Aerobic training prior to myocardial infarction increases cardiac GLUT4 and partially preserves heart function in spontaneously hypertensive rats

2017 ◽  
Vol 42 (3) ◽  
pp. 334-337 ◽  
Author(s):  
Maximiliano Isoppo Schaun ◽  
Rafael Aguiar Marschner ◽  
Thiago Rodrigues Peres ◽  
Melissa Medeiros Markoski ◽  
Alexandre Machado Lehnen
Keyword(s):  
Myocardial Infarction ◽  
Spontaneously Hypertensive Rats ◽  
Glucose Transporter ◽  
Aerobic Training ◽  
Heart Function ◽  
Glucose Transporter 4 ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Glut4 Expression ◽  
And Training

We assessed cardiac function (echocardiographic) and glucose transporter 4 (GLUT4) expression (Western blot) in response to 10 weeks of aerobic training (treadmill) prior to acute myocardial infarction (AMI) by ligation of the left coronary artery in spontaneously hypertensive rats. Animals were allocated to sedentary+sham, sedentary+AMI, training+sham, and training+AMI. Aerobic training prior to AMI partially preserves heart function. AMI and/or aerobic training increased GLUT4 expression. However, those animals trained prior to AMI showed a greater increase in GLUT4 in cardiomyocytes.

Dexamethasone and Training-Induced Cardiac Remodeling Improve Cardiac Function and Arterial Pressure in Spontaneously Hypertensive Rats

2020 ◽  
pp. 107424842095327
Author(s):  
Francine Duchatsch ◽  
Lidieli P. Tardelli ◽  
Naiara A. Herrera ◽  
Thalles F. R. Ruiz ◽  
Carlos A. Vicentini ◽  
...  
Keyword(s):  
Arterial Pressure ◽  
Cardiac Remodeling ◽  
Spontaneously Hypertensive Rats ◽  
Low Dose ◽  
Collagen Deposition ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Deposition Area ◽  
Systolic And Diastolic Function ◽  
And Training

Introduction: Dexamethasone (DEX)-induced hypertension and cardiac remodeling are still unclear, especially in spontaneously hypertensive rats (SHR). On the other side, exercise training is a good strategy to control hypertension. Therefore, this study investigated the effects of DEX treatment and physical training on arterial pressure and cardiac remodeling in SHR. Material and Methods: SHR underwent treadmill training (5 days/week, 1h/session, at 50-60% of maximal capacity, 0% degree, 75 days) and received low-dose of DEX (50µg/kg, s.c.) during the last 15 days. Sedentary Wistar rats (W) were used as control. Echocardiography and artery catheterization were performed for cardiac remodeling and function, arterial pressure and autonomic nervous system analyses. In addition, left ventricle (LV) capillary density, myocyte diameter and collagen deposition area were analyzed using specific histological staining. Results: Low-dose of DEX treatment did not exacerbate arterial pressure of SHR and trained groups had lower values, regardless of DEX. DEX and training decreased relative left ventricle wall thickness (RWT) and determined LV angiogenesis (+19%) and lower collagen deposition area (−22%). In addition, it determined increased left ventricular diastolic diameter. These changes were followed by improvements on systolic and diastolic function, since it was observed increased posterior wall shortening velocity (PWSV) and reduced isovolumetric relaxation time (IVRT). Conclusion: In conclusion, this study is unique to indicate that low-dose of DEX treatment does not exacerbate arterial pressure in SHR and, when associated with training, it improves LV systolic and diastolic function, which may be due to LV angiogenesis and reduction of wall collagen deposition area.

Ranolazine improves diastolic function in spontaneously hypertensive rats

2014 ◽  
Vol 306 (6) ◽  
pp. H867-H881 ◽  
Author(s):  
Sarah Williams ◽  
Marc Pourrier ◽  
Donald McAfee ◽  
Shunping Lin ◽  
David Fedida
Keyword(s):  
Diastolic Dysfunction ◽  
Diastolic Function ◽  
Spontaneously Hypertensive Rats ◽  
Heart Function ◽  
Sodium Current ◽  
Left Ventricular ◽  
Hypertensive Rats ◽  
Late Sodium Current ◽  
Spontaneously Hypertensive ◽  
Ventricular Relaxation

Diastolic dysfunction can lead to heart failure with preserved ejection fraction, for which there is no effective therapeutic. Ranolazine has been reported to reduce diastolic dysfunction, but the specific mechanisms of action are unclear. The effect of ranolazine on diastolic function was examined in spontaneously hypertensive rats (SHRs), where left ventricular relaxation is impaired and stiffness increased. The objective of this study was to determine whether ranolazine improves diastolic function in SHRs and identify the mechanism(s) by which improvement is achieved. Specifically, to test the hypothesis that ranolazine, by inhibiting late sodium current, reduces Ca2+ overload and promotes ventricular relaxation and reduction in diastolic stiffness, the effects of ranolazine or vehicle on heart function and the response to dobutamine challenge were evaluated in aged male SHRs and Wistar-Kyoto rats by echocardiography and pressure-volume loop analysis. The effects of ranolazine and the more specific sodium channel inhibitor tetrodotoxin were determined on the late sodium current, sarcomere length, and intracellular calcium in isolated cardiomyocytes. Ranolazine reduced the end-diastolic pressure-volume relationship slope and improved diastolic function during dobutamine challenge in the SHR. Ranolazine and tetrodotoxin also enhanced cardiomyocyte relaxation and reduced myoplasmic free Ca2+ during diastole at high-stimulus rates in the SHR. The density of the late sodium current was elevated in SHRs. In conclusion, ranolazine was effective in reducing diastolic dysfunction in the SHR. Its mechanism of action, at least in part, is consistent with inhibition of the increased late sodium current in the SHR leading to reduced Ca2+ overload.

