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  • Ovid Technologies (Wolters Kluwer Health)  (20)
  • Amour, Julien  (20)
  • 1
    Online Resource
    Online Resource
    Ovid Technologies (Wolters Kluwer Health) ; 2015
    In:  Anesthesiology Vol. 122, No. 4 ( 2015-04-01), p. 876-883
    In: Anesthesiology, Ovid Technologies (Wolters Kluwer Health), Vol. 122, No. 4 ( 2015-04-01), p. 876-883
    Abstract: Acute respiratory acidosis is associated with alterations in diaphragm performance. The authors compared the effects of respiratory acidosis and metabolic acidosis in the rat diaphragm in vitro. Methods: Diaphragmatic strips were stimulated in vitro, and mechanical and energetic variables were measured, cross-bridge kinetics calculated, and the effects of fatigue evaluated. An extracellular pH of 7.00 was obtained by increasing carbon dioxide tension (from 25 to 104 mmHg) in the respiratory acidosis group (n = 12) or lowering bicarbonate concentration (from 24.5 to 5.5 mM) in the metabolic acidosis group (n = 12) and the results compared with a control group (n = 12, pH = 7.40) after 20-min exposure. Results: Respiratory acidosis induced a significant decrease in maximum shortening velocity (−33%, P & lt; 0.001), active isometric force (−36%, P & lt; 0.001), and peak power output (−59%, P & lt; 0.001), slowed relaxation, and decreased the number of cross-bridges (−35%, P & lt; 0.001) but not the force per cross-bridge, and impaired recovery from fatigue. Respiratory acidosis impaired more relaxation than contraction, as shown by impairment in contraction–relaxation coupling under isotonic (−26%, P & lt; 0.001) or isometric (−44%, P & lt; 0.001) conditions. In contrast, no significant differences in diaphragmatic contraction, relaxation, or contraction–relaxation coupling were observed in the metabolic acidosis group. Conclusions: In rat diaphragm, acute (20 min) respiratory acidosis induced a marked decrease in the diaphragm contractility, which was not observed in metabolic acidosis.
    Type of Medium: Online Resource
    ISSN: 0003-3022
    RVK:
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2015
    detail.hit.zdb_id: 2016092-6
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  • 2
    In: Anesthesiology, Ovid Technologies (Wolters Kluwer Health), Vol. 104, No. 1 ( 2006-01-01), p. 60-64
    Abstract: Plastic single-use laryngoscope blades are inexpensive and carry a lower risk of infection compared with metal reusable blades, but their efficiency during rapid sequence induction remains a matter of debate. The authors therefore compared plastic and metal blades during rapid sequence induction in a prospective randomized trial. Methods Two hundred eighty-four adult patients undergoing general anesthesia requiring rapid sequence induction were randomly assigned on a weekly basis to either plastic single-use or reusable metal blades (cluster randomization). After induction, a 60-s period was allowed to complete intubation. In the case of failed intubation, a second attempt was performed using metal blade. The primary endpoint of the study was the rate of failed intubations, and the secondary endpoint was the incidence of complications (oxygen desaturation, lung aspiration, and oropharynx trauma). Results Both groups were similar in their main characteristics, including risk factors for difficult intubation. On the first attempt, the rate of failed intubation was significantly increased in plastic blade group (17 vs. 3%; P & lt; 0.01). In metal blade group, 50% of failed intubations were still difficult after the second attempt. In plastic blade group, all initial failed intubations were successfully intubated using metal blade, with an improvement in Cormack and Lehane grade. There was a significant increase in the complication rate in plastic group (15 vs. 6%; P & lt; 0.05). Conclusions In rapid sequence induction of anesthesia, the plastic laryngoscope blade is less efficient than a metal blade and thus should not be recommended for use in this clinical setting.
    Type of Medium: Online Resource
    ISSN: 0003-3022
    RVK:
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2006
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  • 3
    In: Anesthesiology, Ovid Technologies (Wolters Kluwer Health), Vol. 122, No. 2 ( 2015-02-01), p. 334-342
    Abstract: In the senescent heart, the positive inotropic response to β-adrenoceptor stimulation is reduced, partly by dysregulation of β1- and β3-adrenoceptors. The multidrug resistance protein 4 (MRP4) takes part in the control of intracellular cyclic adenosine monophosphate concentration by controlling its efflux but the role of MRP4 in the β-adrenergic dysfunction of the senescent heart remains unknown. Methods: The β-adrenergic responses to isoproterenol were investigated in vivo (stress echocardiography) and in vitro (isolated cardiomyocyte by Ionoptix® with sarcomere shortening and calcium transient) in young (3 months old) and senescent (24 months old) rats pretreated or not with MK571, a specific MRP4 inhibitor. MRP4 was quantified in left ventricular homogenates by Western blotting. Data are mean ± SD expressed as percent of baseline value. Results: The positive inotropic effect of isoproterenol was reduced in senescent rats in vivo (left ventricular shortening fraction 120 ± 16% vs. 158 ± 20%, P & lt; 0.001, n = 16 rats) and in vitro (sarcomere shortening 129 ± 37% vs. 148 ± 35%, P = 0.004, n = 41 or 43 cells) as compared to young rats. MRP4 expression increased 3.6-fold in senescent compared to young rat myocardium (P = 0.012, n = 8 rats per group). In senescent rats, inhibition of MRP4 by MK571 restored the positive inotropic effect of isoproterenol in vivo (143 ± 11%, n = 8 rats). In vitro in senescent cardiomyocytes pretreated with MK571, both sarcomere shortening (161 ± 45% vs. 129 ± 37%, P = 0.007, n = 41 cells per group) and calcium transient amplitude (132 ± 25% vs. 113 ± 27%, P = 0.007) increased significantly. Conclusion: MRP4 overexpression contributes to the reduction of the positive inotropic response to β-adrenoceptor stimulation in the senescent heart.
