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E Deflandre

Publications and source records attributed to E Deflandre.

17 recordsLinked to original sources
PubMed2006

Correlation and agreement between bispectral index and state entropy of the electroencephalogram during propofol anaesthesia.

BACKGROUND: Bispectral index (BIS) and state entropy (SE) monitor hypnosis. We evaluated the correlation and the agreement between those parameters during propofol anaesthesia and laryngoscopy with and without muscle relaxation. METHODS: A total of 25 patients were anaesthetized with propofol. At steady state (SS: BIS 40-50), they randomly received rocuronium (R) or saline (S); 3 min thereafter, a 20 s laryngoscopy was performed. Correlation (regression analysis) and agreement (Bland-Altman analysis) were evaluated before induction (baseline), at loss of eyelash reflex (LER), at SS and during the first 3 min after laryngoscopy (L). RESULTS: The correlation coefficient r (95% CI), the mean difference (MD) (95% CI), and the limits of agreement [lower-upper limits of 95% CI of MD (sd 1.96)] between BIS and SE were as follows. Overall recordings: 0.87 (0.83 to 0.90), 2.5 (1.2 to 3.0), and [-19.5 to 24.6]; Baseline: 0.45 (0.06 to 0.72), 7.6 (6.0 to 9.2), and [-2.7 to 17.9]; LER: 0.74 (0.47 to 0.88), 8.3 (3.5 to 13.2), and [-22.6 to 39.3]; SS, all patients: 0.41 (0.14 to 0.63), 2.0 (-0.5 to 4.6), and [-19.0 to 23.3]; SS, Group S: 0.36 (-0.07 to 0.68), 1.9 (-2.5 to 6.3), and [-25.0 to 28.8]; SS, Group R: 0.63 (0.32 to 0.82), 0.2 (-2.0 to 2.3), and [-14.0 to 14.4]; L, all patients: 0.49 (0.32 to 0.63), 0.7 (-1.6 to 3.0), and [-25.6 to 27.1]; L, Group S: 0.41 (0.13 to 0.63), 2.3 (-2.4 to 7.1), and [-36.7 to 41.3]; L, Group R: 0.72 (0.56 to 0.83), -0.6 (-2.2 to 1.0), and [-14.3 to 13.1]. The correlation was good except for SS in Group S. The MD was significantly different from 0 for overall recordings, during baseline and LER, but not for the other conditions. The agreement was poor except for baseline, and SS and L in Group R. CONCLUSIONS: BIS and SE are globally well correlated. In contrast, agreement is poor as differences of more than 20 units are frequently observed, except for awake and paralysed patients.

Adult↗
PubMed2004

[The sleep obstructive apnea and hypopnea syndromes].

Since two decades, sleep breathing disorders are more wisely recognized by the Belgian medical community. Among these, the Obstructive Sleep Apnea Syndrome (OSA) is the best known but its frontiers with others syndromes such as the Upper Airway Resistance Syndrome (UARS), the Central Sleep Apnea Syndrome (CSAS) or the Overlap Syndrome are still matter of discussion. Its causes are plurifactorial, and many recent publications draw the attention to its long term effects in the cardiovascular and neuropsychiatric fields. This article summarizes the present definitions and features associated with OSA, from clinical and neurophysiological perspectives, and the different consequences to which untreated or underdiagnosed patients are exposed.

Cardiovascular Diseases↗
PubMed2002

[Diagnosis of internal carotid artery dissection. Two case reports].

Two cases of acute internal carotid dissection are presented. Typical symptoms, pathogeny and imaging features are reviewed. Magnetic Resonance is actually the best technique for the diagnosis of internal carotid artery dissection, which should be searched in young patients presenting neurologic and cervico-facial symptoms.

Age Factors↗
PubMed2002

[Narcolepsy-cataplexy].

The diagnosis of narcolepsy-cataplexy is based on three axes: 1) the medical history is strongly suggestive when diurnal sleep attacks (narcolepsy) and drop attacks (cataplexy) are reported or observed; 2) the polysomnography is mandatory and shows nocturnal and diurnal (multiple sleep latency test) REM sleep onsets; 3) HLA typing, practically helps to exclude the diagnosis when HLA DR15-DQB1*0602 is not present. New pathogenetic hypotheses have been proposed, mostly based the absence of hypocretin in narcoleptic cerebrospinal fluid. This neurotransmitter was previously known exclusively by its involvement in alimentary behaviours. The new therapies remain symptomatic, but they are powerful to prevent somnolence, daytime sleepiness, cataplexy and insomnia associated with this syndrome.

