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Biomedical subjects

C Guimond

Publications and source records attributed to C Guimond.

18 recordsLinked to original sources
PubMed2003

The interaction of MS and pregnancy: a critical review.

Previous research on the effects of pregnancy on multiple sclerosis (MS) is somewhat flawed, and well-controlled, well-designed studies are needed to validate trial findings. In general, pregnancy appears to have a protective effect on MS course, with fewer, less severe relapses, especially in the third trimester. The exacerbation rate is increased in the first 3 months after delivery, but the overall relapse rate is no different to that observed in non-pregnant MS patients. A woman's past history of relapses may be the best indicator of clinical course during and immediately after pregnancy. Pregnancy does not appear to affect the long-term course of MS.

Estrogens↗
PubMed2003

The immune system and hormones: review and relevance to pregnancy and contraception in women with MS.

Two-thirds of multiple sclerosis (MS) patients are women, and the average age of onset overlaps the childbearing years. Clinicians are frequently asked, therefore, about the most appropriate form of contraception and the risk of an MS relapse/exacerbation during pregnancy and the post-partum period. This paper reviews the literature on the immune system and the effects of pregnancy, oral contraceptives and hormone replacement therapy on MS.

B-Lymphocytes↗
PubMed2003

Reproductive counselling for MS: a rationale.

Many questions arise when counselling multiple sclerosis (MS) patients on the effects of MS on pregnancy, and vice versa. Reassurance can often be given regarding contraception, fertility, pregnancy management, pregnancy outcome, and the risk of the child developing MS. Much more information is needed, however, on the effects and implications of MS therapies on pregnancy and breast-feeding.

Counseling↗
PubMed1999

Elevated levels of polyamines and trypanothione resulting from overexpression of the ornithine decarboxylase gene in arsenite-resistant Leishmania.

The levels of trypanothione, a glutathione-spermidine conjugate, are increased in the protozoan parasite Leishmania selected for resistance to the heavy metal arsenite. The levels of putrescine and spermidine were increased in resistant mutants. This increase is mediated by overexpression of ornithine decarboxylase (ODC), the rate-limiting enzyme in polyamine biosynthesis. Gene overexpression is generally mediated by gene amplification in Leishmania but, here, the mRNA and the enzymatic activity of ODC are increased without gene amplification. This RNA overexpression is stable when cells are grown in the absence of the drug and does not result from gene rearrangements or from an increased rate of RNA synthesis. Transient transfections suggest that mutations in the revertant cells contribute to these elevated levels of RNA. Stable transfection of the ODC gene increases the level of trypanothione, which can contribute to arsenite resistance. In addition to ODC overexpression, the gene for the ABC transporter PGPA is amplified in the mutants. The co-transfection of the ODC and PGPA genes confers resistance in a synergistic fashion in partial revertants, also suggesting that PGPA recognizes metals conjugated to trypanothione.

Animals↗
PubMed1989

Characterization of the peripheral action of neurokinins and neurokinin receptor selective agonists on the rat cardiovascular system.

The effects on mean arterial pressure (MAP) and heart rate (HR) of increasing doses (0.65-65 nmol/kg) of substance P (SP), neurokinin A (NKA), neurokinin B (NKB) and selective agonists for neurokinin receptors were measured after intravenous (i.v.) injection in urethane anaesthetized rats. Neurokinins (NKs) elicited a vasodepressor effect with the following rank order of potency: SP (100%) greater than NKB (17.5%) greater than NKA (10%). The two undecapeptide NK-1 selective agonists, [Pro9, Met(O2)11]SP (787%) and [Sar9, Met(O2)11]SP (697%), evoked a significantly (P less than 0.05) greater vasodepressor response than SP, while the potency of the octapeptide NK-1 selective agonist [beta-Ala4, Sar9, Met(O2)11]SP (4-11) (316%) was not significantly different from SP. Conversely, the NK-2 selective agonist NKA (4-10) (less than 2%) caused only a small effect. The vasodepressor effect elicited by [MePhe7]NKB (112%) and [beta-Asp4, MePhe7]NKB (4-10) (92%), two NK-3 selective agonists, were not significantly different from that of SP. Senktide (1,095%) is the most potent NK-3 agonist, and is significantly (P less than 0.01) more potent than SP. No cross-desensitization, of the vasodepressor response, was observed between NK-1 and NK-3 selective agonists. I.V. injection of 32.5 nmol/kg of NKA, NKA (4-10) and [beta-Ala4, Sar9, Met(O2)11]SP (4-11) raised HR, while NKB and the NK-3 selective agonists produced a rapid and marked bradycardia. SP and the two undecapeptide, NK-1 selective agonists, produced an initial increase in HR and a latent long-lasting bradycardia. The bradycardia elicited by [Sar9, Met(O2)11]SP (32.5 nmol/kg) was blocked by methylatropine, hexamethonium, indomethacin and by treatment with capsaicin or compound 48/80. Although the bradycardia elicited by [beta-Asp4, MePhe7]NKB (4-10) (32.5 nmol/kg) was also blocked by hexamethonium, methylatropine, and by bilateral vagotomy, it remained unaffected after indomethacin, or in rats pretreated with either capsaicin or compound 48/80. The drop in MAP produced by the NK-1 and NK-3 agonists were reduced by hexamethonium, methylatropine and bilateral vagotomy (NK-3 agonist), but remained unaffected by indomethacin, capsaicin, and compound 48/80. The tachycardia to NKA (4-10) (65 nmol/kg) was blocked entirely by sotalol or metoprolol and potentiated by hexamethonium. Guanethidine and bilateral adrenalectomy (48 h) failed to affect the tachycardia induced by the agonist, whereas the combination of both treatments abolished the response. Rats sympathectomized with 6-hydroxydopamine (48 h) reduced the increase in HR to NKA (4-10) only at 1 min post-administration.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1984