Reduction of Cardiac Norepinephrine Improves Postischemic Heart Function in Stroke-Prone Spontaneously Hypertensive Rats

2001 ◽  
Vol 38 (6) ◽  
pp. 821-832 ◽  
Author(s):  
Hong Chen ◽  
Hideaki Higashino ◽  
Kana Maeda ◽  
Zhiwei Zhang ◽  
Yoshio Ohta ◽  
...  
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Heart Function ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive

scholarly journals Cholinergic Stimulation Improve Renal Inflammation After Myocardial Infarction in Spontaneously Hypertensive Rats

2020 ◽  
Vol 34 (S1) ◽  
pp. 1-1
Author(s):  
Pamela Nithzi Bricher Choque ◽  
Maria Helena Mattos Porter ◽  
Luiz Fernando Pereira ◽  
Humberto Dellè ◽  
Maria Claudia Irigoyen ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Spontaneously Hypertensive Rats ◽  
Cholinergic Stimulation ◽  
Hypertensive Rats ◽  
Renal Inflammation ◽  
Spontaneously Hypertensive

scholarly journals ADENOVIRUS ASSOCIATED THIOREDOXIN ‐1 GENE DELIVERY INDUCES HO‐1 MEDIATED CARDIOPROTECTION IN MYOCARDIAL INFARCTION MODEL OF SPONTANEOUSLY HYPERTENSIVE RATS

2007 ◽  
Vol 21 (6) ◽  
Author(s):  
Samson Mathews Samuel ◽  
Srikanth Koneru ◽  
Suresh Varma Penumathsa ◽  
Lijun Zhan ◽  
Mahesh Thirunavukkarasu ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Gene Delivery ◽  
Spontaneously Hypertensive Rats ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Thioredoxin 1

Abstract 69: Reduction of Diastolic Dysfunction by Treatment of a Combination of Agonists of Adenosine Receptor in Spontaneously Hypertensive Rats Submitted to Myocardial Infarction

2015 ◽  
Vol 117 (suppl_1) ◽  
Author(s):  
Gisele Zapata-Sudo ◽  
Tais N Frazão ◽  
Jaqueline S da Silva ◽  
Eliezer J Barreiro ◽  
Carlos A Fraga ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Blood Pressure ◽  
Spontaneously Hypertensive Rats ◽  
Volume Fraction ◽  
Left Ventricular ◽  
Mean Blood Pressure ◽  
Heart Weight ◽  
Hemodynamic Parameters ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive

Introduction: This work investigated the cardioprotective actions of the combination of a positive inotropic agent (LASSBio-294 ) and a potent vasodilator (LASSBio-897) in spontaneously hypertensive rats (SHR) submitted to myocardial infarction (MI). Methods: Twenty four SHR (180-200 g) were randomly divided in sham-operated (SO) and infarcted groups (MI) and each group subdivided in two: treatment with vehicle (DMSO) or with LASSBio-294 + LASSBio-897 (5mg/kg each, p.o.) during 8 weeks. After treatment period, the animals were submitted to echocardiography to determine the anterior wall thickness (AWT), ejection fraction (EF), fractional shortening (FS) and the ratio of early and late transmitral filling velocity (E/A). In addition, the following hemodynamic parameters were evaluated: mean blood pressure (MBP), left ventricular end diastolic pressure (LVEDP), left ventricular end-systolic pressure (LVESP) and LV contractility and relaxation (dp/dt max ). Hypertrophy was measured using the relation between heart weight to body weight (HW/BW). The volume fraction of collagen (%) was determined by measuring the area of H&E stained tissue within a given field. Results: MI induced in SHR promoted a decrease in AWT; EF; FS and E/A from 2.0 ± 0.4 to 1.6 ± 0.9 mm; from 53.1 ± 7.5 to 25.3 ± 6.4 %; from 40.0 ± 0.9 to 25.3 ± 11.0 %; and from 1.4 ± 0.1 to 0.9 ± 0.1, respectively. Treatment with the combination of drugs, increased AWT to 2.5 ± 0.6 mm; EF to 73.2 ± 1.0 %; FS to 43.5 ± 6.6%; and E/A to 1.3 ± 0.1. Increase of LVEDP from 4.6 ± 0.3 to 30.0 ± 3.6 mmHg and duplicated oxygen consumption were observed in MI-SHR. The negative dP/dt was reduced from 6152 ± 1015 to 3957 ± 1225 mm Hg/s. After treatment, all hemodynamic parameters were restored to values similar to SO group. Mean blood pressure which was increased after MI from 168. 2 ± 18.6 to 197.7 ± 10.7 returned to 137.0 ± 19.3 mm Hg after treatment. Increased deposition of colagen from 15.1 ± 3.9 to 24.0 ± 0.9 % induced by MI was prevented with treatment with the combination of drugs (12.9 ± 3.8 %). Conclusion: Oral administration of the combination of LASSBio-294 and LASSBio-897 could be considered promising in preventing cardiac dysfunction in SHR submitted to MI.

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