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Biomedical subjects

L Drouet

Publications and source records attributed to L Drouet.

At least 127 records · Page 7Linked to original sources
PubMed1984

Prothrombin Salakta: an abnormal prothrombin characterized by a defect in the active site of thrombin.

An abnormal prothrombin has been detected in a 17 yr-old female originating from Tunisia. There was no history of excessive bleeding. Prothrombin time and activated partial thromboplastin time were moderately prolonged. Prothrombin activity was 15-18% when measured using either the classical one-stage and two-stage assays, or assays with Echis carinatus venom or staphylocoagulase, whereas prothrombin antigen was 100%. In keeping with current nomenclature practices, the abnormal molecule has been designated prothrombin Salakta. The electrophoretic behaviour and calcium binding properties of the abnormal prothrombin did not differ significantly from normal, as assessed by crossed immunoelectrophoresis. Prothrombin Salakta was isolated by chromatography on DEAE-Sephadex and Dextran sulphate sepharose. Electrophoretic migration of purified prothrombin Salakta on SDS polyacrylamide gels or alkaline disc gels was normal. Upon activation by either bovine factor Xa or Echis carinatus venom, thrombin activity produced by prothrombin Salakta was only 15% of normal, even when the incubation period was prolonged for 24 hours. The pattern of factor Xa-catalyzed proteolysis of prothrombin Salakta, investigated by SDS polyacrylamide gel electrophoresis, was found to be normal. These results indicated that prothrombin Salakta was characterized by a defective thrombin enzymatic activity. Thrombin Salakta was therefore isolated by heparin-sepharose chromatography. Affinity for heparin and molecular weight of thrombin Salakta were found to be normal. Biological activity of thrombin Salakta, determined by clotting assay, was 535 u/mg versus 3 200 u/mg for normal thrombin. Amidolytic activity of thrombin Salakta parallelled its clotting activity, suggesting that the defect resides either in the catalytic site or in the residues adjacent to the catalytic site and implicated as contact residues, rather than in the fibrinogen recognition site.

Adolescent↗
PubMed1984

Monoamine oxidase activity in the cerebral vasculature: comparison between fresh microvessels from different structures and cell cultures derived from microvessels.

Monoamine oxidase (MAO) activity was studied in various preparations of porcine brain microvessels to explore further the role of this enzyme in the blood-brain barrier to catecholamines. No difference was noted (Vm and Km) between microvessels isolated from three structures (caudate nucleus, thalamus, and cerebral cortex) in which the responses to circulating catecholamines in vivo are markedly different. Large and small microvessels from the caudate nucleus and the thalamus presented the same specific activity. Cell cultures obtained from small microvessels were rich in endothelial cells as identified by the presence of Factor VIII-related antigen. These preparations displayed an MAO activity about ninefold less than freshly isolated microvessels, although their prostaglandin synthetase activity appeared normal. These results suggest that MAO activity is not the main factor determining the regional differences in the cerebrovascular reactions to catecholamines, that MAO is not specifically localized in the endothelium but must be also present in the smooth muscle, and that the MAO activity is greatly decreased during cell culture.

Animals↗
PubMed1984

[Traumatic left ventricular aneurysm disclosed by systemic emboli. Value of platelet labelling with indium].

The authors report a case of traumatic left ventricular aneurysm, presenting with recurrent cerebral embolism, 36 years after a thoraco-brachial bullet wound. The 58 year old man had no symptoms of angina or particular cardiovascular risk factors. The ECG showed changes of chronic anterior wall infarction, observed 10 years previously on a routine preoperative recording. There was a calcified circular para-apical shadow on chest X-Ray. The antero-apical region showed hypofixation on myocardial scintigraphy, and hypokinesia on isotopic angiography. The coronary arteries were normal. Indium III platelet marking revealed a focus of hyperfixation within the left ventricle. At surgery, a true calcific para-apical left ventricular aneurysm was discovered, containing a fresh thrombus. This lesion was resected. Peroperative Indium III platelet test confirmed that the thrombus was the site of high uptake. The surgical result was good at 6 months follow-up. This case illustrates: the value of the Indium test which would appear to be a very specific and sensitive method of detecting intraventricular thrombi. This test, which appreciates the thrombotic activity of intracardiac masses is a useful complement to other non-invasive methods such as 2D echocardiography; the special characteristics of post-trauma left ventricular aneurysms which are rare, often diagnosed late, at the time of complications such as systemic embolism, commonly pose medico-legal problems, and for which surgical treatment seems to be indicated in symptomatic patients.