Streptokinase thrombolysis of a chronically thrombosed mitral prosthetic valve.

Thrombus obstruction of a prosthetic heart valve is usually treated surgically. We report a well-documented case of an obstructed mitral prosthetic valve where fibrinolytic treatment was successful. Furthermore the thrombus formation probably had occurred 6 months earlier. Thus fibrinolysis appears to be a safe alternative to surgery although late occurrence of thrombosis may be possible.

Adult↗
PubMed1983

Intracardiac electrophysiological study of S-2395 in intact and chemically sympathectomized dogs.

S-2395 is a new, long-acting, non-selective beta-receptor blocking agent without apparent intrinsic cardiodepressive action and no receptor selectivity. Its electrophysiological actions were studied in intact and chemically sympathectomized dogs. In normal dogs, S-2395 very slightly increased atrial monophasic action potential (MAPa) duration, atrioventricular functional (FRP) and ventricular effective (ERP) refractory periods. The onset of the atrial supernormal conduction phenomenon (SNCP) was delayed and the ventricular SNCP was abolished. These results are consistent with the action of low concentrations of beta-blocking agents. In contrast S-2395 reduced the ventricular MAPv and increased the ERP/MAPv ratio of sympathectomized animals. Such modifications are usually seen with concentrations higher than necessary for simple beta-receptor blockade. In conclusion S-2395, like several others beta-blockers, had minor effects on the classical electrophysiological parameters of normal dogs. However, it suppressed ventricular SNCP and had a more pronounced action in sympathectomized dogs who are known to have higher levels of circulating catecholamines and who present post-synaptic supersensitivity. The SNCP has been linked with re-entrant arrhythmias. Considering that beta-blockers prevent arrhythmias specially in hyperadrenergic states, the suppression of the ventricular SNCP by S-2395 could thus be the mechanism by which this drug and possibly other beta-blockers might exert their antiarrhythmic action.

Adrenergic beta-Antagonists↗
PubMed1983

Electrophysiological effects of ouabain in 6-hydroxydopamine pretreated dogs.

Chemical sympathectomy and bilateral vagotomy were used to evaluate the contribution of each division of the autonomic nervous system in the electrophysiological actions of ouabain. Intact and chemically sympathectomized dogs were given successive and cumulative doses of ouabain until toxicity became manifest (ventricular extrasystoles and (or) ventricular tachycardia). An additional group of normal and sympathectomized animals was also submitted to bilateral vagotomy in the presence of a therapeutic dose of ouabain. Sinus cycle length, AH interval of the His bundle electrogram, atrioventricular junctional effective and functional refractory periods were increased by ouabain at therapeutic doses. These effects were no different in sympathectomized dogs than in intact dogs, indicating the absence of any significant contribution of efferent sympathetic neural activity. However, our results suggested that vagal enhancement was the main mechanism whereby ouabain produced sinus bradycardia and depression of atrioventricular conduction. Sympathectomy with 6-OHDA did not modify nor abolish ouabain toxicity. However, toxic doses were significantly higher in sympathectomized animals than in normal animals. Considering that increasing heart rate by cardiac pacing or vagotomy significantly lowered toxic doses of ouabain in both intact and sympathectomized dogs, it is possible that sympathectomy could influence ouabain toxicity by altering heart rate alone.

Animals↗
PubMed1982

Electrophysiology of the chemically sympathectomised dog.

