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Biomedical subjects

C Jacquot

Publications and source records attributed to C Jacquot.

At least 127 records · Page 7Linked to original sources
PubMed1988

[Registration of peranesthetic cases of malignant hyperthermia in France. An update].

Sixty-two suspected crises of anaesthetic malignant hyperthermia (MH) were collected between 1969 and 1988 by a retrospective inquiry which lasted four years. 33 patients (53%) died whilst 29 survived. 20 cases were confirmed to be MH, either directly or indirectly by way of muscle biopsy and halothane and caffeine contracture tests carried out according to the European MH group protocol by two laboratories. This group included 11 of the deaths, one family member of whom, at least, is sensitive (MHS), 7 MHS survivors and 2 survivors too young to undergo muscle biopsy but belonging to MHS families. 21 cases were highly suspect of MH: 15 of the deaths which occurred in a typical way, and 6 patients of three different families who have suffered from anaesthetic deaths which, clinically, suggested MH. Another 15 were possible MH cases, all survivors, including one case of Steinert's disease and a brother of a case of central core disease. 2 cases were still being debated, because they had equivocal results for the caffeine test (MHEc); the last 4 had negative muscle biopsies and were excluded. 33 close relatives of the MH patients were diagnosed as MHS. 44 others were found to be free from the genetic predisposition. It was strongly recommended to yet 11 others that they carry the MHS card because they were MHEc. The clinical, surgical and anesthetic pictures were always as described in the literature. The anaesthetic protocols included inhalational agents in 90% of cases; these were combined with suxamethonium in 55% of cases. Dantrolene was only used in 32% of cases, and then at inadequate doses and very often too late; this probably explains the large number of treatment failures. The number of severe forms of MH was also very high in this series (70%). The need to increase the means of prevention and screening for MH in France is stressed.

Adolescent↗
PubMed1988

Effects of high magnesium intake on central catecholamines in spontaneously hypertensive rat.

Spontaneously hypertensive rats (SHR) received a highly magnesium enriched diet during the development of hypertension, which caused plasma Mg concentrations to be markedly increased. Arterial blood pressure was reduced in supplemented animals. Levels of noradrenaline, 3-dihydroxyphenylacetic acid and homovanillic acid in cortex, hypothalamus, striatum and brain stem remained unchanged. Dopamine levels in the cortex, hypothalamus and striatum were also unchanged. Dopamine levels in brain stem increased. However the correlation between treatment with magnesium, dopamine-related variables in the brain and decrease in blood pressure in SHR remains hypothetical.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1987

Benzodiazepine receptors are involved in tabernanthine-induced tremor: in vitro and in vivo evidence.

Tabernanthine, an indol alkaloid, is structurally related to carbolines (harmane, harmaline) which, in vitro, displace specific flunitrazepam binding to brain benzodiazepine receptors. In vivo, both tabernanthine and carbolines cause a fine general tremor, suggesting that a possible interaction with benzodiazepine receptors could be involved in the activity of tabernanthine. This hypothesis was validated by the in vitro and in vivo antagonism of benzodiazepine by tabernanthine. In vitro, tabernanthine inhibited specific flunitrazepam binding in a competitive manner with an affinity (IC50 150 microM) in the same range as harmane. Tabernanthine appeared as a benzodiazepine receptor inverse agonist in a discriminant in vitro binding assay. In vivo, the time course of tremorigenic activity was related to the tabernanthine concentration in brain (half-life = 2 h). Moreover, tabernanthine-induced tremor was inhibited reversibly by flunitrazepam or by Ro-15 1788 (an antagonist of benzodiazepine-receptors). These results suggest that part of the action of tabernanthine may be mediated by an interaction at the benzodiazepine receptor level.

Alkaloids↗
PubMed1987

Antithrombin III and heparin cofactor II in patients with chronic renal failure undergoing regular hemodialysis.

Heparin enhances the inhibition rate of thrombin by both antithrombin III (AT III) and heparin cofactor II (HC II). We studied the activity of these two plasma proteins in patients with chronic renal failure (CRF) undergoing regular hemodialysis as their heparin requirements varied widely. In 77 normal blood donors, normal ranges (mean +/- 2 SD) were 82-122% for AT III and 65-145% for HC II. When compared with these controls 82 dialyzed CRF patients had a subnormal AT III activity and a significantly (p less than 0.001) lower HC II activity. To evaluate the effect of hemodialysis we compared AT III, HC II and total proteins in plasma before and after dialysis in 24 patients (12 with normal and 12 with low basal HC II activity). AT III and HC II activities significantly (p less than 0.001) increased in absolute value. When related to total plasma proteins, in order to suppress the influence of hemoconcentration induced by dialysis, AT III decreased significantly (p less than 0.01) whereas HC II increased slightly but significantly (p less than 0.01) in the 12 patients with low initial HC II activity. The decrease of AT III induced by heparin administrated during dialysis is likely to account for this relative decrease of AT III activity. A modification of the distribution of both HC II and heparin between the vascular wall and the circulating blood is evoked to explain the relative increase in HC II activity and the need for higher heparin dosage in patients with low HC II levels.

