Mitochondrial adaptations during myocardial hypertrophy induced by abdominal aortic constriction

2014 ◽  
Vol 23 (5) ◽  
pp. 283-288 ◽  
Author(s):  
Zhusong Mei ◽  
Xinxing Wang ◽  
Weili Liu ◽  
Jingbo Gong ◽  
Xiujie Gao ◽  
...  
Keyword(s):  
Myocardial Hypertrophy ◽  
Aortic Constriction ◽  
Abdominal Aortic ◽  
Mitochondrial Adaptations

scholarly journals Cholecystokinin Expression in the Development of Myocardial Hypertrophy

Scanning ◽  
2021 ◽  
Vol 2021 ◽  
pp. 1-10
Author(s):  
Zhongshu Han ◽  
Sheng Bi ◽  
Yongsheng Xu ◽  
Xiaoying Dong ◽  
Lixia Mei ◽  
...  
Keyword(s):  
Myocardial Hypertrophy ◽  
Morphological Changes ◽  
Left Ventricular ◽  
Enzyme Linked Immunosorbent Assay ◽  
Gastrointestinal Hormone ◽  
Sham Operation ◽  
Aortic Constriction ◽  
Sham Operation Group ◽  
Protein Levels ◽  
Abdominal Aortic

Background. Expression of cholecystokinin is found in myocardial tissues as a gastrointestinal hormone and may be involved in cardiovascular regulation. However, it is unclear whether there is an increase in cholecystokinin expression in myocardial hypertrophy progression induced by abdominal aortic constriction. The study is aimed at exploring the relationship between cholecystokinin expression and myocardial hypertrophy. Methods. We randomly divided the 70 Sprague-Dawley rats into two groups: the sham operation group and the abdominal aortic constriction group. The hearts of rats were measured by echocardiography, and myocardial tissues and blood were collected at 4 weeks, 8 weeks, and 12 weeks after surgery. Morphological changes were assessed by microscopy. The cholecystokinin expression was evaluated by immunochemistry, Western blotting, quantitative real-time polymerase chain reaction, and enzyme-linked immunosorbent assay. Results. The relative protein levels of cholecystokinin were significantly increased in the abdominal aortic constriction groups compared with the corresponding sham operation groups at 8 weeks and 12 weeks. The cholecystokinin mRNA in the abdominal aortic constriction groups was significantly higher than the time-matched sham operation groups. Changes in the left ventricular wall thickness were positively correlated with the relative protein levels of cholecystokinin and the mRNA of cholecystokinin. Conclusions. The development of myocardial hypertrophy can affect the cholecystokinin expression of myocardial tissues.

scholarly journals AntimiR-132 Attenuates Myocardial Hypertrophy in an Animal Model of Percutaneous Aortic Constriction

2021 ◽  
Vol 77 (23) ◽  
pp. 2923-2935
Author(s):  
Rabea Hinkel ◽  
Sandor Batkai ◽  
Andrea Bähr ◽  
Tarik Bozoglu ◽  
Sarah Straub ◽  
...  
Keyword(s):  
Animal Model ◽  
Myocardial Hypertrophy ◽  
Aortic Constriction

scholarly journals Chronic Stress Promotes the Progression of Pressure Overload-Induced Cardiac Dysfunction Through Inducing More Apoptosis and Fibrosis

2015 ◽  
pp. 325-334 ◽  
Author(s):  
W. LIU ◽  
X. WANG ◽  
Z. MEI ◽  
J. GONG ◽  
X. GAO ◽  
...  
Keyword(s):  
Chronic Stress ◽  
Cardiac Dysfunction ◽  
Cardiac Fibroblasts ◽  
Pressure Overload ◽  
Chronic Restraint Stress ◽  
Neonatal Rats ◽  
Aortic Constriction ◽  
Collagen Expression ◽  
Abdominal Aortic ◽  
High Level

Stress serves as a risk factor in the etiology of hypertension. The present study was designed to decipher the effect and mechanism of chronic stress on the progression of pressure overload-induced cardiac dysfunction. We used abdominal aortic constriction (AAC) to induce pressure overload with or without chronic restraint stress to establish the animal models. Echocardiographic analysis showed pressure overload-induced cardiac dysfunction was worsened by chronic stress. Compared with the AAC rats, there is a significant increase in cardiac hypertrophy, injury, apoptosis and fibrosis of the AAC + stress rats. Furthermore, we found the secretion of norepinephrine (NE) increased after the AAC operation, while the level of NE was higher in the AAC + stress group. Cardiomyocytes and cardiac fibroblasts isolated from neonatal rats were cultured and separately treated with 1, 10, 100 μM NE. The higher concentration NE induced more cardiomyocytes hypertrophy and apoptosis, cardiac fibroblasts proliferation and collagen expression. These results revealed that high level of NE-induced cardiomyocytes hypertrophy and apoptosis, cardiac fibroblasts proliferation and collagen expression further contributes to the effect of chronic stress on acceleration of pressure overload-induced cardiac dysfunction.

scholarly journals Leonurine Attenuates Pressure-Overload Cardiac Hypertrophy Induced By Abdominal Aortic Constriction In Rats

2021 ◽  
Author(s):  
Ding Xiaoli ◽  
Yuan Qingqing ◽  
Qian Haibing
Keyword(s):  
Angiotensin Ii ◽  
Cardiac Hypertrophy ◽  
Pressure Overload ◽  
Ventricular Myocardium ◽  
Left Ventricular ◽  
Left Ventricular Myocardium ◽  
Ang Ii ◽  
Aortic Constriction ◽  
Qrt Pcr ◽  
Abdominal Aortic