Carrier Proteins↗
PubMed1987

[Exploration of endogenous mechanisms controlling the inflammatory reaction, by the study of counter-irritation: release of prostaglandins, formation of kinins and accumulation of leukocytes].

This review was focused on counter irritation by turpentine in the rat. The involvement of sympathetic system, adrenal steroids, beta-endorphin, axon reflexes, haptoglobin, alpha-2-macroglobulin, complement activation, prostaglandin synthesis, kinin formation and leukocyte accumulation was considered as possible explanation of the anti-inflammatory effect of counter irritation by turpentine. The main mechanism consists of the reduction of leucocyte accumulation.

Animals↗
PubMed1986

Further studies of the mechanism of counter irritation by turpentine.

The influence of counter irritation by turpentine (0.2 ml) on zymosan- and carrageenan-oedemas was investigated in the rat. Zymosan-oedema was inhibited by mepyramine and methysergide and by leucopenia. It was not modified by captopril and developed normally in kininogendeficient Brown Norway rats. Leucocytes and mast cell amines but not kinins are thus involved in zymosan-oedema. The last phase of this reaction was inhibited by counter irritation alone, but the odema was largely depressed by counter irritation in rats pretreated with mepyramine and methysergide. Carrageenan-oedema was increased by kininase inhibitors and inhibited by leucopenia in normal rats. This inflammatory reaction had a small developement and was not increased by kininase inhibitors in kininogen-deficient BN rats. Leucocytes and kinins participate in the developement of this inflammatory reaction in normal rats while kinins are lacking in deficient rats. Counter irritation depressed carrageenan-oedema in deficient Brown Norway rats and suppressed the potentiating effect of kininase inhibitors in normal rats. Carrageenan oedema was nearly abolished in turpentine-treated leucopenic rats. These results suggest that the anti-inflammatory effect of counter irritation by turpentine could depend on a reduction of leucocyte accumulation into zymosan-oedema and on a reduction of both kinin formation and of leucocyte accumulation into carrageenan-oedema. The significance of T-kininogen as acute phase reactant is discussed.

Animals↗
PubMed1986

[Anti-inflammatory effect of ACTH in the rat].

In rats, ACTH reduced the oedemas induced by zymosan and lambda carrageenan. ACTH reduced the volume of the exudate induced by sponge implantation and its content in proteins, beta-galactosidase, beta-glucuronidase and PGE2. The inhibitory effect of ACTH was suppressed by adrenalectomy which increased the carrageenan-oedema. The inhibitory effect of ACTH was also suppressed by 17 alpha-methyltestosterone. Corticosterone reduced carrageenan-oedema. The inhibitory effect of corticosterone was suppressed by cycloheximide and actinomycin D. These results suggest that rat adrenal steroids, among which corticosterone, can modulate the reactivity of the animal towards irritating processes. The anti-inflammatory effect of rat adrenal steroids would depend on the formation of lipocortin-like peptides.

Adrenocorticotropic Hormone↗
PubMed1984

The mechanism of the anti-inflammatory effect of turpentine in the rat.

The influence of counter irritation by turpentine on carrageenan-oedema, leucocyte count, plasma kininogen stores and composition of sponge-induced exudates has been investigated in the rat. Counter irritation reduced the carrageenan-oedema in normal as well as in adrenalectomized rats. It induced leucopenia with lymphopenia but did not modify the plasma kininogen stores. In turpentine-pretreated rats, the exudates induced by sponge implantation 18 h previously had a lower content in leucocytes. Their levels in beta-glucuronidase and beta-galactosidase were slightly reduced, their content in PGE2 was not modified and their level in malonaldehyde was increased. The exudates induced by sponge implantation 4 h previously had a lower content in leucocytes and PGE2 while their level in kinins was not modified. The mechanism of the anti-inflammatory effect of counter irritation by turpentine is discussed. We suggest that the main factor involved is a decrease in leucocyte accumulation into the exudates.

