Effects of hypothyroidism and aortic constriction on mitochondria during cardiac hypertrophy

1995 ◽  
Vol 27 (11) ◽  
pp. 1500???1508 ◽  
Author(s):  
MARY L. NISHIO ◽  
OLGA I. ORNATSKY ◽  
DAVID A. HOOD
Keyword(s):  
Cardiac Hypertrophy ◽  
Aortic Constriction

THE EFFECT OF DIFFERENT DEGREES OF SUBDIAPHRAGMATIC AORTIC CONSTRICTION ON HEART WEIGHT AND BLOOD PRESSURE OF NORMAL AND HYPOPHYSECTOMIZED RATS

1955 ◽  
Vol 33 (1) ◽  
pp. 985-994 ◽  
Author(s):  
Margaret Beznák
Keyword(s):  
Blood Pressure ◽  
Cardiac Hypertrophy ◽  
Blood Pressure Response ◽  
Pressure Response ◽  
Heart Weight ◽  
Aortic Constriction ◽  
Hypophysectomized Rats ◽  
Intact Rats

The aortae of groups of normal and hypophysectomized rats were constricted with rings of five different sizes (0.93, 0.83, 0. 74, 0.71, and 0.63 mm. diameter). In normal rats constriction caused an increase in heart weight and blood pressure which was the greater the narrower the constriction. If constriction exceeded 0.74 mm., cardiac hypertrophy reached extremely high values, while the blood pressure was lower than in groups with less constriction. The blood pressure response to Adrenalin or Infundin increased in proportion to the degree of constriction down to 0.74 mm.; greater constriction reduced the response. In hypophysectomized rats no degree of aortic constriction produced hypertension or cardiac hypertrophy, yet the increase in blood pressure after Adrenalin or Infundin was as great as in the normal intact rats.

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.

ANTAGONIZING THE CX3CR1 RECEPTOR MARKEDLY REDUCES DEVELOPMENT OF CARDIAC HYPERTROPHY AFTER TRANSVERSE AORTIC CONSTRICTION IN MICE

2021 ◽  
Vol Publish Ahead of Print ◽  
Author(s):  
Simona Nemska ◽  
Max Gassmann ◽  
Marie-Louise Bang ◽  
Nelly Frossard ◽  
Reza Tavakoli
Keyword(s):  
Cardiac Hypertrophy ◽  
Transverse Aortic Constriction ◽  
Aortic Constriction

Effect of Growth Hormone Preparations on Cardiac Hypertrophy and Blood Pressure of Hypophysectomized Rats

1956 ◽  
Vol 184 (3) ◽  
pp. 563-566 ◽  
Author(s):  
Margaret Beznák
Keyword(s):  
Blood Pressure ◽  
Growth Hormone ◽  
Cardiac Hypertrophy ◽  
Body Growth ◽  
Bovine Growth Hormone ◽  
Aortic Constriction ◽  
Hypophysectomized Rats ◽  
Crystalline Growth

Of three growth hormone preparations only one (PGH 163-208A, Armour) restored cardiac hypertrophy and hypertension on aortic constriction in hypophysectomized rats near to the level seen in normal rats. The same aortic constriction caused no increase in the weight of the heart and no hypertension in untreated hypophysectomized rats and in similar rats treated with a bovine growth hormone preparation (R 285-174, Armour) or crystalline growth hormone (Dr. Li, Berkeley). The different action of the three preparations was not connected with their effect on appetite and on body growth. ACTH, 5 mg/rat/day, caused adrenal hypertrophy in hypophysectomized rats without raising their blood pressure. The weight of the heart and particularly the blood pressure after aortic constriction were, however, greater in hypophysectomized rats treated with ACTH than in their nontreated controls.

scholarly journals LCZ696, an Angiotensin Receptor-Neprilysin Inhibitor, Improves Cardiac Hypertrophy and Fibrosis and Cardiac Lymphatic Remodeling in Transverse Aortic Constriction Model Mice

