scholarly journals Excessive Treadmill Training Produces different Cardiac-related MicroRNA Profiles in the Left and Right Ventricles in Mice

Author(s):  
Jing Yang ◽  
Lin Xu ◽  
Xin Yin ◽  
Yi Li Zheng ◽  
Hai Peng Zhang ◽  
...  

AbstractHigh-volume training followed by inadequate recovery may cause overtraining. This process may undermine the protective effect of regular exercise on the cardiovascular system and may increase the risk of pathological cardiac remodelling. We evaluated whether chronic overtraining changes cardiac-related microRNA profiles in the left and right ventricles. C57BL/6 mice were divided into the control, normal training, and overtrained by running without inclination, uphill running or downhill running groups. After an 8-week treadmill training protocol, the incremental load test and training volume results showed that the model had been successfully established. The qRT-PCR results showed increased cardiac miR-1, miR-133a, miR-133b, miR-206, miR-208b and miR-499 levels in the left ventricle of the downhill running group compared with the left ventricle of the control group. Similarly, compared with the control group, the downhill running induced increased expression of miR-21, miR-17–3p, and miR-29b in the left ventricle. Unlike the changes in the left ventricle, no difference in the expression of the tested miRNAs was observed in the right ventricle. Briefly, our results indicated that overtraining generally affects key miRNAs in the left ventricle (rather than the right ventricle) and that changes in individual miRNAs may cause either adaptive or maladaptive remodelling with overtraining.

2012 ◽  
Vol 22 (3) ◽  
pp. 335-340 ◽  
Author(s):  
Sevim Karaarslan ◽  
Hayrullah Alp ◽  
Tamer Baysal ◽  
Derya Çimen ◽  
Rahmi Örs ◽  
...  

AbstractIntroductionThe aim of this study was to investigate the importance of myocardial performance index as an additive criterion to Sarnat criteria in differential diagnosis of newborn babies with moderate and severe hypoxic–ischaemic encephalopathy.MethodsOur study group included 50 healthy term newborn babies and 20 newborn babies with hypoxic–ischaemic encephalopathy. The 20 newborn babies with hypoxic–ischaemic encephalopathy were scored using Sarnat grades. Left and right ventricular functions were determined on the first day and thereafter in the 1, 3–4, 6–7, and 11–12 months of life by M-Mode and pulsed Doppler.ResultsMyocardial performance indexes of the left ventricle were significantly higher in the severe hypoxic–ischaemic encephalopathy group than in the control group during the first, second, and third analyses (p = 0.01, p = 0.02, p = 0.02, respectively) and only during the first analysis (p = 0.01) in the moderate hypoxic–ischaemic encephalopathy group. In addition, the myocardial performance indexes of the right ventricle were significantly higher during the first, second, and third analyses in both severe and moderate hypoxic–ischaemic encephalopathy groups than in the control group (p = 0.01, all). Hypoxia-induced alterations last longer in the right ventricle than in the left ventricle in the moderate group, as during the second and third analyses myocardial performance index continues to be higher than the control group.ConclusionMyocardial performance indexes for the left and right ventricles were significantly higher in both severe and moderate hypoxic–ischaemic encephalopathy groups than in the control group during the first analysis, and myocardial performance index greater than or equal to 0.5 can be used in order to distinguish moderate and severe hypoxic–ischaemic encephalopathy babies according to Sarnat grades as a discriminative additive criterion.


2006 ◽  
Vol 397 (3) ◽  
pp. 427-436 ◽  
Author(s):  
Neslihan Toyran ◽  
Peter Lasch ◽  
Dieter Naumann ◽  
Belma Turan ◽  
Feride Severcan

Diabetes mellitus is associated with a high incidence and poor prognosis of cardiovascular disease. The aim of the present study was to examine the effect of relatively short-term (5 weeks) Type I diabetes on the left ventricle, the right ventricle and the vessel (vein) on the left ventricle of the myocardium at molecular level by FTIR (Fourier-transform infrared) microspectroscopy. The rats were categorized into two groups: control group (for the left ventricle myocardium, n=8; for the right ventricle myocardium, n=9; for the vein, n=9) and streptozotocin-induced diabetic group (for the left ventricle myocardium, n=7; for the right ventricle myocardium, n=9; for the vein, n=8). Two adjacent cross-sections of 9 μm thickness were taken from the ventricles of the hearts in two groups of rats by using a cryotome. The first sections were used for FTIR microspectroscopy measurements. The second serial sections were stained by haematoxylin/eosin for comparative purposes. Diabetes caused an increase in the content of lipids, an alteration in protein profile with a decrease in α-helix and an increase in β-sheet structure as well as an increase in glycogen and glycolipid contents in both ventricles and the vein. Additionally, the collagen content was found to be increased in the vein of the diabetic group. The present study demonstrated that diabetes-induced alterations in the rat heart can be detected by correlating the IR spectral changes with biochemical profiles in detail. The present study for the first time demonstrated the diabetes-induced alterations at molecular level in both ventricle myocardia and the veins in relatively short-term diabetes.


