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Biomedical subjects

P Carpentier

Publications and source records attributed to P Carpentier.

At least 73 records · Page 4Linked to original sources
PubMed1995

Partial interruption of the inferior vena cava: ten-year evolution in protocols at Grenoble University Hospital. Study of 621 patients.

An evolution in protocols regarding indications and modalities for Partial Interruption of the Inferior Vena Cava (PIIVC) on 621 patients at Grenoble University Hospital is reported and the influence of new methods in diagnosis (vascular sonography) and therapy (percutaneous filters) is assessed. This comparative study covers the intervals from 1982-1984 (Period A - 333 patients), and 1989-1991 (Period B - 288 patients). The percentage of patients with venous thromboembolic disease who underwent PIIVC clearly decreased (21.8% in period A vs. 13% in period B, p < 0.01). The incidence of what are currently miscalled "prophylactic", but are in fact adjunctive indications also diminished (115 patients in period A, or 34.5% of the PIIVC cases vs. 60 patients in period B, or 20.8% of the PIIVC cases, p < 0.05). There was a reduction in the use of Miles caval clips (59 patients or 17.7% for period A vs. 34 patients or 11.8% for period B, p < 0.05). Although there has been an increase in the use of percutaneous caval filters, the use of percutaneous filters has not lead to an increase in the real rate of PIIVC performed by an Angiology Unit with a large experience in the diagnosis and follow-up of patients with venous thromboembolic disease.

Combined Modality Therapy↗
PubMed1995

[Antegrade scrotal sclerotherapy in the treatment of varicocele].

The antegrade scrotal sclerotherapy is a minimally invasive surgical technique in the treatment of the varicocele. Through a small scrotal incision a straight vein merging in the spermatic vein is isolated and cannulated. An antegrade phlebography is performed and ethoxysclerol is injected in the vein. We have performed this technique in 35 patients with a follow-up of at least 3 months. All patients except one (97%) show no more varicocele. This technique has a low morbidity, is cheap and as effective as the other treatment modalities. The antegrade sclerotherapy is competitive to the retrograde embolisation and has the advantage that the treatment can be performed in all cases, even in cases of recidive.

Adolescent↗
PubMed1995

Clinical diagnosis compared with findings of magnetic resonance imaging in 242 patients with internal derangement of the TMJ.

The aim of this study was to compare the provisional diagnosis based on an initial clinical examination with subsequent findings of magnetic resonance imaging in patients with internal derangement of the temporomandibular joint. Clinical examinations were conducted on 242 patients (198 women and 44 men) who had unilateral (51%) or bilateral (49%) temporomandibular joint internal derangement. They were divided into the following categories: (1) disc displacement with reduction; (2) disc displacement without reduction; (3) "stuck" disc; (4) degenerative arthrosis with or without one of the above; and (5) normal temporomandibular joint of the contralateral side. There was no statistically significant difference in the distribution of disorders on a unilateral or bilateral basis or in the prevalence of disorders in right versus left joints. Based on the high occurrence of matching true-negative data, this study showed a highly statistically significant correlation between the magnetic resonance findings and the clinical data for all categories of derangement. Despite this high correlation, the magnetic resonance imaging and clinical diagnoses matched exactly in only 287 of the 484 joints studied. There was only partial agreement in the remaining 197 joints. The best clinical diagnosis in relation to the magnetic resonance findings was observed in the arthrosis category followed by the categories of normal joint, disc displacement with reduction, stuck disc, and disc displacement without reduction, in descending order. This study strongly suggests that degenerative arthrosis is a result of a long-term displaced disc. The clinical examination alone did not correctly indicate all the structural defects; therefore, it is insufficient for determining the status of the joint.

Adult↗
PubMed1994

Modulation of soman-induced neuropathology with an anticonvulsant regimen.

Rat hippocampus and piriform cortex were examined for pathological changes 48 hours after exposure to a convulsant dose of soman. Animals were treated with a low dose of atropine just after soman and were then injected, after 10 or 40 minutes of seizures, with both the anticonvulsant drugs NBQX and TCP. Atropine given alone counteracted the extensive neuronal loss due to soman in both areas without prevention of neuronal suffering. Comparatively, the complete anticonvulsant regimen, given before 40 minutes of seizures, totally prevented hippocampal soman-induced neuropathology. Neurones of piriform cortex were still suffering whatever the time of injection of the drugs. This emphasizes the need for a rapid and definitive anticonvulsant treatment just after soman intoxication to block the subsequent neurotoxic effect of nerve-agent exposure.

