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Biomedical subjects

L Chartier

Publications and source records attributed to L Chartier.

At least 19 recordsLinked to original sources
PubMed1999

Free-floating thrombi in the right heart: diagnosis, management, and prognostic indexes in 38 consecutive patients.

BACKGROUND: Floating right heart thrombi (FRHTS) are a rare phenomenon, encountered almost exclusively in patients with suspected or proven pulmonary embolism and diagnosed by transthoracic echocardiography. Their management remains controversial. METHODS AND RESULTS: We report on a series of 38 consecutive patients encountered over the past 12 years. Thirty-two patients were in NYHA class IV, 20 in cardiogenic shock. Echocardiography usually demonstrated signs of cor pulmonale: right ventricular overload (91.7% of the population), paradoxical interventricular septal motion (75%), and pulmonary hypertension (86. 1%). The thrombus was typically wormlike (36 of 38 patients). It extended from the left atrium through a patent foramen ovale in 4 patients. Pulmonary embolism was confirmed in all but 1. Mortality was high (17 of 38 patients) irrespective of the therapeutic option chosen: surgery (8 of 17), thrombolytics (2 of 9), heparin (5 of 8), or interventional percutaneous techniques (2 of 4). The in-hospital mortality rate was significantly linked with the occurrence of cardiac arrest. Conversely, the outcome after discharge was usually good, because 18 of 21 patients were still alive 47.2 months later (range, 1 to 70 months). CONCLUSIONS: Severe pulmonary embolism was the rule in our series of FRHTS (mortality rate, 44.7%). The choice of therapy had no effect on mortality. Emergency surgery is usually advocated. However, thrombolysis is a faster, readily available treatment and seems promising either as the only treatment or as a bridge to surgery. In patients with contraindications to surgery or lytic therapy, interventional techniques may be proposed.

Adult↗
PubMed1997

[Mobile thrombi of the right heart in pulmonary embolism].

Systematic transthoracic echocardiography in all cases of pulmonary embolism may demonstrate right heart thrombi. The results of this monocentric series of 28 consecutive cases observed between 1987 and 1996 were analysed. Twenty-four patients were in NYHA Class IV: thirteen were in cardiogenic shock. Echocardiographic signs of acute cor pulmonale were usually observed: 96.3% of patients had right ventricular dilatation, 85.2% paradoxical interventricular septal motion, 88.9% pulmonary hypertension. The thrombus was typical serpentine (27/28 cases) arising from the lower limb veins. Passage into the left heart chambers through a patent foramen ovale was observed in 3 cases. Pulmonary embolism was confirmed in all cases. This is an extreme therapeutic emergency and 13 patients (46.4%) died despite treatment: surgery (7/16), thrombolysis (2/5), heparin (3/4) or interventional radiology (1/3). After the acute phase, the prognosis was generally good, as demonstrated by the 100% survival rate at 28.6 +/- 25 months. This study confirms the gravity of mobile right heart thrombi in pulmonary embolism. The diagnosis is echocardiographic. No significant difference in mortality was observed between the different therapeutic approaches used in this series. The echocardiographic finding of these thrombi is a traditional indication for emergency surgical embolectomy. Thrombolysis is rapid and readily available and seems to provide promising results alone or before surgery. In patients with contraindications to thrombolysis, interventional radiology or simple heparin therapy may be proposed.

Adult↗
PubMed1992

Changes in the cytoskeleton of 3T3 fibroblasts induced by the phosphatase inhibitor, calyculin-A.

Addition of the protein phosphatase inhibitor, calyculin-A, to 3T3 fibroblasts causes a marked change in cell morphology. Initially the cells become rounded, develop surface blebs and then detach from the substratum. In the detached cells an unusual ball-like structure is observed. This study focuses on the cytoskeleton during these calyculin-A-induced morphological changes. Stress fibres disappear as the cells begin to round and aggregates of actin are formed towards the apical surface of the cell. These aggregates condense, in the detached cells, to form the ball structure of approximately 3 microns diameter. Between the ball and the nucleus are cables of intermediate filaments that appear to be attached to the surface of the ball and to the nuclear lamina. Using a procedure designed for the isolation of nuclei the nucleus-ball complex can be obtained. Analysis of the nucleus-ball preparation by immunofluorescence and electron microscopy demonstrate that the ball contains actin and that intermediate filaments are located between the ball and the nucleus. In this preparation, the intermediate filaments also appear to attach to the surfaces of the ball and the nucleus. Electrophoretic analysis of the nucleus-ball preparation indicates that, in addition to actin, a major component of the ball is myosin. It is suggested that the formation of the ball is caused by an actin-myosin-based contractile process, initiated by the phosphorylation of myosin. The aggregation of the actomyosin draws together the intermediate filaments into the area between the ball and nucleus. This hypothesis requires that vimentin binds both to the nucleus and to some component of the ball.

