As early as the 15th post-operative day, a myo-intimal layer of myofibroblastic cells develops; the origin and control of these cells are still unknown. A better knowledge of the histological development of vein grafts and underlying mechanisms appears to be essential to improvements in surgical procedures and subsequent long-term functional performance of the grafts.

Animals↗