Animals↗
PubMed1994

Coadministration of atropine, NBQX and TCP against soman-induced seizures.

The ability of relatively low doses of atropine, NBQX and TCP administered in combination to prevent or stop seizures induced by soman, was studied in rats. While these drugs injected together early after soman prevented the onset of seizures, their delayed concomitant administration after 5 or 30 min of epileptic activity only mildly attenuated the intensity of seizures. Conversely, a total arrest of epileptic activity was observed in 80 to 100% of animals when NBQX and TCP were given together after 5 to 50 min of seizures to atropine pretreated rats. The large time-window for antiepileptic effectiveness of this 'three drug treatment', provided that atropine is administered early after soman, is discussed in relation to reciprocal potentiations of the antiepileptic effects of atropine, NBQX and TCP in combination.

Animals↗
PubMed1994

[Epidemiology of chronic venous insufficiency].

From an epidemiological point of view, at least three different entities of chronic venous insufficiency (CVI) can be defined: heavy legs syndrome is experienced by about half the working people of industrialized countries. It is most frequently linked to varicosis, nevertheless, in one case out of three, no venous incompetence is associated. Female sex, prolonged standing position and overweight are other significant risk factors; varicosis comes with modern civilization. Its prevalence is very low in African and Asian or Australasian aborigen populations although immigrant subjects from these regions have the same risk as the population of their host country. Sedentarity, overweight, tight clothing may provide part of the explanation. But the main factor is probably linked to the low fiber diet in industrialized countries through induced constipation and increased abdominal pressure, or because of the associated low vitamin F intake. Varicosis is rarely seen before adulthood, and its prevalence increases with aging. Sex ratio is unbalanced (F/M estimates: 1.5 to 3.5), that is mainly explained by childbearing and hormonal gactors. A familial factor has also been evidenced, with a relative risk of 2, when one parent has varicosis, and about 3 when both are involved; epidemiological data regarding cutaneous trophic changes in CVI are restricted to leg ulcers: 1% of the general population, and 4 to 5% of people aged 80 and more are afflicted. Leg ulcers are frequently found in the post-thrombotic syndrome, but female sex and varicosis are other significant risk factors. Up to now, epidemiological data are too scarce for a definite demonstration of the natural history of the different subsets of CVI. On the other hand, they clearly show that major medical, social and economical problems are involved.

Adult↗
PubMed1994

[Functional anatomy of the venous system of the lower limbs].

Surgical techniques including CHIVA and ambulatory phlebectomy and angiographic methods provide a new approach to the anatomy of the venous system in the lower limbs. The endothelium develops fibrous folds of the intima which form valves preventing backward flow. Staged pairs of valves are found throughout the network. The venous wall has three layers: the inner layer, the intima, acts as a mechanical barrier and regulates coagulation and vasomotricity and plays an important role in exchanges. Venous constriction is produced by the middle layer, the media, and the adventitia, the outer layer, connects the vein to surrounding supportive tissue. The anatomy of the venous system in the lower limbs is divided into a superficial network lying over the superficial aponevrosis. This system drains the teguments. The deep system, below the aponevrosis, drains all the blood flow coming from the muscles. These two systems are connected by perforating veins with valves guaranteeing one-way flow. Communicating veins link together the different veins within each network.

Humans↗
PubMed1994

[Venous hemodynamics of the lower limbs].

Low pressure venous return results from several different pump systems. Blood flow and velocity depend on sympathetic tone and contraction of the veins modulating distensibility. In patients with chronic venous insufficiency, different components including hyperdistensibility, hyperpressure, valve failure, back-flow and stasis, lead to a vicious circle. These elements modify the venous wall and lead to hyperdistension producing modified distensibility and/or formation of varicose veins. Endothelial and smooth muscle cells participate in these changes. Smooth muscle cells play a major role: some hypertrophy and/or lose their contractility, synthesizing and sometimes rapidly destroying tissue. These changes in the circulation, sometimes increased by inflammation and thrombosis, affect microcirculatory haemodynamics with a variable delay. The venous system, even when pathological (as long as it is not totally invaded by fibrosis) responds to a large number of relaxing or constricting pharmacological agents, justifying their therapeutic value.

