Pathogenesis of left ventricular aneurysms: An experimental study in the rat model

1982 ◽  
Vol 50 (1) ◽  
pp. 83-88 ◽  
Author(s):  
Judith S. Hochman ◽  
Bernadine Healy Bulkley
2013 ◽  
Vol 850-851 ◽  
pp. 1255-1258
Author(s):  
Ming San Miao ◽  
Shu Yan Yu ◽  
Shuai Shao

Abstract. Mice model of the endurance and rat model of atmospheric oxygen were prepared in this paper. Study on the effect of Shenqi Pollen Tablet on altitude sickness. Shenqi Pollen Tablet could prolong survival time of mice、significantly reduce weight of rat right ventricular (RV) 、reduce leverage of the weight of right ventricular(RV) and left ventricular increases septum(LV+S),significantly reduce MDA level、NO level and NOS level、increase SOD level, improve hypoxia tolerance of organism.


2020 ◽  
Vol 18 (3) ◽  
pp. 260-265
Author(s):  
Xu Lin ◽  
Zheng Xiaojun ◽  
Lv Heng ◽  
Mo Yipeng ◽  
Tong Hong

The purpose of this study was to evaluate the protective effect of swertiamarin on heart failure. To this end, a rat model of heart failure was established via left coronary artery ligation. Infarct size of heart tissues was determined using triphenyl tetrazolium chloride staining. Echocardiography was performed to evaluate cardiac function by the determination of ejection fraction, left ventricular internal dimension in diastole and left ventricular internal dimension in systole. The effect of swertiamarin on oxidative stress was evaluated via enzyme-linked immunosorbent assay. The mechanism was evaluated using western blot. Administration of swertiamarin reduced the infarct size of heart tissues in rat models with heart failure. Moreover, swertiamarin treatment ameliorated the cardiac function, increased ejection fraction and fractional shortening, decreased left ventricular internal dimension in diastole and left ventricular internal dimension in systole. Swertiamarin improved oxidative stress with reduced malondialdehyde, while increased superoxide dismutase, glutathione, and GSH peroxidase. Furthermore, nuclear-factor erythroid 2-related factor 2, heme oxygenase and NAD(P)H dehydrogenase (quinone 1) were elevated by swertiamarin treatment in heart tissues of rat model with heart failure. Swertiamarin alleviated heart failure through suppression of oxidative stress response via nuclear-factor erythroid 2-related factor 2/heme oxygenase-1 pathway providing a novel therapeutic strategy for heart failure.


2011 ◽  
Vol 10 (1) ◽  
pp. 75 ◽  
Author(s):  
James T Thackeray ◽  
Jerry Radziuk ◽  
Mary-Ellen Harper ◽  
Erik J Suuronen ◽  
Kathryn J Ascah ◽  
...  

2016 ◽  
Vol 28 (3) ◽  
pp. 203-209 ◽  
Author(s):  
Vladimir Grigorjevich Bespalov ◽  
Galina Sergeevna Kireeva ◽  
Olesya Alexandrovna Belyaeva ◽  
Konstantin Yurjevich Senchik ◽  
Alexandr Nikolaevich Stukov ◽  
...  

Microsurgery ◽  
2002 ◽  
Vol 22 (8) ◽  
pp. 347-351 ◽  
Author(s):  
Mohamed M. El-Shazly ◽  
Assem H. Kamel ◽  
Mostafa A. El-Sonbaty ◽  
Mohamed S. Zaki ◽  
Ruediger G. Baumeister
Keyword(s):  

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Zejuan Sheng ◽  
Xiaoyan Qiang ◽  
Guoyu Li ◽  
Huimin Wang ◽  
Wenxin Dong ◽  
...  

Introduction: Phosphodiesterase 9 (PDE9) controls natriuretic-peptide-stimulated cyclic guanosine monophosphate in cardiac myocytes and is stongly upregulated in human heart failure, suggesting its potential as a promising therapeutic target in heart failure. Here we investigated the potential effects of TT-00920, a clinical stage novel and highly selective PDE9 inhibitor, on heart failure in a rat model of myocardial infarction. Methods: Myocardial infarction was induced by left anterior descending coronary artery (LAD) ligation in male Sprague Dawley rats. After 4-week treatment of vehicle, LCZ696, TT-00920, or TT-00920/Valsartan by oral gavage, efficacy was assessed by echocardiography and cardiac histopathology. Results: TT-00920 had remarkably improved cardiac function, protected against cardiac remodeling and fibrosis in a dose-dependent manner. TT-00920/Valsartan combination showed superior beneficial efficacy when compared to TT-00920 or LCZ696 single agent.Figure 1. TT-00920 improved cardiac function and ventricular remodeling.Figure 2. TT-00920 attenuated cardiac fibrosis in peri-infarct zone. Conclusions: TT-00920 reversed LAD-induced left ventricular dysfunction and remodeling, supporting its potential as a novel therapeutic agent for heart failure. The superior efficacy of TT-00920/Valsartan combination suggests that TT-00920 and renin-angiotensin-aldosterone system inhibitors may have additive therapeutic effects in heart failure.TT-00920 is currently being evaluated in Phase 1 clinical study for safety, tolerability, pharmacokinetics and pharmacodynamics in healthy volunteers (NCT04364789).


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