3T3 Cells↗
PubMed1991

Calyculin-A increases the level of protein phosphorylation and changes the shape of 3T3 fibroblasts.

Calyculin-A, an inhibitor of type 1 and 2A phosphatases, was applied extracellularly to 3T3 fibroblasts. At 0.1 microM, calyculin-A caused a marked increase in protein phosphorylation in both the cytosolic and insoluble cellular fractions. This effect was independent of external Ca2+. An immunoprecipitate, formed with an antibody to myosin, contained several cytoskeletal components. Increased phosphorylation following treatment with calyculin-A was observed in vimentin, the 20-kD myosin light chain, and an unidentified 440-kD component. An enhanced level of vimentin phosphorylation was found in intermediate filament preparations from treated cells. Calyculin-A also caused marked shape changes of 3T3 cells. Within minutes after addition of calyculin-A (0.1 microM) cells became rounded and lost attachment to the substratum. Stress fibers, intermediate filaments, and microtubules, prominent in the attached control cells, were not evident in the rounded cells. Shape changes were reversible and after removal of calyculin-A the rounded cells attached to the substratum, resumed a flattened shape, and were active mitotically. In the cells treated with calyculin-A an unusual "ball-like" structure was observed with transmission electron microscopy. This unique structure was 2-3 microM in diameter and was located close to the nucleus. The use of calyculin-A adds further support to the idea that cell shape is controlled, at least in part, by concerted actions of a kinase-phosphatase couple.

Animals↗
PubMed1991

[Initial validation of a new scale for needs: the inventory of family needs].

This article presents the initial validation study results of a new scale to measure family needs: l'Inventaire des besoins des familles (IBF) (Chartier & Coutu-Wakulczyk, 1988). The scale is available in both French and English. Based on the perceptual theory, the IBF is a self-report scale composed of 33 items. It also offers three (3) different sub-scores of the importance of needs: the Global Score of Needs (GSN), the Intensity Need Index (INN) and the Total Number of Needs (TNN). The IBF was first validated on a sample of 207 subjects drawn from the adult population of immediate family members visiting a patient in a surgical intensive care unit in the CHUS in Sherbrooke. The reliability yielded a 0.91 Cronback Alpha coefficient and the homogeneity coefficient for Spearman-Brown and Guttman procedures were 0.89 and 0.86 respectively. The principal component factor analysis and factorial matrices lead to examine the conceptual structure of five independent factors.

Adolescent↗
PubMed1991

[Transcultural validation of a measurement scale].

This monography presents the validation study results of a new scale to measure family needs: The Family Needs Inventory (IBF) (Chartier and Coutu-Wakulczyk, 1988). The scale is available in both French and English from the Departement des sciences infirmières of the Université de Sherbrooke. Based on a perceptual framework, the IBF is a self-report scale composed of 33 items. It offers three different subscores of the importance of needs: the global score of needs, the intensity need index and the total number of needs. The IBF was validated on a sample of 400 subjects. These subjects were drawn from the adult population of immediate family members visiting a patient in surgical or medical intensive care units in three different geographical regions, in Québec, northeast Ontario and France. The reliability yielded a 0.90 Cronback Alpha coefficient and the homogeneity coefficient for Spearman-Brown and Guttman procedures were 0.88 respectively. The principal component factor analysis and factorial matrices lead to examine the conceptual structure of five independent factors.

Cross-Cultural Comparison↗
PubMed1990

French validation of the critical care family needs inventory.

This study is a contribution to the French validation of Molter and Leske Critical Care Family Needs Inventory (CCFNI). The importance of this validation study is based on the presumption that evaluation of family needs relies on the use of measures that are reliable and valid for a specific population. The preliminary validation of the French text of the CCFNI was carried out by back translation method of the French form into English by three translators. Then the final French version was selected. The study was conducted in the surgical intensive care unit of the University Hospital in Sherbrooke, Canada. The sample consisted of 207 voluntary subjects selected from adult members of the immediate family visiting a patient in the intensive care unit. The data collection was spread over a 10-week period. The French version of the CCFNI was given to subjects for self-reporting at the end of a 15-minute face-to-face interview. The reliability of the French version yielded 0.91 as Cronbach alpha coefficient. The Spearman-Brown split-half coefficient was 0.89, and the Guttman split-half coefficient was 0.88. Principal-component analysis and factorial matrices were used to examine the clustering structure of the French version of this instrument.

Adult↗
PubMed1989

Families in ICU: their needs and anxiety level.