Hemodynamics↗
PubMed1994

[Microcirculation and rheology].

Microvessels, especially in the skin and muscles are organized in functional units. These units are controlled by the adrenergic system and hormones but also have autonomous metabolic and myogenic regulatory systems independent of vasomotion. Microcirculatory blood flow is affected by special rheologic properties: a low arteriolar haematocrit rises to the systemic level in the venules. The flow rate in the venules is low, and together with the raised haematocrit, explains the microvenular sensitivity to hyperviscosity. Capillarovenular microangiopathy, recently described by standard and fluorescent capillaroscopy, develops during chronic venous insufficiency. The capillary loops appear dilated and knotted together with fibrous deposits and pericapillary oedema. Venous hyperpressure is the cause of this microangiopathy. Together these phenomena disrupt normal haemodynamics and physiology of the microcirculatory unit: baseline hyperhaemia, lowered vasomotor and vasomotion reactivity, development of rheologic disorders (haemoconcentration, hyperfibrinogenaemia, erythrocyte agregation) and decreased fibrinolysis. Modifications in the transcapillary exchange is related to hypoxia and is aggravated by depressed lymphatic drainage. The main consequence is oedema. Inflammation, a characteristic of these microangiopathies could occur when the endothelium is activated by the hypoxia. The classical mediators of inflammation would activate interactions between the different cells: endothelium, granulocytes, monocytes and platelets. Several pharmacological models have been developed for the analysis of these data including exploration of the permeability and capillary resistance and rheological analysis. Objective observation of the microangiopathy with capillaroscopy, together with modern haemodynamical, biological and pharmacological methods are essential for a better understanding of microvascular disorders in chronic venous insufficiency.

Capillary Permeability↗
PubMed1994

Antiepileptic effects of NBQX against soman-induced seizures.

The ability of NBQX, a potent antagonist of AMPA glutamatergic receptors, to prevent or stop seizures induced by the organophosphate soman, an irreversible inhibitor of AChE, was studied in rats. NBQX administered concomitantly with soman prevents the onset of seizures (ED50: 29.2 mg kg-1, i.p.). Administered 5 min after the onset of seizures, NBQX greatly reduces the intensity of the epileptic activity. The same decrease of epileptic activity is observed, in the presence of atropine, when the administration of NBQX is delayed 15 min after the onset of seizures. NBQX thus appears as a promising antiepileptic candidate against soman-induced seizures. The roles of AMPA and muscarinic receptors in the onset and propagation of soman-induced epileptic activity are discussed.

Animals↗
PubMed1994

Anticonvulsant and antilethal effects of the phencyclidine derivative TCP in soman poisoning.

The protection afforded by TCP (thienylcylohexylpiperidine), a non-competitive blocker of N-methyl-D-aspartate (NMDA) receptors, against the seizures and lethality produced by 2 x LD50 of soman (62 micrograms/kg, sc), an irreversible inhibitor of cholinesterase, was studied in guinea-pigs. In the presence of additional anticholinergic medication (pyridostigmine: 0.2 mg/kg, sc, 30min prior to soman; atropine sulphate: 5mg/kg, im, 1 min post-soman), TCP pretreatment (2.5mg/kg, im, 30 or 15 min prior to soman) did not generally prevent the appearance of soman-induced status epilepticus but did arrest it after 30-40 min in 80% (TCP-30min) or 100% (TCP-15min) of the convulsing subjects. Moreover, in all subjects treated curatively, TCP was able to interrupt ongoing status epilepticus in approximately 20, 10 or 8 min when it was administered 5, 30 or 60min respectively after the onset of epileptiform tracings on EEG. All of these curatively administered animals survived and recovered remarkably well. On every criteria examined (latency-to-seizure arrest, 24hr-survival rate, clinical recovery), injection of 2.5mg/kg TCP after 90min of seizures appeared slightly less efficient compared to earlier curative administration. Therefore, our study (a) establishes that the previously reported capacity of MK-801 (dibenzocyclohepneimine) to counteract soman toxicity is not unique and could be extended to other non-competitive inhibitors of NMDA receptors; (b) shows that TCP could easily prevent and, above all, interrupt soman-induced seizures; furthermore, TCP appears the first compound ever tested on soman poisoning that still displays satisfactory anticonvulsant activity after such a long duration of initial status epilepticus (90min); therefore, TCP might be of special value for the delayed therapy for soman poisoning; (c) confirms that NMDA receptors are involved in the maintenance of seizures and play an important role in other processes implicated in the overall toxicity (including the lethal respiratory effects) of soman poisoning.

