Calculation of volumes and systolic indices of heart ventricle fromHalobatrachus didactylus: Echocardiographic noninvasive method

Coucelo, J; Joaquim, Natércia

doi:10.1002/(sici)1097-010x(20000501)286:6<585::aid-jez5>3.0.co;2-z

Cited by 23 publications

(18 citation statements)

References 12 publications

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“…2). We observed no consistent effect on heart rate; however, applying an algorithm previously validated in another fish species allowed us to assess the ventricular enddiastolic and end-systolic volumes using time-lapse recordings of the beating zebrafish hearts (Coucelo et al, 2000). This revealed a TCDD-induced decrease in stroke volume at 8 h (80 hpf).…”

Section: Resultsmentioning

confidence: 95%

“…The volume of the ventricle at end-diastole and end-systole and heart rate were measured in larvae to calculate stroke volume, ejection fraction, and cardiac output. The volume of the ventricle was approximated from linear dimensions taken from two-dimension images with Simpson's method, also called the method of discs (Schiller et al, 1989;Coucelo et al, 2000). This method approximates a ventricle volume by dividing the ventricle into slices of finite thickness from the apex to base and calculates the ventricle volume by addition of the individual slice volumes using the…”

Section: Heart-specific Transcriptional Response To Tcdd 551mentioning

confidence: 99%

See 1 more Smart Citation

Aryl Hydrocarbon Receptor Activation Produces Heart-Specific Transcriptional and Toxic Responses in Developing Zebrafish

Carney¹,

Chen²,

Burns³

et al. 2006

Molecular Pharmacology

154

166

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Proper regulation of the aryl hydrocarbon receptor (AHR), a ligand-activated transcription factor, is required for normal vertebrate cardiovascular development. AHR hyperactivation by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) during zebrafish (Danio rerio) development results in altered heart morphology and function, culminating in death. To identify genes that may cause cardiac toxicity, we analyzed the transcriptional response to TCDD in zebrafish hearts. Zebrafish larvae were exposed to TCDD for 1 h at 72 h after fertilization (hpf), and the hearts were extracted for microarray analysis at 1, 2, 4, and 12 h after exposure (73, 74, 76, and 84 h postfertilization). The remaining body tissue was also collected at each time for comparison. TCDD rapidly induced expression in 42 genes within 1 to 2 h of exposure. These genes function in xenobiotic metabolism, proliferation, heart contractility, and pathways that regulate heart development. Furthermore, these expression changes preceded signs of cardiovascular toxicity, characterized by decreased stroke volume, peripheral blood flow, and a halt in heart growth. This identifies strong candidates for important AHR target genes. It is noteworthy that the TCDDinduced transcriptional response in the hearts of zebrafish larvae was substantially different from that induced in the rest of the body tissues. One of the biggest differences included a cluster of genes that were down-regulated 12 h after exposure in heart tissue, but not in the body samples. More than 70% of the transcripts in this heart-specific cluster promote cellular growth and proliferation. Thus, the developing heart stands out as being responsive to TCDD at both the level of toxicity and gene expression.

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Section: Resultsmentioning

confidence: 95%

Section: Heart-specific Transcriptional Response To Tcdd 551mentioning

confidence: 99%

Aryl Hydrocarbon Receptor Activation Produces Heart-Specific Transcriptional and Toxic Responses in Developing Zebrafish

Carney¹,

Chen²,

Burns³

et al. 2006

Molecular Pharmacology

154

166

View full text Add to dashboard Cite

show abstract

“…To calculate stroke volume we separately averaged EDV and then ESV for a given fish across three consecutive beats. Volume was calculated using the Simpson method of stacked discs (8,37). Briefly, two-dimensional cross sectional images of the ventricle were obtained (end diastole and end systole determined as the largest and smallest 2D sections, respectively), and the ventricular space was divided into a series of bands representing the three-dimensional chamber.…”

Section: Methodsmentioning

confidence: 99%

Systems proteomics of cardiac chromatin identifies nucleolin as a regulator of growth and cellular plasticity in cardiomyocytes