In the course of their care-giving activities nurses deal with family members as well as with patients. The dimension of family involvement becomes even more crucial when patients are hospitalised in the Intensive Care Unit (ICU). The purpose of this study was to identify: 1. The perceived needs and anxiety levels of adult family members of ICU patients; 2. The relationship between perceived needs and situational anxiety levels; and 3. The sociodemographic factors having an influence on the needs and anxiety level of family members. Over a 10-week-period, a convenience sample of 207 subjects was formed from the total adult population of immediate family members visiting a patient in a 9-bed ICU of a 388-bed university hospital. The data were gathered by a face to face interview, a self-report questionnaire of the French version of the Critical Care Family Needs Inventory (Molter & Leske, 1983), and the A-Scale of the State Trait Anxiety Inventory (Spielberger, 1970). The major variables investigated were: family needs; situational anxiety; on-site sources of worry; level of knowledge with respect to the ICU setting from experience or pre-surgery education; and finally, sociodemographic data. The sample was predominantly female (75%) and the mean age was 45.43 s.d.-15.19, ranging from 18 to 91 years. The average number of respondents per family was 2.3 with a range of 1 to 5. The Situational Anxiety Scale of the STAI yielded a mean score of 47.88 +/- 12.02 ranging from 21 to 76.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1987

Atrial natriuretic peptide inhibits the effect of endogenous angiotensin II on plasma aldosterone in conscious sodium-depleted rats.

Previous studies have shown that atrial natriuretic peptide (ANP) inhibits the secretion of aldosterone by isolated adrenal glomerulosa cells stimulated by angiotensin II, adrenocorticotropic hormone and potassium in vitro. We have also demonstrated that this inhibitory effect of ANP on plasma aldosterone induced by angiotensin II and adrenocorticotropic hormone can be reproduced in vivo in conscious unrestrained rats. In this study, we have investigated the effect of an intravenous infusion of ANP on plasma aldosterone in conscious unrestrained sodium-depleted rats. During sodium depletion, the rise in plasma renin activity which determines an increment in the circulating concentration of angiotensin II was accompanied by a rise in aldosterone secretion as expected. ANP infused intravenously at a dose which increased the plasma concentration of the peptide three- to five-fold, produced a significant decrement in the concentration of aldosterone in plasma after an infusion period of 120 min. There was no significant effect of ANP on plasma renin activity and plasma corticosterone concentration. Since the increase in plasma aldosterone levels in sodium-depleted rats is mainly dependent on the activation of the renin-angiotensin system, we conclude that ANP may modulate the effect of endogenous as well as exogenous angiotensin II on plasma aldosterone secretion.

Aldosterone↗
PubMed1987

Role of calcium in effects of atrial natriuretic peptide on aldosterone production in adrenal glomerulosa cells.

Atrial natriuretic peptide (ANP) inhibits the stimulation of aldosterone secretion by isolated adrenal glomerulosa cells produced by angiotensin II (ANG II), ACTH, and potassium. The effect of ANP on the dose-response curve of aldosterone stimulated by ANG II, ACTH, and potassium on isolated rat adrenal glomerulosa cells was studied. In the presence of ANP the maximal response of aldosterone output stimulated by ANG II or potassium decreased and the half-maximum (EC50) of the response to ACTH was displaced to the right. Because these effects resemble those of calcium-channel blockers, we investigated the effect of different concentrations of nifedipine, a dihydropyridine calcium-channel blocker, on the dose-response curve of aldosterone stimulated by ANG II, ACTH, and potassium. Nifedipine produced effects similar to ANP. The maximal response of aldosterone stimulated by ANG II and potassium was decreased and the dose-response curve to ACTH was displaced to the right. ANP decreased the maximal response of aldosterone to the dihydropyridine derivative BAY K8644, a calcium-channel "activator," without change in its EC50. In contrast, nifedipine displaced the dose-response curve to BAY K8644 to the right as expected of a competitive inhibitor. The effect of ANP and nifedipine on basal and stimulated 45Ca influx into isolated rat adrenal glomerulosa cells was studied. Basal calcium influx was not significantly affected by ANP or nifedipine. Angiotensin II-, ACTH-, potassium-, and BAY K8644-stimulated calcium influx were significantly decreased by 1 nM ANP or 30 microM nifedipine. ANP may act on the rat adrenal glomerulosa cells at least in part by interference with calcium entry.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1986

Atrial natriuretic peptide inhibits the stimulation of aldosterone secretion by ACTH in vitro and in vivo.