2020 ◽  
Vol 21 (Supplement_1) ◽  
Author(s):  
N M Popa-Fotea ◽  
M M Micheu ◽  
M Dorobantu

Abstract Funding Acknowledgements CREDO Project - ID: 49182, financed through the SOP IEC -A2-0.2.2.1-2013-1 cofinanced by the ERDF Introduction One important cause of sudden cardiac death in hypertrophic cardiomyopathy (HCM) are ventricular arrhythmias. In patients with HCM, non-sustained ventricular arrhythmias were analysed in relation with 2D speckle tracking mechanical dispersion of left ventricle (LVMD), but not in relation with mechanical dispersion of the right ventricle. Purpose To investigate the possible associations between mechanical dispersion and other echocardiographic parameters and the development of non-sustained ventricular tachycardias (NSVT) in HCM patients. Methods Clinical, 24 hours ECG-Holter, 2D and 3D echocardiography data were registered in HCM patients and in a healthy control group (with normal echocardiography). The 24 hours ECG-Holter was used for detecting NSVT. LVMD was calculated as the standard deviation of time to peak negative strain in the sixteenth segments of the left ventricle. The right ventricle mechanical dispersion (RVMD) was calculated on a three free wall segments model (FWMD), but also in six segments (three RV free wall segments plus three septal segments). Right and left ventricle function was evaluated by conventional echography and 2D speckle tracking imaging. Results Fifty-two patients with HCM and thirty-six age and sex matched subjects were included in the study. In HCM group, 6 patients (11,5%) associated biventricular hypertrophy, while 15 (28.8%) had NSVT on ECG monitoring (group HCM1). HCM1 patients had a much higher LVMD (77.38 ± 11.19 ms) compared with HCM patients without NSVT (group HCM2) (55.8 ± 23.85 ms, p = 0.001, CI:-33.9,-9.3) or compared with controls (43.07 ± 14.19 ms, p <0.001, CI: -44.68, -25.99). The 6 segments RVMD (60.23 ± 10.2 ms) was significantly higher in the CMH1 group compared with CMH2 (45.22 ± 9.8 ms, p = 0.01, CI: -32.1, -28.1) or with the control group (22 ±14 ms, p < 0.001,CI: -36.28, -30.12) independently of the existence of RV hypertrophy. Also, FWMD (55.2 ± 4.8 ms) was significantly higher in CMH1 group in comparation with CMH2 (42.3 ± 5.6 ms, p = 0.02, CI: -27.1, -8.2) or controls (32.1 ± 2.2 ms, p = 0.006, CI: -28.1, -12.1). The presence of NSVT correlated with global longitudinal strain (GS) 2C (-0.442, p = 0.009), GS LAX (r=-0.373, p = 0.03), GS mean value (r=-0.345, p = 0.046), LVMD (r = 0.462, p = 0.006), FWMD (r = 0.51, p = 0.004), 6 segments RVMD (r = 0.46, p = 0.05), 2D and 3D left atrial volume (r = 0.446, p = 0.008 and respectively, r = 0.512, p = 0.002). In a logistic regression, the only parameters associated with NSVT were LVMD (OR = 1.046, p = 0.05), FWMD (OR = 1.03, p = 0.05) and 6 segments MD (OR = 1.1, p = 0.04). Conclusions Increased mechanical dispersion of the left, but also right ventricle is associated with the risk of non-sustained ventricular tachycardias in HCM patients.


2004 ◽  
Vol 96 (6) ◽  
pp. 2265-2272 ◽  
Author(s):  
Tannis A. Johnson ◽  
Alrich L. Gray ◽  
Jean-Marie Lauenstein ◽  
Stephen S. Newton ◽  
V. John Massari