    Type of Medium: Online Resource
    ISSN: 0003-3022
    RVK:
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2015
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  • 4
    Online Resource
    Online Resource
    Ovid Technologies (Wolters Kluwer Health) ; 2010
    In:  Anesthesiology Vol. 113, No. 3 ( 2010-09-01), p. 750-751
    In: Anesthesiology, Ovid Technologies (Wolters Kluwer Health), Vol. 113, No. 3 ( 2010-09-01), p. 750-751
    Type of Medium: Online Resource
    ISSN: 0003-3022
    RVK:
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2010
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  • 5
    Online Resource
    Online Resource
    Ovid Technologies (Wolters Kluwer Health) ; 2008
    In:  Critical Care Medicine Vol. 36, No. 10 ( 2008-10), p. 2740-2745
    In: Critical Care Medicine, Ovid Technologies (Wolters Kluwer Health), Vol. 36, No. 10 ( 2008-10), p. 2740-2745
    Type of Medium: Online Resource
    ISSN: 0090-3493
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2008
    detail.hit.zdb_id: 2034247-0
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  • 6
    Online Resource
    Online Resource
    Ovid Technologies (Wolters Kluwer Health) ; 2004
    In:  Anesthesiology Vol. 100, No. 5 ( 2004-05-01), p. 1179-1187
    In: Anesthesiology, Ovid Technologies (Wolters Kluwer Health), Vol. 100, No. 5 ( 2004-05-01), p. 1179-1187
    Abstract: Diabetes induces significant myocardial abnormalities, but the effects of halogenated anesthetics on this diseased myocardium remain a matter of debate. Methods Left ventricular papillary muscles and triton-skinned cardiac fibers were provided from control and streptozotocin-induced diabetic rats. The effects of halothane and sevoflurane were studied on inotropic and lusitropic responses, under low (isotony) and high (isometry) loads in papillary muscles and then on isometric tension-Ca2+ concentration (pCa) relations obtained in triton-skinned cardiac fibers. Data are presented as mean +/- SD. Results Sevoflurane and halothane induced a negative inotropic effect that was more important in diabetic rats (active force: 1.5% halothane, 19+/-6 vs. 24+/-6% of baseline, P & lt; 0.05; 3.6% sevoflurane, 47+/-14 vs. 69+/-17% of baseline, P & lt; 0.05). However, when differences in minimum alveolar concentration were considered, no significant difference was observed between groups for halothane. The effects of halothane and sevoflurane on isotonic relaxation and postrest potentiation were not significantly different between groups. In contrast, the decrease in Ca myofilament sensitivity produced by each anesthetic agent was greater in diabetic rats than in control rats (0.65% halothane, -0.15+/-0.07 vs. -0.05+/-0.04 pCa unit, P & lt; 0.05; 1.8% sevoflurane, -0.12+/-0.06 vs. -0.06+/-0.04 pCa unit, P & lt; 0.05). Conclusions The negative inotropic effect of halothane and sevoflurane was greater in diabetic rats, mainly because of a significant decrease in myofilament Ca sensitivity.