Blood Platelets↗
PubMed1983

Plasminogen Paris I: congenital abnormal plasminogen and its incidence in thrombosis.

An abnormal plasminogen was discovered because of a decreased level of plasminogen activity in plasma contrasting with a normal level of plasminogen antigen concentration. The same discrepancy was found in the purified plasminogen. The molecular abnormality seems to be inherited. The patient is a heterozygote. The experimental findings can be explained by assuming that half of the plasminogen is normal, while the other half is an inactive mutant protein, without catalytic activity after SK or UK addition. There was no binding of labeled DFP and a decreased binding of TLCK to the abnormal plasminogen. The role of the abnormal plasminogen in thrombotic tendency is uncertain since the patient is the only one who has suffered a thrombotic accident, while her relatives who present the same defective plasminogen have not had thrombotic problems.

Blood Coagulation↗
PubMed1983

[Pure defibrination after timber rattlesnake bite].

The only disorder of coagulation observed after a timber rattlesnake (Crotalus horridus) bite was a total absence of fibrinogen which lasted 64 hours despite hourly administration of cryoprecipitates. The pure defibrination experimentally obtained with this particular species of crotalid snakes underlines the specificity of the coagulation disorder and the impossibility of identifying the coagulopathy induced by venom poisoning without laboratory examination.

Adult↗
PubMed1983

[Molecular abnormalities in recurrent thromboembolic disease].

The diagnosis and treatment of apparently idiopathic recurrent thromboembolic disease (RTED) still raise difficult problems. However, recent data suggest that abnormalities of coagulation and fibrinolysis factors are important. Hereditary antithrombin III (AT III) deficiency or abnormal AT III, and hereditary protein C deficiency with autosomal dominant transmission have been associated with severe familiar RTED. More recently, we described a dysfibrinogenemia characterized by abnormal fibrin polymerization and abnormal plasminogen binding to the fibrin clot, responsible for familial RTED. Disorders of fibrinolytic activity in RTED are represented, in 70% of the cases, by reduced release or lack of production by endothelial cells of a vascular plasminogen activator. Hereditary plasminogen deficiency or abnormal plasminogen, although rare, are regularly responsible for RTED.

Antithrombin III Deficiency↗
PubMed1982

[PDGF (platelet derived growth factor): a regulator of connective tissue proliferation or an artefact?].

Platelets carry, and release after stimulation, mitotic activities for connective tissue cells in culture. One of these activities has been studied carefully: the PDGF, it is a peptide, molecular weight 30,000, pHi 9.8-10, heat stable. Beside this mitotic activity, PDGF bears migrative, chemotactic and metabolic functions. Hypothetical theories have implicated PDGF in different pathological conditions (atherosclerosis, myelofibrosis, ...) but there is no direct proof that PDGF is active in vivo. Recently there has been experimental data suggesting that the mitotic activity of PDGF in vitro could be a technical artefact.

Blood Platelets↗
PubMed1981

Monoclonal antibody to human platelet glycoprotein I. II. Effects on human platelet function.

The effect on platelet function of a monoclonal platelet antibody to platelet membrane glycoprotein I was tested. This antibody, AN51, inhibited ristocetin or bovine factor VIII-induced aggregation but did not modify ADP, collagen type I or type III, thrombin or arachidonic acid induced aggregations. Furthermore, the adhesion-aggregation of platelets induced by microfibrils was also inhibited by the antibody. Platelet adhesion to rabbit aorta subendothelium was impaired by the antibody. The persistent adhesion of platelets to collagenase-treated subendothelium was also inhibited. These findings strongly suggested that platelet membrane glycoprotein I could interact with a non-collagenic microfibrillar component of subendothelium. The binding of factor VIII/von Willebrand factor to platelet membrane in the presence of ristocetin was decreased in the binding site for factor VIII/von Willebrand factor to allow platelet adhesion to subendothelium.

Antibodies, Monoclonal↗
PubMed1981

Time course of plasma growth hormone during exercise in humans at altitude.