The locations, projections, and functions of the intracardiac ganglia are incompletely understood. Immunocytochemical labeling with the general neuronal marker protein gene product 9.5 (PGP 9.5) was used to determine the distribution of intracardiac neurons throughout the cat atria and ventricles. Fluorescence microscopy was used to determine the number of neurons within these ganglia. There are eight regions of the cat heart that contain intracardiac ganglia. The numbers of neurons found within these intracardiac ganglia vary dramatically. The total number of neurons found in the heart (6,274 ± 1,061) is almost evenly divided between the atria and the ventricles. The largest ganglion is found in the interventricular septum (IVS). Retrogradely labeled fluorescent tracer studies indicated that the vagal intracardiac innervation of the anterior surface of the right ventricle originates predominantly in the IVS ganglion. A cranioventricular (CV) ganglion was retrogradely labeled from the anterior surface of the left ventricle but not from the anterior surface of the right ventricle. These new neuroanatomic data support the prior physiological hypothesis that the CV ganglion in the cat exerts a negative inotropic effect on the left ventricle. A total of three separate intracardiac ganglia innervate the left ventricle, i.e., the CV, IVS, and a second left ventricular (LV2) ganglion. However, the IVS ganglion provides the major source of innervation to both the left and right ventricles. This dual innervation pattern may help to coordinate or segregate vagal effects on left and right ventricular performance.


1981 ◽  
Vol 240 (6) ◽  
pp. H896-H900
Author(s):  
W. P. Santamore ◽  
R. Carey ◽  
D. Goodrich ◽  
A. A. Bove

To better understand biventricular mechanics, an algorithm was developed to simultaneously calculate right and left ventricular volumes from randomly placed subendocardial radiopaque markers. Mathematically, the ventricle is represented as a stack of circular discs. The radius R of each disc is calculated as the distance from the subendocardial radiopaque marker to a computer generated base-to-apex line, and the height H of each disc is determined by the projected distance between radiopaque markers along the base-to-apex line. Accordingly, the volume (V) is calculated as V = pi . sigma Hi . Ri2. The validity of this algorithm was tested on 10 canine left ventricular casts, on 10 human right ventricular casts, and in five experiments. For the left ventricle, the regression line between the casts (VT) and calculated (VC) volumes was VC = 0.55 VT + 6.6, with r = 0.95, standard error of estimate (Sy) = 1.9 ml, and the standard deviation of percent error = 12.6%. For the right ventricle, VC = 1.75 VT = 42.5, with r = 0.86, Sy = 16.2 ml, and the standard deviation of percent error = 24.8%. In five animal experiments, radiopaque markers were implanted into the endocardium of the left and right ventricles and comparisons were made between angiographic- and marker-determined ventricular volumes. For the five experiments, the mean correlation coefficient, relating the marker volumes to the angiographic volumes, were 0.92 +/- 0.01 for the left ventricle and 0.89 +/- 0.02 for the right ventricle. The results, which are similar to other volume-determination methods, indicate that this method can be applied to determine right and left ventricular volume. Once implanted, fluoroscopy of these markers provides a noninvasive means of calculating ventricular volume.


1997 ◽  
Vol 272 (2) ◽  
pp. H884-H893 ◽  
Author(s):  
R. Sethi ◽  
K. S. Dhalla ◽  
R. E. Beamish ◽  
N. S. Dhalla

The status of beta-adrenergic receptors and adenylyl cyclase in crude membranes from both left and right ventricles was examined when the left coronary artery in rats was occluded for 4, 8, and 16 wk. The adenylyl cyclase activity in the presence of isoproterenol was decreased in the uninfarcted (viable) left ventricle and increased in the right ventricle subsequent to myocardial infarction. The density of beta1-adrenergic receptors, unlike beta2-receptors, was reduced in the left ventricle, whereas no change in the characteristics of beta1- and beta2-adrenergic receptors was seen in the right ventricle. The catalytic activity of adenylyl cyclase was depressed in the viable left ventricle but was unchanged in the right ventricle. In comparison to sham controls, the basal, as well as NaF-, forskolin-, and 5'-guanylyl imidodiphosphate [Gpp(NH)p]-stimulated adenylyl cyclase activities were decreased in the left ventricle and increased in the right ventricle of the experimental animals. Opposite alterations in the adenylyl cyclase activities in left and right ventricles from infarcted animals were also seen when two types of purified sarcolemmal preparations were employed. These changes in adenylyl cyclase activities in the left and right ventricles were dependent on the degree of heart failure. Furthermore, adenosine 3',5'-cyclic monophosphate contents were higher in the right ventricle and lower in the left ventricle from infarcted animals injected with saline, isoproterenol, or forskolin in comparison to the controls. The results suggest differential changes in the viable left and right ventricles with respect to adenylyl cyclase activities during the development of congestive heart failure due to myocardial infarction.