Animals↗
PubMed1994

[Prevention and treatment of status epilepticus induced by soman].

Treatment of the convulsive and neuropathologic actions of organophosphates comprise the major unsolved problem in defending against this class of chemical nerve agents. Understanding and preventing these central actions are important goals of chemical defense research. It is generally accepted that inhibition of acetylcholinesterase results in an accumulation of acetylcholine (ACh) which may be responsible for the acute toxic effects of nerve agents. Although atropine has long been used in the treatment of poisoning, it does not significantly reduce convulsions and seizures nor does it drastically alter the acute toxicity. Inasmuch as antimuscarinic agents do not provide sufficient antidotal activity, it follows that ACh may not be the only transmitter involved in the CNS actions of organophosphates. Benzodiazepines, the most potent of the clinically available anticonvulsants are potentially useful as antidote against nerve agent poisoning. However, significant disadvantages are associated with the im administration of benzodiazepines particularly diazepam the now anticonvulsant fielded drug. The present report was undertaken to compare the effectiveness of thienyl phencyclidine (TCP), a non-competitive antagonist at N-methyl-D-aspartate (NMDA) glutamate receptors, to diazepam both administered im for protection against soman toxicity (convulsions, seizures, incidence on death, brain damage). In a first set of experiments, male wistar rats were pretreated with diazepam (1 mg/kg) given im. Fifteen minutes later 1 x LD50 of soman was injected sc and the incidence of seizures and death were recorded for 24 hr. The therapeutic efficacy of a post-poisoning treatment of diazepam was also studied. In this case diazepam was administered 45 min after the onset of seizures. In a second set of experiments, guinea-pigs were pretreated with pyridostigmine (0.2 mg/kg, sc) in combination with atropine (5 mg/kg, im) 30 min before soman (62 micrograms/kg, sc) and the protective effect of TCP (2.5 mg/kg, im) evaluated when the drug was administered either before soman (15 or 30 min) or after the onset of EEG seizures (5, 30 or 60 min). Pretreatment with diazepam alone did reduce soman-induced seizures but did not reduce mortality of rats. Neuropathology was not observed in non-seizuring rats. When given 45 min after the onset of seizures, diazepam failed to protect against status epilepticus and neuropathology. Thus, diazepam was more effective when given before, rather than after, seizure initiation. Systemic injection of TCP blocked the seizures induced by 2 x LD50 of soman in guinea-pigs pretreated by pyridostigmine and atropine. The anticonvulsant potency of TCP was particularly obvious when the compound was administered curatively.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1993

Transient impairment of the gabaergic function during initiation of soman-induced seizures.

The changes in extracellular gamma-aminobutyric acid (GABA) levels, the modifications in binding capacities of GABA-receptor subtypes A and B and of the Cl- ionophore sites localized in the ionic-channel associated to the GABAA receptors were studied in hippocampus of rats subjected to a convulsive dose of the acetylcholinesterase inhibitor soman. Whereas extracellular GABA levels, just as binding on GABAA and GABAB receptors, were not modified under soman, a significant transient decrease in the binding capacities of the Cl- ionophore site of the GABAA receptor complex occurred within the first 10 min of seizures in CA1, CA3 areas, and in the dentate gyrus with return to basal values after 30 min. Accordingly, a transient decrease of the brain muscimol-gated Cl- influx was observed after 10 min of seizures. An increased ability of diazepam to potentiate the GABAA gated Cl- influx occurred at the same time. Altogether, these data demonstrated that an impairment of the GABAA receptor function occurs at the beginning of seizures. This suggests that a temporary decrease of GABAAergic function may contribute to the onset of seizures.