The effects of hypoxia on growth hormone release during submaximal exercise were studied 1) in eight highlanders (HL) at 3,800 m (La Paz, Bolivia); and 2) in five lowlanders (LL) at sea level, after 5 days' sojourn at 2,850 m, and while breathing a hypoxic gas mixture (FIO2 - 0.15 corresponding to PIO2 at 2,850 m) 1 mo after returning to sea level. Concentrations of immunoreactive human growth hormone ([IRHGH]), blood glucose ([G]), free fatty acids ([FFA]), and lactate ([LA]) were determined repeatedly at rest, during 1 h of exercise, and after 1 h of recovery. Compared with LL, in HL, the resting value of [IRHGH] is higher, the rate of increase at the beginning of exercise is faster and earlier, but the mean maximal value reached at the end of exercise is similar. The response pattern in LL during the early stages of exposure to hypoxia resembles that of HL. No correlation was found between peak values of [IRHGH] and maximal values of [LA] and [FFA] or minimal values of [G]. The possible causes of the different time sequence observed in growth hormone dynamics during hypoxia are suggested: an alteration of the clearance of the hormone through a more pronounced reduction of hepatic blood flow or a difference in the state of the pituitary gland before the exercise begins. The study emphasizes the importance of characterizing time sequence of [IRHGH] by parameters other than the maximal value, e.g., by mean concentration computed over exercise period.

Acclimatization↗
PubMed1981

[Congenital deficiency of platelet alpha-granules and medullary reticulinic fibrosis. Physiopathogenic hypothesis (author's transl)].

Hematological investigations of two propositus from a family with congenital thrombopathia characterised by a moderate thrombopenia and a specific platelet alpha granule deficiency revealed that the thrombopathia was associated with a constitutive reticulinic myelofibrosis, without any sign of evolutivity. This association led us to present an hypothesis to explain the genesis of this myelofibrosis. This hypothesis is based on the potential role of a mitogenic factor(s) synthetized in megakaryocytes and transported normally by platelets in alpha granules, to induce fibroblastic proliferation and increased synthesis of collagen type III by bone marrow. This myelofibrosis is similar to that found in most of myeloproliferative disorders at some step of evolutivity. In these diseases myelofibrosis is associated with qualitative and quantitative abnormalities of platelets and megakaryocytes. These abnormalities give elements to sustain our hypothesis.

Blood Platelet Disorders↗
PubMed1981

[Relation between the wall structure and modifications of the blood content (author's transl)].

In view of its anatomical position, physical characteristics and metabolism, the endothelial cell plays a major part in maintaining the integrity of the vascular system and in the relation between the blood content, both plasma and blood cells, and the wall structure. Where this continuous single layer undergoes anatomical or functional changes, a new equilibrium is set up, an equilibrium which is multifactorial and dynamic. It is governed by the vascular and blood components and by their interrelation; it varies as a function of time and of the biorheological conditions. The interrelationship between the blood content and the wall plays an important part in vascular pathology, especially of the degenerative and thrombotic type. A better understanding of these factors will enhance the possibility of preventing atherogenesis and lay the basis for a coherent and effective therapeutic attitude thrombosis.

Blood Vessels↗
PubMed1980

[Interaction between the platelets and the vessel wall. Part 3: Investigation].

Numerous techniques are now suggested for the investigation of interactions between the platelets and the vessel wall. These techniques offer the possibility of precise diagnosis of the majority of haemorrhagic diseases of primary haemostasis. A critical study nevertheless shows that few tests of haemostasis are of use in defining a state predisposing to thrombosis and amongst others, biological study of the vessel remains very limited.

Animals↗
PubMed1980

[Interactions between the platelets and the vessel wall. Part 2: physiopathology (author's transl)].

The role of the blood platelets in the aetiogenesis of arterial lesions has been underlined in recent years by studies of platelet elastase and above all the mitogenic factor of smooth muscle cells. A truly thrombogenic theory of atherosclerosis can now be envisaged. In the context of arterial thromboses, it is interaction between the damaged vessel wall, the lesion most often being atherosclerosis, and blood platelets which gives rise to the thrombus. In certain conditions such as diabetes abnormalities in the interaction between platelets and vessel walls may favour the development of vascular lesions and thromboses. With regard to venous thrombosis, the participation of the vessel and/or platelets is less clear. However, recently described platelet procoagulant activities could activate coagulation mechanisms. Knowledge of diseases of primary haemostasis has benefited from studies of platelet-vessel interaction. Whilst the spontaneous haemorrhagic syndrome of major thrombocytopaenia remains mysterious, platelet membrane molecular abnormalities in thrombopathies such as Bernard Soulier syndrome or thrombasthenia offer an explanation for their mechanisms. By their interaction with the vessel, platelets finally participate in mechanisms of inflammation, immunological conflicts, disseminated intravascular coagulation and metastatic dissemination.

Arteries↗