Previous studies have shown that atrial natriuretic peptide (ANP) inhibits the secretion of aldosterone by isolated adrenal glomerulosa cells stimulated by angiotensin II, ACTH and potassium in vitro and by angiotensin II in conscious unrestrained rats. In this study we investigated further the effects of synthetic ANP on the dose-response curve of aldosterone secretion stimulated by ACTH in vitro. ANP displaced the dose-response curve of aldosterone to ACTH to the right with a significant change in EC50. A similar effect of ANP was reproduced in vivo in conscious unrestrained rats. There was no significant effect of ANP on the corticosterone response to ACTH in vivo. ANP is a potent regulator of aldosterone secretion which may modulate the effects of ACTH on the adrenal in vitro and in vivo.

Adrenal Cortex↗
PubMed1985

Identification of a biologically active circulating form of rat atrial natriuretic factor.

An atrial natriuretic peptide has been isolated from plasma of morphine treated rats by means of glass beads extraction, immunoaffinity chromatography, and reverse phase HPLC. 1.3 micrograms of immunoreactive material was obtained. The biological activity of this material was found comparable to that of ANF (Arg 101 - Tyr 126) on the inhibition of basal aldosterone secretion by rat adrenal zona glomerulosa cells and the displacement curve of iodinated ANF from ANF receptors in a mesenteric artery preparation. Gas phase amino acid sequencing indicated that it is related to ANF (Ser 99 - Tyr 126). These results suggest that the maturation of ANF may require a tryptic-like cleavage after a single Arg residue.

Adrenal Cortex↗
PubMed1985

Vascular and adrenal receptors for atrial natriuretic factor in the rat.

Previous studies have shown that atrial natriuretic factor, a powerful vasorelaxant of precontracted vessels, inhibits the secretion of aldosterone stimulated by angiotensin II, adrenocorticotropic hormone, and potassium. We now report the presence of specific binding sites for atrial natriuretic factor in rat blood vessels (mesenteric and renal arteries) and adrenal capsules. Radioiodinated synthetic atrial natriuretic factor bound to a single class of high-affinity (KD = 0.1 nM) low-capacity receptors in a particulate fraction from blood vessels and adrenals. Unrelated peptides did not displace atrial natriuretic factor. Fragments of atrial natriuretic factor displaced the labeled ligand with decreasing potency after cleavage at the N-terminal. The cleavage of the C-terminal tyrosine did not decrease the potency of atrial natriuretic factor, but further cleavage at the C-terminal dramatically reduced the affinity of the resulting peptides. The potency of the atrial natriuretic factor fragments in the radioligand assay was in proportion to their potency to inhibit aldosterone secretion by isolated rat glomerulosa cells. Our results suggest that these binding sites mediate the biological actions of atrial natriuretic factor in blood vessels and the adrenal, and that both receptors have similar specificities.

Adrenal Glands↗
PubMed1984

Effect of atrial natriuretic factor (ANF)-related peptides on aldosterone secretion by adrenal glomerulosa cells: critical role of the intramolecular disulphide bond.

We previously demonstrated that synthetic 48-73 atrial natriuretic factor (ANF) (previously called 8-33 ANF) blocked the response of rat adrenal glomerulosa cells to angiotensin II, ACTH and potassium. We have now investigated the effects of natural 43-73 ANF, oxidised synthetic 48-73 ANF and the natural 1-73 ANF on aldosterone output by rat glomerulosa cells. The natural 43-73 ANF and the natural 1-73 ANF were equipotent to 48-73 ANF in inhibiting the stimulation of aldosterone secretion produced by angiotensin II with an IC50 of 2 X 10(-9)M. Similar results were obtained with ACTH and potassium. After oxidation with performic acid, 48-73 ANF was completely devoid of activity on the response of aldosterone to angiotensin II, ACTH and potassium. We conclude that the intramolecular disulphide bond in 48-73 ANF is critical for maintaining the active conformation of ANF.

Adrenal Cortex↗
PubMed1984

Atrial natriuretic factor inhibits the stimulation of aldosterone secretion by angiotensin II, ACTH and potassium in vitro and angiotensin II-induced steroidogenesis in vivo.

Since atrial natriuretic factor (ANF) blocks the contractile effect of angiotensin II on vascular strips, we investigated the action of the synthetic 48-73 ANF (previously called 8-33 ANF) on another target tissue of angiotensin II, the adrenal glomerulosa. ANF did not affect basal aldosterone output by isolated rat adrenal glomerulosa cells. ANF inhibited aldosterone secretion stimulated by 10(-8)M angiotensin II with an IC50 of 1.3 X 10(-9)M. Aldosterone secretion stimulated by 2.9 X 10(-10)M ACTH and by 15 mM potassium was similarly inhibited by ANF. In vivo, ANF blocked the effect of angiotensin II infused iv on aldosterone secretion in conscious unrestrained rats. We conclude that ANF is a non-selective inhibitor of stimulated aldosterone output.

Adrenal Glands↗