2020 ◽  
Vol 2020 ◽  
pp. 1-10 ◽  
Author(s):  
Qing Ge ◽  
Li Zhao ◽  
Chen Liu ◽  
Xiaoming Ren ◽  
Yi-hui Yu ◽  
...  
Keyword(s):  
Cardiac Hypertrophy ◽  
Protein Expression ◽  
Lymphatic System ◽  
Lymphatic Vessels ◽  
Mouse Heart ◽  
Transverse Aortic Constriction ◽  
Aortic Constriction ◽  
Expression Levels ◽  
Factor C ◽  
Proinflammatory Factors

Cardiac hypertrophy and ventricular remodeling following heart failure are important causes of high mortality in heart disease patients. The cardiac lymphatic system has been associated with limited research, but it plays an important role in the improvement of myocardial edema and the promotion of fluid balance. LCZ696 is a novel combination of angiotensin and neprilysin inhibitors. Here, we studied the role played by LCZ696 during transverse aortic constriction (TAC) induced cardiac hypertrophy and changes in the lymphatic system. Mice undergoing aortic coarctation were constructed to represent a cardiac hypertrophy model and then divided into random groups that either received treatment with LCZ696 (60 mg/kg/d) or no treatment. Cardiac ultrasonography was used to detect cardiac function, and hematoxylin and eosin (H&E) and Masson staining were used to detect myocardial hypertrophy and fibrosis. The proinflammatory factors interleukin-6 (IL-6), IL-1β, and tumor necrosis factor-α (TNF-α) were detected in the blood and heart tissues of mice. The protein expression levels of lymphatic-specific markers, such as vascular endothelial growth factor C (VEGF-C), VEGF receptor 3 (VEGFR3), and lymphatic vessel endothelial hyaluronan receptor 1 (LYVE-1) were detected in mouse heart tissues. We also examined the colocalization of lymphatic vessels and macrophages by immunofluorescence. The results showed that LCZ696 significantly improved heart dysfunction, cardiac hypertrophy, and fibrosis and inhibited the expression of proinflammatory factors IL-6, IL-1β, and TNF-α in the circulating blood and heart tissues of mice. LCZ696 also decreased the protein expression levels of VEGF-C, VEGFR3, and LYVE-1 in mouse heart tissues, ameliorated the transport load of lymphatic vessels to macrophages, and improved the remodeling of the lymphatic system in the hypertrophic cardiomyopathy model induced by TAC.

CARDIAC PERFORMANCE IN HEART–LUNG PREPARATIONS OF RATS WITH EXPERIMENTAL CARDIAC HYPERTROPHY

1966 ◽  
Vol 44 (1) ◽  
pp. 21-27 ◽  
Author(s):  
B. Korecky ◽  
M. Beznak ◽  
M. Korecka
Keyword(s):  
Cardiac Output ◽  
Left Ventricle ◽  
Arterial Pressure ◽  
Cardiac Hypertrophy ◽  
Cardiac Performance ◽  
Aortic Constriction ◽  
Chronic Anemia ◽  
Stepwise Increase ◽  
Thyroxine Treatment ◽  
Made In

Heart-lung preparations (h.l.p.) were made in normal rats and in rats with cardiac hypertrophy produced by aortic constriction, thyroxine treatment, or chronic anemia. In the h.l.p., arterial pressure was kept constant at 100 mm Hg, and maximum cardiac output (m.c.o.) was measured by stepwise increase in the inflow of blood until no further rise in cardiac output occurred. The m.c.o. of enlarged hearts was above normal, but not if it was expressed per gram of left ventricle weight. This latter value was not above normal in any of the enlarged hearts, contrary to earlier findings in whole animals. In fact, in one group of severely anemic rats it was significantly below normal.

scholarly journals Apocynum Tablet Protects against Cardiac Hypertrophy via Inhibiting AKT and ERK1/2 Phosphorylation after Pressure Overload

2014 ◽  
Vol 2014 ◽  
pp. 1-9
Author(s):  
Jianyong Qi ◽  
Qin Liu ◽  
Kaizheng Gong ◽  
Juan Yu ◽  
Lei Wang ◽  
...  
Keyword(s):  
Chinese Medicine ◽  
Cardiac Hypertrophy ◽  
Protein Expression ◽  
Molecular Mechanisms ◽  
Cardiac Fibrosis ◽  
Pressure Overload ◽  
Study Groups ◽  
Transverse Aortic Constriction ◽  
Aortic Constriction ◽  
Cardioprotective Effects

