Impact of Anesthesia on Echocardiographic Evaluation of Systolic and Diastolic Function in Rats

Plante, Eric; Lachance, Dominic; Roussel, Élise; Drolet, Marie‐Claude; Arsenault, Marie; Couët, Jacques

doi:10.1016/j.echo.2006.06.011

Cited by 44 publications

(47 citation statements)

References 31 publications

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“…Adaptive hypertrophy enhances the contractile force via increased muscle mass to match peripheral demands. Thus, our observation of exerciseinduced hypertrophy is in harmony with our earlier finding that the isolated EXAC left ventricle generates greater pressure than that of EX hearts (31). In contrast to the quantitative effect of training on the morphometric features of both trained groups, the EX and EXAC cardiac phenotypes showed differential contractile features.…”

Section: What Can We Learn From Echocardiography?supporting

confidence: 89%

“…Although the effects of sedation on cardiovascular hemodynamics and contractility depend on the anesthetic agent used, our between-groups comparisons are valid because all of our experimental animals were sedated similarly, using the same anesthetic agent. Likewise, the morphometric and physiological parameters reported here do not differ significantly among the drugs usually used in rat echocardiography, hence data are provided with values close to those obtained from conscious rats (31,37).…”

Section: What Can We Learn From Echocardiography?supporting

confidence: 67%

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Heat acclimation and exercise training interact when combined in an overriding and trade-off manner: physiologic-genomic linkage

Kodesh

Nesher

Simaan

et al. 2011

American Journal of Physiology-Regulatory, Integrative and Comp

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Combined heat acclimation (AC) and exercise training (EX) enhance exercise performance in the heat while meeting thermoregulatory demands. We tested the hypothesis that different stress-specific adaptations evoked by each stressor individually trigger similar cardiac alterations, but when combined, overriding/trade-off interactions take place. We used echocardiography, isolated cardiomyocyte imaging and cDNA microarray techniques to assay in situ cardiac performance, excitationcontraction (EC) coupling features, and transcriptional programs associated with cardiac contractility. Rat groups studied were controls (sedentary 24°C); AC (sedentary, 34°C, 1 mo); normothermic EX (treadmill at 24°C, 1 mo); and heat-acclimated, exercise-trained (EXAC; treadmill at 34°C, 1 mo). Prolonged heat exposure decreased heart rate and contractile velocity and increased end ventricular diastolic diameter. Compared with controls, AC/EXAC cardiomyocytes demonstrated lower L-type Ca 2ϩ current (ICaL) amplitude, higher Ca 2ϩ transient (Ca 2ϩ T), and a greater Ca 2ϩ T-to-ICaL ratio; EX alone enhanced I CaL and Ca 2ϩ T, whereas aerobic training in general induced cardiac hypertrophy and action potential elongation in EX/ EXAC animals. At the genomic level, the transcriptome profile indicated that the interaction between AC and EX yields an EXACspecific molecular program. Genes affected by chronic heat were linked with the EC coupling cascade, whereas aerobic training upregulated genes involved with Ca 2ϩ turnover via an adrenergic/ metabolic-driven positive inotropic response. In the EXAC cardiac phenotype, the impact of chronic heat overrides that of EX on EC coupling components and heart rate, whereas EX regulates cardiac morphometry. We suggest that concerted adjustments induced by AC and EX lead to enhanced metabolic and mechanical performance of the EXAC heart. echocardiography; isolated cardiomyocytes; Ca 2ϩ signaling; genomic responses HEAT ACCLIMATION (AC) and exercise training (EX) are powerful stressors, causing structural cardiac remodeling and improving mechanical performance. Each stressor has its own adaptive requirements, e.g., increased peripheral blood flow to enhance heat dissipation, required for AC, or increased muscle blood flow to augment the oxygen supply and muscle power output needed during bouts of exercise. Evidence derived from isolated rat heart preparations prompted the hypothesis that different stress-specific adaptive signaling mechanisms trigger the similar cardiac alterations evoked by each stressor alone. Upon AC, an increase in left cardiac ventricular compliance and systolic pressure with a concomitant decrease in oxygen consumption suggests enhanced cardiac efficiency (25-26). At the cellular level, greater Ca 2ϩ transient amplitude compensates for decreased myofilament Ca 2ϩ responsiveness and plays a major role in greater force development (4). Myosin isoform redistribution from the predominantly fast myosin isoform (V1) to slow myosin isoform (V3) predominance and the altered expression of Ca 2ϩ r...