Adrenalectomy↗
PubMed1984

[Natriuria during immersion of brief duration].

During immersion in sitting position to the neck of 10 normal adult males, natriuria is significantly increased even after pretreatment with captopril (2 mg X kg-1, p.o.). Inhibition of the renin-angiotensin-aldosterone cascade does not completely block the mechanisms causing natriuria during immersion.

Adult↗
PubMed1983

Prostaglandin biosynthesis is not affected by the anti-inflammatory effect of turpentine.

In turpentine-pretreated rats, the development of carrageenan induced oedema is reduced, while dextran and PGE2-induced oedemas are not influenced. In these pretreated rats, carrageenan oedema is potentiated by arachidonic acid, the hypotensive effect of arachidonic acid is not decreased and the production of malonaldehyde by platelets is not inhibited. Thus, the reduction of carrageenan oedema in turpentine treated-rats does not appear to depend on an endogenous PG synthesis inhibition, while plasma level of acute phase reactants is greatly increased.

Animals↗
PubMed1982

[Inhibition of prostaglandin synthesis by (phenylthio-4 phenylamino)-2 nicotinic acids].

In the rat, (phenylthio-4 phenylamino)-2 nicotinic and [(chloro-4 phenylthio)-4 phenylamino]-2 nicotinic acids inhibit the hypotensive prostaglandin-mediated action of arachidonic acid. They inhibit also the formation from arachidonic acid, of prostaglandin-like substances by chopped rat lungs and of malonaldehyde by rat platelets. They are prostaglandin synthetase inhibitors, three to ten times less active as indomethacin.

Animals↗
PubMed1981

[Cardiovascular reactivity to arachidonic acid, prostaglandin E2, prostacyclin and bradykinin in carrageenan treated rats].

In the rat, during carrageenan-induced peritonitis, the hypotensive activity of arachidonic acid, which depends on PG biosynthesis, is increased during the first hours, and thereafter is not modified. The vasodilator action of PGE2 is reduced during the first day while the actions of PGI2 and bradykinin are not modified. The concentrations of plasma albumin and haptoglobin, two inhibitors of PG biosynthesis are reduced during the first hours. Thereafter the concentration of haptoglobin is increased by 100% while the concentration of albumin remains diminished. During this peritonitis, no plasmatic inhibitory influence on PG synthesis is seen. The anti-inflammatory action of carrageenans does not depend on PG synthesis inhibition.

Animals↗
PubMed1980

[Platelet stimulation in rats by lambda carrageenan and fibrinogen].

Defibrinogenation by defibrase does not modify the hypotensive activity of lambda carrageenan in the Brown Norway rat. Defibrinogenation by defibrase and kininogen depletion by ellagic acid do not change this activity in the Wistar rat. This hypotensive action of lambda carrageenan which depends on platelet stimulation, is unaffected by the lack of fibrinogen.

Animals↗
PubMedDate not supplied

[The influence in the rat of counter-irritation by turpentine on the leukocyte content of exudates induced by sponge implants].

In normal rats, PGE1, arachidonic acid, indomethacin and diclofenac did not modify the leucocyte content of sponge exudates withdrawn 4 hours after implantation while arachidonic acid increased the level in PGE2 and indomethacin reduced it. The leucocyte content of sponges exudates withdrawn 18 hours after implantation was not modified by PGE1 and TXB2, but diminished by indomethacin and NDGA and increased by arachidonic acid. As the chemotactic effect of arachidonic acid was slightly reduced by indomethacin and abolished by NDGA, it could depend on the formation of lipoxygenase derivatives. In normal rats, the leucocyte content of sponge exudates withdrawn 18 hours after implantation was increased slightly by normal serum and largely by serum from turpentine-treated rats. The blood leucocyte content was not modified in turpentine-treated rats. However in these rats, the leucocyte content of sponge exudates was low comparatively to the leucocyte content in normal rats. This low level was not affected by indomethacin, arachidonic acid and normal serum. The leucocytes of turpentine-treated rats seem to be desensitizated towards chemotactic factors. Similar desensitization was observed in rats treated by iota carrageenan.

Animals↗