Adult↗
PubMed1987

Cholecystokinin and bombesin in vagotomized or intact lean and obese rats: effects on neurotransmitters in brain.

Cholecystokinin (CCK) and Bombesin (BBS) are two neuropeptides which induce changes in monoamines in the brain after peripheral administration. A vagal mediation of these effects was investigated since the satiety responses to both peptides are affected differently by vagotomy. This work was performed on genetically obese and lean Zucker rats and on "cafeteria-fed" and lean Sprague-Dawley rats as the effects of the peptides are dissimilar in these different groups. Vagotomy either inhibited or potentiated the peptide-induced effects, or created new variations. With CCK, the inhibition occurred mainly in the serotonergic system and in the Zucker strain, while new effects appeared in the dopaminergic system of lean rats of both strains. With bombesin, vagotomy inhibited the effects in the dopaminergic system in all lean rats, while new effects were observed in the serotonergic system in the Zucker strain. These data enable the differentiation of the mechanisms of action of both peptides and their selective effects, according to the strain of rat and the presence or absence of obesity.

Animals↗
PubMed1987

Metabolism of 6,7-dimethoxy 4-(4'-chlorobenzyl)isoquinoline. II. Role of liver catechol O-methyltransferase and glutathione.

1. On i.v. administration to rats of 14C-6,7-dimethoxy 4-(4'-chlorobenzyl)isoquinoline (PV2) 23% dose of 14C was excreted in urine and 72% in faeces. The pattern of metabolites showed ten 14C-PV2 derivatives and unchanged PV2. Seven metabolites have been characterized by comparison with authentic compounds e.g. the ketone of PV2, the N-oxide PV2, the demethylated metabolites 6-hydroxy-PV2, 7-hydroxy-PV2 and 6,7-dihydroxy PV2, the benzyl ring-hydroxylated metabolites, 3'-hydroxy-PV2 and 6,7,3'-trihydroxy-PV2. Unchanged PV2 and its metabolites are excreted both free and conjugated. 2. Enzymic O-methylation of 6,7-dihydroxy-PV2 by liver catechol-O-methyl transferase (COMT) in vitro produced 6-hydroxy,7-methoxy-PV2. After blockade of COMT by pyrogallol in vivo, the excretion of 6,7-dihydroxy-PV2 was increased and the excretion of 6-hydroxy, 7-methoxy-PV2 decreased. 3. Hydroxylation of the benzyl ring of PV2 and its metabolites indicates the formation of an intermediate epoxide followed by glutathione conjugation. After glutathione depletion in vivo by diethyl maleate (DEM) liver covalent binding of 14C-PV2 metabolites was increased and biliary excretion of benzyl ring-hydroxylated PV2 metabolites decreased. Replacement of glutathione depletion by a cysteine derivative restored liver covalent binding and the excretion of PV2 metabolites to levels similar to those observed in control rats, indicating that glutathione conjugation may be an important metabolic pathway for the detoxication of PV2 and its metabolites in vivo.

Animals↗
PubMed1987

Glomerulonephritis, B monoclonal small lymphocytic lymphoma and mixed cryoglobulinemia.

A novel association in the same patient with small lymphocytic lymphoma, type II cryoglobulinemia and glomerulonephritis is reported. This case is also characterized by a quite unusual sequence of glomerular alterations. A first renal biopsy showed severe endocapillary proliferative glomerulonephritis due to monocytic infiltration without any evidence of deposition of immune reactants. The immune deposits associated with type II cryoglobulinemia were only observed at a second renal biopsy performed five months later. This case shows that mononuclear cells can be responsible in and of themselves for severe glomerular damage, without deposition of immune material, and suggests that monocytic infiltration might be the first stage of type II cryoglobulinemia associated glomerulonephritis.

B-Lymphocytes↗
PubMed1987

[Phenotype of plasma cholinesterase in prolonged apnea and sensitivity to succinylcholine].