Background. Cardiac hypertrophy occurs in many cardiovascular diseases. Apocynum tablet (AT), a traditional Chinese medicine, has been widely used in China to treat patients with hypertension. However, the underlying molecular mechanisms of AT on the hypertension-induced cardiac hypertrophy remain elusive. The current study evaluated the effect and mechanisms of AT on cardiac hypertrophy.Methods. We created a mouse model of cardiac hypertrophy by inducing pressure overload with surgery of transverse aortic constriction (TAC) and then explored the effect of AT on the development of cardiac hypertrophy using 46 mice in 4 study groups (combinations of AT and TAC). In addition, we evaluated the signaling pathway of phosphorylation of ERK1/2, AKT, and protein expression of GATA4 in the cardioprotective effects of AT using Western blot.Results. AT inhibited the phosphorylation of Thr202/Tyr204 sites of ERK1/2, Ser473 site of AKT, and protein expression of GATA4 and significantly inhibited cardiac hypertrophy and cardiac fibrosis at 2 weeks after TAC surgery (P<0.05).Conclusions. We experimentally demonstrated that AT inhibits cardiac hypertrophy via suppressing phosphorylation of ERK1/2 and AKT.

scholarly journals Different roles of myocardial ROCK1 and ROCK2 in cardiac dysfunction and postcapillary pulmonary hypertension in mice

2018 ◽  
Vol 115 (30) ◽  
pp. E7129-E7138 ◽  
Author(s):  
Shinichiro Sunamura ◽  
Kimio Satoh ◽  
Ryo Kurosawa ◽  
Tomohiro Ohtsuki ◽  
Nobuhiro Kikuchi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Pulmonary Hypertension ◽  
Cardiac Hypertrophy ◽  
Cardiac Dysfunction ◽  
High Throughput Screening ◽  
Histological Analysis ◽  
Rho Kinase ◽  
Pressure Overload ◽  
Aortic Constriction ◽  
Patients With Heart Failure

Although postcapillary pulmonary hypertension (PH) is an important prognostic factor for patients with heart failure (HF), its pathogenesis remains to be fully elucidated. To elucidate the different roles of Rho-kinase isoforms, ROCK1 and ROCK2, in cardiomyocytes in response to chronic pressure overload, we performed transverse aortic constriction (TAC) in cardiac-specific ROCK1-deficient (cROCK1−/−) and ROCK2-deficient (cROCK2−/−) mice. Cardiomyocyte-specific ROCK1 deficiency promoted pressure-overload-induced cardiac dysfunction and postcapillary PH, whereas cardiomyocyte-specific ROCK2 deficiency showed opposite results. Histological analysis showed that pressure-overload-induced cardiac hypertrophy and fibrosis were enhanced in cROCK1−/− mice compared with controls, whereas cardiac hypertrophy was attenuated in cROCK2−/− mice after TAC. Consistently, the levels of oxidative stress were up-regulated in cROCK1−/− hearts and down-regulated in cROCK2−/− hearts compared with controls after TAC. Furthermore, cyclophilin A (CyPA) and basigin (Bsg), both of which augment oxidative stress, enhanced cardiac dysfunction and postcapillary PH in cROCK1−/− mice, whereas their expressions were significantly lower in cROCK2−/− mice. In clinical studies, plasma levels of CyPA were significantly increased in HF patients and were higher in patients with postcapillary PH compared with those without it. Finally, high-throughput screening demonstrated that celastrol, an antioxidant and antiinflammatory agent, reduced the expressions of CyPA and Bsg in the heart and the lung, ameliorating cardiac dysfunction and postcapillary PH induced by TAC. Thus, by differentially affecting CyPA and Bsg expressions, ROCK1 protects and ROCK2 jeopardizes the heart from pressure-overload HF with postcapillary PH, for which celastrol may be a promising agent.

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