The contribution of the sympathetic nervous system in the definition of various electrophysiological variables was studied in chemically sympathectomised dogs. Chemical sympathectomy was obtained following intravenous injection of 50 mg X kg-1 of 6-hydroxydopamine. Sympathectomised dogs presented significant increases in: basic sinus period, sino-atrial conduction time (SACT), AH and HV intervals of the His bundle electrogram, atrial functional (AFRP) and effective (AERP) refractory periods, atrio-ventricular node functional (AVNFRP) and effective (AVNERP) refractory periods, ventricular functional (VFRP) and effective (EVRP) refractory periods and atrial (AMAP) and ventricular (VMAP) monophasic action potential durations. Corrected sinus recovery time (CSRT) was not affected by chemical sympathectomy. Neither was the atrial ERP/MAP duration ratio. This new form of sympathectomy affects all the levels of the cardiac conduction system. Such results are in accordance with those obtained with surgical sympathectomy or the use of beta-blocking agents.

Animals↗
PubMed1979

Computer processing of intracardiac electrograms for conduction studies.

Computer techniques developed to process intracardiac signals recorded in dogs are presented. The signals under measurement are the auricular and ventricular monophasic action potentials and the His bundle electrogram. Computerized measurement of significant timing parameters on simultaneous recordings of these signals can assess quite precisely changes in the normal conduction scheme of the heart provoked by different experimental protocols. Increased accuracy is mainly due to the objective way of defining wave onsets and the processing power of the system used. Signal recording, signal acquisition, automatic waveform measurements, interactive process and production of end result graphs by computer are all described.

Action Potentials↗
PubMed1978

[The supernormal phase of cardiac conduction. An experimental study in the dog].

The existence of a cardiac phase of supernormal excitability is not fully proved at the cellular level. As far as the whole heart is concerned, the phenomenon of supernormal conduction is still under discussion. Intracardiac conduction has been studied both in the right atrium (13 dogs) and in the right ventricle (14 dogs) by programmed stimulation (extrastimulus technique), while monophasic action potential (MAP) was recorded. The phenomenon of supernormal conduction was noted in 67.7% of cases, starting at 59.0% and ending at 78.0% of the basic cycle, hence occuring shortly after phase 3 of the MAP. In the ventricle, a phase of supernormal conduction was present in 52.4% of cases, starting at 66.1% and ending at 77.9% of the basic cycle. After ajmaline, the supernormal conduction was moved towards the end of the cycle. The mechanism of supernormal conduction, and its implications in the study of arrhythmias are discussed.

Action Potentials↗
PubMed1976

Intra-His bundle blocks (102 cases).

Some intra-His bundle (intra-HB) blocks escape the routine exploration of the His bundle and are confused with supra- or infrahisian blocks. We believe that a more accurate exploration (recording of His bundle activity successively at the proximal end and the distal end of the His bundle, dynamic tests and drug injection) is needed to detect some concealed cases, mostly paroxysmal intra-HB blocks. In this series of 102 cases of intra-HB blocks, 20% had no criteria of AV block on the surface electrocardiogram, and only 4% had an intact conduction pattern (normal PR interval and normal QRS complexes.) A first degree intra-HB block was found in 35% (15 cases with a normal PR interval), a second degree intra-HB block in 23% and a thired degree intra-HB block in 42% of the cases (unidirectional in 4 cases). Of the 43% having an isolated intra-HB block, most were elderly women with a chronic third degree AV block.

Adolescent↗
PubMed1976

[Analysis of the electrophysiological effects of amiodarone using simultaneous recordings of monophasic and bundle-of-his action potentials].

The effects of amiodarone given by rapid intravenous injection at a dosage of 10 mg/kg have been studied in the dog. The peak activity is found between the fifth and the tenth minute. The rate of discharge of the sinus is lowered by 36%. At the atrial level, the duration of the monophasic action potential (MAP) is increased by 9% and its dv/dt is lowered slightly, the total refractory period is increased by 22%, the effective refractory period is increased by 27%, the functional refractory period is increased by 19%, the ratio of the length of the effective period/duration of the MAP becomes slightly greater than unity, conduction facilitation disappears, and the period of slow conduction increases. In the A/V node the AH interval increases by 44% under normal rhythm, while atrial stimulation at 200/min. results in conversion to total AV block in more than half of the cases. The potential of the bundle of His and the HV interval are not altered. At ventricular level the duration of the monophasic action potential increases by 25%, its dv/dt decreases slightly, the total refractory period is increased by 8%, and the effective refractory period is increased by 14%.

Action Potentials↗