90% of the injected dose of succinylcholine is hydrolysed by serum cholinesterase (E.C.3.I.I.8) Abnormal variants of serum cholinesterase lead to prolonged apnea. This report presents the results of 62 serum cholinesterase phenotyping including 12 cases of prolonged apneas. One clinical case of prolonged apnea in a patient homozygous for the atypical cholinesterase gene is presented with a study of his genealogy. The phenotypes were established on the basis of dibucaïne, fluorure, chloride and propranolol differential inhibition. The frequency and significance of the various phenotypes is discussed.

Anesthesia, General↗
PubMed1986

Putative neurotransmitters in three experimental filariasis models.

Some putative neurotransmitters in three experimental filariasis models were investigated by a new relevant chromatographic method, sensitive and specific. No catecholaminergic compounds have been detected, but serotonin was found in Dipetalonema vitae. However, further investigations revealed very high levels of gamma amino butyric acid (GABA) in the macro-filariae. These data allow us to foresee new fields in filariasis therapeutics.

5-Hydroxytryptophan↗
PubMed1986

Immunohistochemical demonstration of parietal epithelial cells and macrophages in human proliferative extra-capillary lesions.

The cellular composition of crescents in diffuse crescentic glomerulonephritis is still controversial. Ten renal biopsies were studied on serial sections by using antikeratin antibodies as specific markers of epithelial cells of Bowman's capsule and both anti-macrophage and anti-lymphocyte antibodies. Semiautomatic morphometry showed that cellular crescents consisted of epithelial cells of Bowman's capsule (24-61%), of macrophages (19-34%) and of unlabelled cells (12-53%). In each biopsy, parietal epithelial cells outnumbered macrophages within crescents.

Antibodies, Monoclonal↗
PubMed1986

Ontogeny of brain monoamines in lean and obese female Zucker rats.

Differences in monoamine and metabolite levels were previously observed between lean and obese 16 week-old female Zucker rats. In order to test whether these variations exist initially in young animals, catecholamines (CA), serotonin (5-HT) and some of their metabolites were assayed in brain areas of Zucker rats between 5 and 16 weeks of age. The levels of most compounds in all areas studied increased with age in both groups. At 5 weeks of age, there was no difference between lean and obese rats. At 8 weeks, a reduction of dopamine (DA) metabolites appeared in the striatum and cortex of obese rats and persisted up to 16 weeks. A reduction of the 5-HT metabolite, 5-hydroxyindolacetic acid (5-HIAA), occurred at 8 weeks only. At 16 weeks, increases of DA and 5-HT in the hypothalamus and decreases of norepinephrine (NE), 5-HT and 5-HIAA in the hippocampus appeared. These data suggest that the development of obesity occurs before any monoamine alterations.

3,4-Dihydroxyphenylacetic Acid↗
PubMed1986

Rat brain monoamine metabolism and hypobaric hypoxia: a new approach.

A chromatographic method with electrochemical detection was used to measure noradrenaline (NA), dopamine (DA), and serotonin (5-HT), 3,4-dihydroxyphenylacetic acid (DOPAC), homovanillic acid (HVA), 3-methoxytyramine (3-MT) and 5-hydroxyindoleacetic acid (5-HIAA) in several brain areas (hypothalamus, hippocampus, striatum and rest of the brain) of rats exposed to a 7000 m simulated altitude for 3 hr. This new direct approach, not using a pharmacological tool, provides further information on the hypobaric hypoxia effects on the main DA and 5-HT metabolic steps. In the hypothalamus, a decreased NA level with increased DA and DOPAC contents was considered as the result of dopamine-beta-hydroxylase activity impairment. The decrease of both 5-HIAA and DOPAC in all brain areas provides further evidence of the hypoxia-induced decrement in MAO activity. Furthermore, in the striatum, it was shown that catechol-O-methyl transferase, up to now considered unaffected by hypoxia, may also be altered by oxygen deficiency.

Animals↗
PubMed1986

Variability of changes in obese rat brain monoamines in response to cholecystokinin.

The interactions between cholecystokinin (CCK) and brain monoamines have been investigated. The data found in the literature are quite dissimilar. Several reasons for these disparities have been suggested. We have sought to test some of them, such as the strain of rat, the nutritional state (by the use of two models of obesity), the length of the peptide (CCK 8 and CCK 33), the route of administration (i.p. and i.c.v.) and the time of sacrifice. We indeed found all these experimental conditions to be the cause of differential effects on brain monoamines and metabolites. However, by repeating the same experiments several times, we did not always obtain the same variations, even under the same conditions. In addition to the different parameters tested, another source of variability exists, possibly due to the molecule itself or to seasonal variations.

Animals↗