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Section: What Can We Learn From Echocardiography?supporting

confidence: 89%

Section: What Can We Learn From Echocardiography?supporting

confidence: 67%

Heat acclimation and exercise training interact when combined in an overriding and trade-off manner: physiologic-genomic linkage

Kodesh

Nesher

Simaan

et al. 2011

American Journal of Physiology-Regulatory, Integrative and Comp

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“…The echocardiogram after 2 weeks was performed to quantify AR before starting the training program to ensure all animals still met the entry criteria. Left ventricular dimensions, wall thickness, ejection fraction, diastolic function, cardiac output, myocardial performance index were evaluated as previously reported [13][14][15] .…”

Section: Echocardiographymentioning

confidence: 99%

Moderate Exercise Training Improves Survival and Ventricular Remodeling in an Animal Model of Left Ventricular Volume Overload

Lachance

Plante

Bouchard-Thomassin

et al. 2009

Circ: Heart Failure

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“…LV dimensions, wall thickness, ejection fraction, diastolic function, cardiac output (ejection volume in the LV outflow tract ϫ heart rate) were evaluated as previously reported (14,33). AR was semiquantified at each time point, as described in the previous section.…”

Section: Echocardiographymentioning

confidence: 99%

Gene profiling of left ventricle eccentric hypertrophy in aortic regurgitation in rats: rationale for targeting the β-adrenergic and renin-angiotensin systems

Champetier¹,

Bojmehrani²,

Beaudoin³

et al. 2009

American Journal of Physiology-Heart and Circulatory Physiology

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profiling of left ventricle eccentric hypertrophy in aortic regurgitation in rats: rationale for targeting the ␤-adrenergic and renin-angiotensin systems. Am J Physiol Heart Circ Physiol 296: H669 -H677, 2009. First published December 26, 2008 doi:10.1152/ajpheart.01046.2008.-Aortic valve regurgitation (AR) imposes a severe volume overload to the left ventricle (LV), which results in dilation, eccentric hypertrophy, and eventually loss of function. Little is known about the impact of AR on LV gene expression. We, therefore, conducted a gene expression profiling study in the LV of rats with acute and severe AR. We identified 64 genes that were specifically upregulated and 29 that were downregulated out of 21,910 genes after 2 wk. Of the upregulated genes, a good proportion was related to the extracellular matrix. We subsequently studied a subset of 19 genes by quantitative RT-PCR (qRT-PCR) to see if the modulation seen in the LV after 2 wk persisted in the chronic phase (after 6 and 12 mo) and found that it did persist. Knowing that the adrenergic and renin-angiotensin systems are overactivated in our animal model, we were interested to see if blocking those systems using metoprolol (25 mg ⅐ kg Ϫ1 ⅐ day Ϫ1 ) and captopril (100 mg ⅐ kg Ϫ1 ⅐ day Ϫ1 ) would alter the expression of some upregulated LV genes in AR rats after 6 mo. By qRT-PCR, we observed that upregulations of LV mRNA levels encoding for procollagens type I and III, fibronectin, atrial natriuretic peptide, transforming growth factor-␤2, and connective tissue growth factor were totally or partially reversed by this treatment. These observations provide a molecular rationale for a medical strategy aiming these systems in the medical treatment of AR and expand the paradigm in the study of this form of LV volume overload. heart hypertrophy; gene expression; renin-angiotensin system; adrenergic system SEVERE AORTIC VALVE REGURGITATION (AR) is associated with a long asymptomatic period during which the left ventricle (LV) progressively dilates and hypertrophies in response to a chronic volume overload. This process is accompanied by a decrease in LV function, occurrence of symptoms, and eventually heart failure (4, 7). No drug has yet been clearly shown in humans to be effective to slow LV dilation, hypertrophy, and loss of systolic function or to have any impact on morbidity or mortality in chronic AR (5, 15).At the microscopic level, AR is associated with cardiomyocyte elongation and excessive but mostly noncollagen myocardial fibrosis (fibronectin) (6, 23). Although gene expression profiling in LV eccentric hypertrophy resulting from volume overload has been studied recently in an aortocaval fistula rat model (25), very little is known about the mechanisms of LV hypertrophy and extracellular matrix (ECM) remodeling associated with a more clinically common form of LV volume overload, namely AR. Aortocaval fistula models relate to a clinically rather rare complication of aortic aneurysm or secondary to abdominal trauma in humans (21). Moreover, aortocaval ...

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Impact of Anesthesia on Echocardiographic Evaluation of Systolic and Diastolic Function in Rats

Abstract: Abstract:Background: Echocardiography is used on rats but general anesthesia is usually

Cited by 44 publications

References 31 publications

Heat acclimation and exercise training interact when combined in an overriding and trade-off manner: physiologic-genomic linkage

Heat acclimation and exercise training interact when combined in an overriding and trade-off manner: physiologic-genomic linkage

Moderate Exercise Training Improves Survival and Ventricular Remodeling in an Animal Model of Left Ventricular Volume Overload

Gene profiling of left ventricle eccentric hypertrophy in aortic regurgitation in rats: rationale for targeting the β-adrenergic and renin-angiotensin systems

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