Computational Approach to Measuring Myocyte Disarray in Animal Models of Heart Disease

2017 ◽  
Vol 93 (1) ◽  
Author(s):  
William Wan ◽  
Leslie Leinwand
Keyword(s):  
Heart Disease ◽  
Animal Models ◽  
Computational Approach ◽  
Myocyte Disarray

Abstract 228: Alterations of Cardiac Morphology and Function Caused by Cardio-Thoracic Surgery in Small Animal Models of Heart Disease

2013 ◽  
Vol 113 (suppl_1) ◽  
Author(s):  
Peter Nordbeck ◽  
Leoni Bönhof ◽  
Karl-Heinz Hiller ◽  
Sabine Voll ◽  
Paula Arias ◽  
...  
Keyword(s):  
Body Weight ◽  
Heart Disease ◽  
Animal Models ◽  
Right Ventricular ◽  
Small Animal ◽  
Cardiac Morphology ◽  
Small Animal Models ◽  
And Function

Background: Surgical procedures in small animal models of heart disease, such as artificial ligation of the coronary arteries for experimental myocardial infarction, can evoke alterations in cardiac morphology and function. Such alterations might induce artificial early or long term effects in vivo that might account for a significant bias in basic cardiovascular research, and, therefore, could potentially question the meaning of respective studies in small animal models of heart disease. Methods: Female Wistar rats were matched for weight and distributed to sham left coronary artery ligation or untreated control. Cardiac parameters were then investigated in vivo by high-field MRI over time after the surgical procedure, determining left and right ventricular morphology and function. Additionally, the time course of several metabolic and inflammatory blood parameters was determined. Results: Rats after sham surgery showed a lower body weight for up to 8 weeks after the intervention compared to healthy controls. Left and right ventricular morphology and function were not different in absolute measures in both groups 1 week after surgery. However, there was a confined difference in several cardiac parameters normalized to the body weight (bw), such as myocardial mass (2.19±0.30/0.83±0.13 vs. 1.85±0.22/0.70±0.07 mg left/right per g bw, p<0.05), or enddiastolic ventricular volume (1.31±0.36/1.21±0.31 vs. 1.14±0.20/1.07±0.17 µl left/right per g bw, p<0.05). Vice versa, after 8 weeks, cardiac masses, volumes, and output showed a trend for lower values in the sham operated rats compared to the controls in absolute measures (782.2±57.2/260.2±33.2 vs. 805.9±84.8/310.4±48.5 mg, p<0.05 for left/right ventricular mass), but not normalized to body weight. Matching these findings, blood testing revealed prolonged metabolic and inflammatory changes after surgery not related to cardiac disease. Conclusion: There is a small distinct impact of cardio-thoracic surgical procedures on the global integrity of the organism, which in the long term also includes circumscribed repercussions on cardiac morphology and function. This impact has to be considered when analyzing data from respective studies and transferring the findings to conditions in patients.

scholarly journals Role of the lysyl oxidase enzyme family in cardiac function and disease

2019 ◽  
Author(s):  
Doa’a Al-u’datt ◽  
Bruce G Allen ◽  
Stanley Nattel
Keyword(s):  
Heart Disease ◽  
Animal Models ◽  
Lysyl Oxidase ◽  
Heart Diseases ◽  
Experimental Studies ◽  
Vital Role ◽  
Cross Linking ◽  
Disease Therapy ◽  
Family Protein ◽  
Oxidase Enzyme

Abstract Heart diseases are a major cause of morbidity and mortality world-wide. Lysyl oxidase (LOX) and related LOX-like (LOXL) isoforms play a vital role in remodelling the extracellular matrix (ECM). The LOX family controls ECM formation by cross-linking collagen and elastin chains. LOX/LOXL proteins are copper-dependent amine oxidases that catalyse the oxidation of lysine, causing cross-linking between the lysine moieties of lysine-rich proteins. Dynamic changes in LOX and LOXL protein-expression occur in a variety of cardiac pathologies; these changes are believed to be central to the associated tissue-fibrosis. An awareness of the potential pathophysiological importance of LOX has led to the evaluation of interventions that target LOX/LOXL proteins for heart-disease therapy. The purposes of this review article are: (i) to summarize the basic biochemistry and enzyme function of LOX and LOXL proteins; (ii) to consider their tissue and species distribution; and (iii) to review the results of experimental studies of the roles of LOX and LOXL proteins in heart disease, addressing involvement in the mechanisms, pathophysiology and therapeutic responses based on observations in patient samples and relevant animal models. Therapeutic targeting of LOX family enzymes has shown promising results in animal models, but small-molecule approaches have been limited by non-specificity and off-target effects. Biological approaches show potential promise but are in their infancy. While there is strong evidence for LOX-family protein participation in heart failure, myocardial infarction, cardiac hypertrophy, dilated cardiomyopathy, atrial fibrillation and hypertension, as well as potential interest as therapeutic targets, the precise involvement of LOX-family proteins in heart disease requires further investigation.

Morphologic analysis of animal models of congenital heart disease

1998 ◽  
Vol 9 (3) ◽  
pp. 139-153 ◽  
Author(s):  
Robert H Anderson ◽  
Sandra Webb ◽  
Nigel A Brown
Keyword(s):  
Congenital Heart Disease ◽  
Heart Disease ◽  
Animal Models ◽  
Congenital Heart ◽  
Morphologic Analysis

scholarly journals Volume load-induced right ventricular dysfunction in animal models: insights in a translational gap in congenital heart disease

2017 ◽  
Vol 20 (4) ◽  
pp. 808-812 ◽  
Author(s):  
Guido P.L. Bossers ◽  
Quint A.J. Hagdorn ◽  
Mark Jan Ploegstra ◽  
Marinus A.J. Borgdorff ◽  
Herman H.W. Silljé ◽  
...  
Keyword(s):  
Congenital Heart Disease ◽  
Heart Disease ◽  
Animal Models ◽  
Right Ventricular ◽  
Congenital Heart ◽  
Ventricular Dysfunction ◽  
Right Ventricular Dysfunction ◽  
Volume Load

scholarly journals The Sydney Heart Bank: improving translational research while eliminating or reducing the use of animal models of human heart disease

2017 ◽  
Vol 9 (4) ◽  
pp. 431-441 ◽  
Author(s):  
C. G. dos Remedios ◽  
S. P. Lal ◽  
A. Li ◽  
J. McNamara ◽  
A. Keogh ◽  
...  
Keyword(s):  
Heart Disease ◽  
Animal Models ◽  
Translational Research ◽  
Human Heart ◽  
Human Heart Disease

scholarly journals Shexiang Baoxin Pills for Coronary Heart Disease in Animal Models: Preclinical Evidence and Promoting Angiogenesis Mechanism

2017 ◽  
Vol 8 ◽  
Author(s):  
Ke-Jian Zhang ◽  
Jia-Zhen Zhu ◽  
Xiao-Yi Bao ◽  
Qun Zheng ◽  
Guo-qing Zheng ◽  
...  
Keyword(s):  
Coronary Heart Disease ◽  
Heart Disease ◽  
Animal Models
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