Animals↗
PubMed1993

Cholinergic activation of phosphoinositide metabolism during soman-induced seizures.

In the present study we investigated the role of the cholinergic pathway in phosphoinositide metabolism activation observed during soman-induced convulsions. We thus studied the effect of atropine sulphate, a muscarinic antagonist (20 mg kg-1, i.p.), on IP3 levels in rat hippocampus. We demonstrated that initially, the increase of IP3 is closely seizure-related. On the other hand, after 10 min of seizures, the IP3 enhancement and the seizure activity are no longer correlated. After 20 min of seizures, atropine failed to inhibit soman-induced IP3 enhancement, suggesting that the activation of another neurotransmitter system(s) linked to PPI turnover succeeds the cholinergic stimulation.

Animals↗
PubMed1993

Neuroprotective activity of glutamate receptor antagonists against soman-induced hippocampal damage: quantification with an omega 3 site ligand.

Previous investigations have indicated that the measurement of omega 3 (peripheral-type benzodiazepine) binding site densities could be of widespread applicability in the localization and quantification of neural tissue damage in the central nervous system. In the first step of the present study, the suitability of this approach for the assessment of soman-induced brain damage was validated. Autoradiographic study revealed marked increases of omega 3 site densities in several brain areas of convulsing rats 2 days after soman challenge. These increases were well-correlated with the pattern and the amplitude of neuropathological alterations due to soman and closely related to both glial reaction and macrophage invasion of the lesioned tissues. We then used this marker to assess, in mouse hippocampus, the neuroprotective activity against soman-induced brain damage of NBQX and TCP which are respective antagonists of non-NMDA and NMDA glutamatergic receptors. Injection of NBQX at 20 or 40 mg/kg 5 min prior to soman totally prevented the neuronal damage. Comparatively, TCP had neuroprotective efficacy when administered at 1 mg/kg 5 min prior to soman followed by a reinjection 1 h after. These results demonstrate that both NBQX and TCP afford a satisfactory neuroprotection against soman-induced brain damage. Since it is known that the neuropathology due to soman is closely seizure-related, the neuroprotective activities of NBQX and TCP are discussed in relation with the respective roles of non-NMDA and NMDA receptors in the onset and maintenance of soman-induced seizures.

Animals↗
PubMed1993

Disc movements over the condylar head. Radiographical study on autopsy materials.

A radiographical study has been performed to evaluate the movement of the disc posterior band over the condylar head during mandibular opening. Six formal free embalmed subjects were selected as 'normal'. Micro stainless steel balls were used as landmarks both into the bone and into the disc for X-ray identification. The data was processed at each phase of movement in selected planes. The true coordinates of each disc landmark gave the potential to calculate the linear length of their path and any distance change between them. It can be concluded that there is a 5% width reduction during the opening movement and it also suggests strongly that a fair amount of translation movement between the disc and the condyle occurs in the lower compartment.

Cadaver↗
PubMed1993

[Carotid stenoses. Non-invasive exploration].

Doppler flowmeter and ultrasound imaging techniques, currently associated (duplex), have made important contributions to the simple and early non invasive diagnosis of carotid stenosis lesions in the cervical region for more than 20 years. These exploratory methods are reliable when a significant degree of stenosis (greater than about 60%) exists. Moderate degrees of stenoses or plaques are evaluated morphologically, calcifications and ulcerations being enhanced by staining techniques. But the evaluations have not really demonstrated exact correlations between anatomicopathologic and ultrasound images. The intracranial arteries and the circle of Willis are explored indirectly during the cervical examination by cautious compressive maneuvers or directly by trans-cranial Doppler. Whereas angiography competes with ultrasound imaging as a standard examination in the neck region, it nevertheless remains effective for the study of the intracranial arteries. Newer techniques, such as high-field MRI angiography, tridimensional ultrasonography or ultrasound recording of vascular flow rate without Doppler, will doubtlessly transform the diagnosis of symptomatic or asymptomatic carotid stenosis. From the strategic point of view, ultrasound imaging techniques will retain their role of a decisional pivot, since they are simple to use and are of very wide accessibility to competent vascular physicians in the context of an organized care network.

Carotid Stenosis↗