Monte

Mouillesseaux

Chen

et al. 2013

American Journal of Physiology-Heart and Circulatory Physiology

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Myocyte hypertrophy antecedent to heart failure involves changes in global gene expression, although the preceding mechanisms to coordinate DNA accessibility on a genomic scale are unknown. Chromatin-associated proteins alter chromatin structure by changing their association with DNA, thereby altering the gene expression profile. Little is known about the global changes in chromatin subproteomes that accompany heart failure, and the mechanisms by which these proteins alter chromatin structure. The present study tests the fundamental hypothesis that cardiac growth and plasticity in the setting of disease recapitulates conserved developmental chromatin remodeling events. We used quantitative proteomics to identify chromatin-associated proteins extracted via detergent and to quantify changes in their abundance during disease. Our study identified 321 proteins in this subproteome, demonstrating it to have modest conservation (37%) with that revealed using strong acid. Of these proteins, 176 exhibited altered expression during cardiac hypertrophy and failure; we conducted extensive functional characterization of one of these proteins, Nucleolin. Morpholino-based knockdown of nucleolin nearly abolished protein expression but surprisingly had little impact on gross morphological development. However, hearts of fish lacking Nucleolin displayed severe developmental impairment, abnormal chamber patterning and functional deficits, ostensibly due to defects in cardiac looping and myocyte differentiation. The mechanisms underlying these defects involve perturbed bone morphogenetic protein 4 expression, decreased rRNA transcription, and a shift to more heterochromatic chromatin. This study reports the quantitative analysis of a new chromatin subproteome in the normal and diseased mouse heart. Validation studies in the complementary model system of zebrafish examine the role of Nucleolin to orchestrate genomic reprogramming events shared between development and disease.

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“…Although valuable, these techniques are invasive and determining the degree of functional change owing to surgery, stress, and tissue modification can be difficult. In recent years, noninvasive echocardiography has been used successfully to study cardiac function and structure in nonmammalian vertebrates (Franklin and Davie, '92a;Young and Saunders, '99;Coucelo et al, 2000;Lai et al, 2004). Echocardiography uses high-frequency sound waves to produce detailed two-dimensional images of the heart and large blood vessels.…”

mentioning

confidence: 99%

“…Echocardiography has been used in fish to estimate cardiac chamber volume and shape (Franklin and Davie, '92a;Coucelo et al, 2000;Claireaux et al, 2005), diagnose cardiomyopathy syndrome (Sande and Poppe,'95), identify ventricular filling and specific hemodynamic patterns (Lai et al, '90, '96, '98, 2004;Coucelo et al, '96;Ho et al, 2002); and determine stroke volume (SV) and ventricle performance (Franklin and Davie, '92a;Coucelo et al, 2000).…”

mentioning

confidence: 99%

Cardiac hemodynamics of the rainbow trout (Oncorhynchus mykiss) using simultaneous Doppler echocardiography and electrocardiography

Cotter

Han

Everson³

et al. 2008

J. Exp. Zool.

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Using Doppler echocardiography and electrocardiography, we characterized cardiac hemodynamics, timing, and electromechanical function, and examined the effects of ventricular hypertrophy on systolic function in anesthetized rainbow trout. Atrial filling (D(SA)), ventricular filling (D(AV)), and ventricular ejection (D(VB)) accounted for 40-77, 13-27, and 22-41% of the cardiac cycle, respectively. Ventricular ejection occurred entirely during atrial filling and ended by the time the QT interval was 80% (SD=9%) completed. Sinoatrial (SA) flow was of longer duration (0.53+/-0.08 sec, mean+/-SD) and lower velocity (32+/-8 cm sec(-1)) than corresponding atrioventricular (AV, 0.19+/-0.02 sec; 87+/-8 cm sec(-1)) and ventriculobulbar (VB, 0.30+/-0.05 sec; 63+/-20 cm sec(-1)) values. Despite a wide range of heart masses, atrioventricular and VB valve dimensions were identical ( approximately 5.5 mm(2)). Ventricle mass (M(V)), but not relative ventricle mass (RVM), and cardiac cycle length were positively correlated (r(2)=0.57, P<0.001); thus, all time-dependent electrical/mechanical measures of cardiac function were significantly related to M(V), but not RVM. All rate-corrected (c) electromechanical event durations (except cD(SA)) and the systolic function index (cPEP (pre-ejection period)/D(VB)) were independent of RVM, suggesting the maintenance of cardiac functional capabilities across maturation stages (males) and different ventricle sizes (males and females). In summary, we define fundamental electrical and mechanical properties of the in vivo teleost myocardium under anesthesia, and report the maintenance of systolic function over a wide range of heart sizes for both sexes and maturation state of males. We also suggest that the short duration of ventricular emptying relative to the QT interval may provide a novel mechanism to adjust stroke volume and cardiac output in teleosts.

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Calculation of volumes and systolic indices of heart ventricle fromHalobatrachus didactylus: Echocardiographic noninvasive method

Cited by 23 publications

References 12 publications

Aryl Hydrocarbon Receptor Activation Produces Heart-Specific Transcriptional and Toxic Responses in Developing Zebrafish

Aryl Hydrocarbon Receptor Activation Produces Heart-Specific Transcriptional and Toxic Responses in Developing Zebrafish

Systems proteomics of cardiac chromatin identifies nucleolin as a regulator of growth and cellular plasticity in cardiomyocytes

Cardiac hemodynamics of the rainbow trout (Oncorhynchus mykiss) using simultaneous Doppler echocardiography and electrocardiography

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