    Type of Medium: Online Resource
    ISSN: 0003-3022
    RVK:
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2004
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  • 7
    Online Resource
    Online Resource
    Ovid Technologies (Wolters Kluwer Health) ; 2008
    In:  Anesthesiology Vol. 109, No. 6 ( 2008-12-01), p. 1045-1053
    In: Anesthesiology, Ovid Technologies (Wolters Kluwer Health), Vol. 109, No. 6 ( 2008-12-01), p. 1045-1053
    Abstract: In senescent heart, beta-adrenergic response is altered in parallel with beta1- and beta2-adrenoceptor down-regulation. A negative inotropic effect of beta3-adrenoceptor could be involved. In this study, the authors tested the hypothesis that beta3-adrenoceptor plays a role in beta-adrenergic dysfunction in senescent heart. Methods beta-Adrenergic responses were investigated in vivo (echocardiography-dobutamine, electron paramagnetic resonance) and in vitro (isolated left ventricular papillary muscle, electron paramagnetic resonance) in young adult (3-month-old) and senescent (24-month-old) rats. Nitric oxide synthase (NOS) immunolabeling (confocal microscopy), nitric oxide production (electron paramagnetic resonance) and beta-adrenoceptor Western blots were performed in vitro. Data are mean percentages of baseline +/- SD. Results An impaired positive inotropic effect (isoproterenol) was confirmed in senescent hearts in vivo (117 +/- 23 vs. 162 +/- 16%; P & lt; 0.05) and in vitro (127 +/- 10 vs. 179 +/- 15%; P & lt; 0.05). In the young adult group, the positive inotropic effect was not significantly modified by the nonselective NOS inhibitor N-nitro-L-arginine methylester (L-NAME; 183 +/- 19%), the selective NOS1 inhibitor vinyl-L-N-5(1-imino-3-butenyl)-L-ornithine (L-VNIO; 172 +/- 13%), or the selective NOS2 inhibitor 1400W (183 +/- 19%). In the senescent group, in parallel with beta3-adrenoceptor up-regulation and increased nitric oxide production, the positive inotropic effect was partially restored by L-NAME (151 +/- 8%; P & lt; 0.05) and L-VNIO (149 +/- 7%; P & lt; 0.05) but not by 1400W (132 +/- 11%; not significant). The positive inotropic effect induced by dibutyryl-cyclic adenosine monophosphate was decreased in the senescent group with the specific beta3-adrenoceptor agonist BRL 37344 (167 +/- 10 vs. 142 +/- 10%; P & lt; 0.05). NOS1 and NOS2 were significantly up-regulated in the senescent rat. Conclusions In senescent cardiomyopathy, beta3-adrenoceptor overexpression plays an important role in the altered beta-adrenergic response via induction of NOS1-nitric oxide.
    Type of Medium: Online Resource
    ISSN: 0003-3022
    RVK:
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2008
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  • 8
    Online Resource
    Online Resource
    Ovid Technologies (Wolters Kluwer Health) ; 2010
    In:  Anesthesiology Vol. 112, No. 5 ( 2010-05-01), p. 1204-1210
    In: Anesthesiology, Ovid Technologies (Wolters Kluwer Health), Vol. 112, No. 5 ( 2010-05-01), p. 1204-1210
    Abstract: Hemodynamic instability is frequent in brain-dead patients and may result, in part, from absolute or relative adrenal insufficiency. Corticosteroid supplementation is widely used to restore hemodynamic stability in septic shock and to reduce the time of shock resolution. The authors verified that supplementation with hydrocortisone may enhance hemodynamic stability in brain-dead patients. Methods All consecutive brain-dead patients with hypotension requiring vasopressor agents were included in this single-center noninterventional clinical observation study. Assessment of baseline and adrenocorticotropic hormone (ACTH)-stimulated plasma cortisol concentrations was performed. Immediately after, patients were systematically treated with a single intravenous injection of hydrocortisone (50 mg), and norepinephrine administration was adjusted every 15 min to maintain mean arterial pressure between 65 and 90 mmHg. Adrenal insufficiency was defined as baseline plasma cortisol concentration less than 15 microg/dl and/or delta plasma cortisol concentration less than 9 microg/dl. Patients were considered as ACTH responders when delta cortisol concentration was more than 9 microg/dl 30 min after ACTH injection. Results Among the 31 patients included, the incidence of adrenal insufficiency was 87% [95% CI, 70-96%]. A significant ( & gt; or =30%) decrease in norepinephrine dose was obtained 180 min after hydrocortisone injection in 18 (59%) patients, from 0.31 [0.16-0.44] microg . kg(-1) . min(-1) to 0.18 [0.10-0.24] microg . kg(-1) . min(-1) (P & lt; 0.01). The incidence of hemodynamic response was greater in ACTH nonresponders than in ACTH responders: 86% versus 50%, respectively, P & lt; 0.05. Conclusions Adrenal insufficiency with hemodynamic instability is frequent in brain-dead patients. After ACTH stimulation testing and hydrocortisone infusion, hemodynamic stability is enhanced especially in patients with true adrenal nonfunction.
    Type of Medium: Online Resource
    ISSN: 0003-3022
    RVK:
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2010
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  • 9
    Online Resource
    Online Resource
    Ovid Technologies (Wolters Kluwer Health) ; 2008
    In:  Anesthesiology Vol. 108, No. 3 ( 2008-03-01), p. 524-530
    In: Anesthesiology, Ovid Technologies (Wolters Kluwer Health), Vol. 108, No. 3 ( 2008-03-01), p. 524-530
    Type of Medium: Online Resource
    ISSN: 0003-3022
    RVK:
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2008
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  • 10
    In: Critical Care Medicine, Ovid Technologies (Wolters Kluwer Health), Vol. 43, No. 7 ( 2015-07), p. e241-e249
    Type of Medium: Online Resource
    ISSN: 0090-3493
    Language: English
    Publisher: Ovid Technologies (Wolters Kluwer Health)
    Publication Date: 2015
    detail.hit.zdb_id: 2034247-0
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