Abstract Background: Myocardial hypertrophy occurs in many cardiovascular diseases. Leonurine (Leo) is commonly used for cardiovascular and cerebrovascular diseases. However, whether it can prevent cardiac hypertrophy is not known. The aim of this study was to investigate the effect and mechanism of Leonurine (Leo) against pressure-overload cardiac hypertrophy induced by abdominal aortic constriction (AAC) in rats. Methods: To answer this question, we prove it in the following way: Cardiac function was evaluated by hemodynamic; the left ventricle enlargement was measured by heart weight index (HWI) and left ventricular mass index (LVWI); myocardial tissue changes and myocardial cell diameter (MD) were determined by Hematoxylin and eosin (HE) staining; theβ-myosin heavy chain(β-MHC)and atrial natriuretic factor (ANF), which are recognized as a marker of cardiac hypertrophy, were determined by Real-time quantitative PCR (qRT-PCR), then another gene phospholipase C (PLC), inositol triphosphate (IP3), which associated with RAS were determined by Western blot(WB). angiotensin II (Ang II), angiotensin II type 1 receptor (AT1R) were determined by ELISA, WB and qRT-PCR methods. Finally, we measured the level of Ca2+ by microplate method and the protooncogene c-fos and c-myc mRNA in left ventricular myocardium by qRT-PCR.Results: Compare with control group, Leonurine can improve systolic dysfunction; inhibit the increase of left cardiac; inhibit myocardial cells were abnormally large and restrain the changes of cardiac histopathology; decrease the expression of β-MHC, ANF, Ang II, AT1R, c-fos and c-myc mRNA and the protein levels of PLC, IP3, AngII and AT1R in left ventricular myocardium, in addition, the content of Ca2+ also decrease. Conclusion: Therefore, Leonurine can inhibit cardiac hypertrophy induced by AAC and its effects may be associated with RAS.

Altered renal dopamine receptors during development of cardiac hypertrophy

1992 ◽  
Vol 262 (5) ◽  
pp. E569-E573
Author(s):  
P. K. Ganguly ◽  
K. Mukherjee ◽  
Y. Chen
Keyword(s):  
Cardiac Hypertrophy ◽  
Dopamine Receptors ◽  
Pressure Overload ◽  
Total Body Weight ◽  
Left Ventricular ◽  
Kidney Cortex ◽  
Sprague Dawley ◽  
Aortic Constriction ◽  
Compensatory Response ◽  
Abdominal Aortic

The characteristics of dopamine receptors were studied in heart and kidney using the radiolabeled receptor assay of [3H]spiperone during the development of cardiac hypertrophy. Male Sprague-Dawley rats (175-200 g) underwent abdominal aortic constriction above the renal arteries and were studied 3, 14, and 28 days thereafter. Sham-operated animals without aortic constriction were used as control. Although the ratio of left ventricular weight to total body weight was significantly increased 14 and 28 days after aortic constriction in animals, [3H]spiperone binding in left ventricular membrane was increased as early as 3 days after aortic constriction. At 14 days, the binding was still elevated and, by 28 days, it returned to control values. In contrast, membranes obtained from kidney cortex showed an elevation of [3H]spiperone binding only at 28 days after aortic constriction; at 3 days the binding values were decreased. A reciprocal correlation was found between the number of dopamine receptors and the activity of Na(+)-K(+)-ATPase at 28 days of aortic constriction; the enzyme activity, as measured by the release of 32Pi from [gamma-32P]ATP, was decreased in kidney cortex. Autoradiographic data also showed an increased number of dopamine receptors in kidney at 28 days after abdominal aortic constriction. These results suggest that the dopamine receptor is increased very early in heart in response to pressure overload as a result of a compensatory response to maintain an optimal left ventricular output. Kidney dopamine receptors are triggered at a later stage possibly to maintain fluid homeostasis secondary to the cardiac hypertrophic process.

Tongsaimai reverses the hypertension and left ventricular remolding caused by abdominal aortic constriction in rats

2020 ◽  
Vol 246 ◽  
pp. 112154 ◽  
Author(s):  
Qinghai Meng ◽  
Yao Guo ◽  
Dini Zhang ◽  
Qichun Zhang ◽  
Yu Li ◽  
...  
Keyword(s):  
Left Ventricular ◽  
Aortic Constriction ◽  
Abdominal Aortic

Effect of a mild exercise program on myocardial function and the development of hypertrophy

1979 ◽  
Vol 46 (2) ◽  
pp. 354-360 ◽  
Author(s):  
A. F. Cutilletta ◽  
K. Edmiston ◽  
R. T. Dowell
Keyword(s):  
Cardiac Index ◽  
Myocardial Function ◽  
Myocardial Hypertrophy ◽  
Exercise Program ◽  
Pressure Overload ◽  
Ascending Aorta ◽  
Sham Operation ◽  
Aortic Constriction ◽  
Sedentary Animal ◽  
Slight Elevation

Cardiac function and the development of myocardial hypertrophy were studied in rats conditioned by an exercise program consisting of 8 wk of running on a treadmill. At the end of the training period a group of exercised and sedentary rats was subjected to hemodynamic evaluation under general anesthesia. Except for a slight elevation in the heart rates of the exercised animals there were no significant differences between the exercised and sedentary rats at rest. Following an increase in afterload or a period of hypoxia, the cardiac index of the exercised animals remained significantly higher than that of the sedentary controls. These differences were related to changes in stroke volume. Another group of exercised and sedentary animals underwent either constriction of the ascending aorta or a sham operation. Sedentary rats developed significant hypertrophy at 3 days but had no hypertrophy at 1 day after aortic constriction. Exercised rats, however, developed significant myocardial hypertrophy by 1 day after pressure overload. These data suggest that the heart from an exercised animal is better able to tolerate increases in afterload and hypoxia and can respond with compensatory myocardial hypertrophy more rapidly than the heart of a sedentary animal.

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