1985 ◽  
Vol 248 (6) ◽  
pp. H883-H889 ◽  
Author(s):  
P. Anversa ◽  
A. V. Loud ◽  
V. Levicky ◽  
G. Guideri

Three days after myocardial infarction involving 57% of the left ventricle in rats, the viable tissue of the left ventricle expanded 29%, whereas myocardial hypertrophy in the right ventricle was 19%. To determine whether tissue oxygenation in the hypertrophied ventricles was supported by a proportional growth of the capillary network, morphometric analysis was used to measure capillary luminal volume and surface densities and the diffusion distance for O2. The volume fraction of capillary lumen and the luminal surface of capillaries, related to O2 availability and diffusion, were altered by -21 and -19%, respectively, in the left ventricle and by -23 and -20%, respectively, in the right ventricle. The path length for O2 transport was found to be increased by 12 and 15% in the left and right ventricle, respectively. In contrast, myocyte mass expanded in proportion to tissue growth in the left ventricle and exceeded tissue growth by 5% in the right ventricle. Myocyte mitochondria and myofibrils both grew in proportion to the cells, so that their volume ratio was not changed in either ventricle. The relatively inadequate adaptation of the capillary vasculature suggests that hypertrophy after severe myocardial infarction may initially leave the heart more vulnerable to additional ischemic episodes.


2017 ◽  
Vol 7 (4) ◽  
pp. 240-247
Author(s):  
O. V. Filatova ◽  
E. Ivanova ◽  
V. Chursina

We conducted a retrospective study of EchoCG from 33 males who had the myocardial infarction. Patients with a diagnosis of "neurocirculatory dystonia" (30 people) entered the control group. We studied the size of the left ventricle, the left atrium, the right ventricle, their relationship to each other, the mass of the myocardium and the mass index of the myocardium of the left ventricle. The study of the morphological structures of the heart revealed a change in the size of the left ventricle, the left atrium and the right ventricle in patients who had an acute myocardial infarction, manifested by an increase in the end-diastolic and end-systolic dimensions of the left ventricle, the left atrium, and the right ventricle. In 2/3 of the patients who had an acute myocardial infarction, the normal geometry of the left ventricle was observed. Around one-quarter of the patients had a concentric remodeling (24%), an eccentric hypertrophy of the left ventricle was the least common (15%). The heart of patients who had an acute myocardial infarction demonstrates a lower functionality being compared to the subjects in the control group. In these groups, the maximum value of the DAC / DDR ratio is observed, the ejection fraction is reduced. To a greater extent, the onset of acute myocardial infarction was determined by the size and mass of the left ventricular myocardium. Important meaning had also the body weight, BMI, surface area of the body, the size of the left atrium, and the right ventricle.


2019 ◽  
Vol 8 (4) ◽  
Author(s):  
Еlena N. Sazonova ◽  
Natalia A. Cimbalist ◽  
Olga V. Kaplieva ◽  
Olga A. Lebed’ko

Objective ― Our study aimed to evaluate the possibility of correcting cardiac consequences of intrauterine hypoxia (IUH) by injecting leu-enkephalin analog, lacking affinity for opiate receptors, in the early postnatal period. Material and Methods ― To model IUH, we placed pregnant Wistar rats in a hypobaric chamber with an oxygen partial pressure of 52 mmHg. The procedure was repeated for 4 h daily over the 15th-19th days of gestation. From the 2nd through the 6th days of their lives, the offspring were injected intraperitoneally with non-opiate leu-enkephalin analog at a dose of 100 μg/kg (NALE: Phe-D-Ala-Gly-Phe-Leu-Arg). This analog did not have affinity for opiate receptors. The 7- and 60-day old offspring of female rats subjected to IUH were investigated. The control group included the descendants of intact animals. We investigated gravimetric indicators, DNA-synthetic activity of cardiomyocytes (CMC) by tritium-labeled thymidine autoradiography method, the size of the CMC nuclei, as well as size and amount of nucleoli in the CMC nuclei. The activity of free radical oxidation was evaluated in cardiac homogenates by chemiluminescence. Results ― In 7-day old rats subjected to IUH vs. control animals, we observed decreases in body mass by 32.6%, in heart mass by 27.3%; in the proportion of 3Н-thymidine labeled CMC nuclei by 32.7% in the left ventricle and by 30.4% in the right ventricle; in the number of nucleoli in the CMC nuclei (in the left ventricle: control – 2.384±0.027, IUH – 2.282±0.027*, p<0.05; in the right ventricle: control – 2.409±0.038; IUH – 2.240±0.012*, p<0, 05). Increase in CML indices of cardiac homogenates was revealed, indicating the activation of free radical oxidation. In 7-day old rats subjected to IUH and administration of the NALE peptide from the 2nd through the 6th days of their lives, the proportion of 3H-thymidine labeled nuclei in the CMC did not differ from the control (in the left ventricle: control – 12.79±0.89%, IUH + NALE – 10.98±0.95%, p>0.05; in the right ventricle: control – 11.61±0.78%; IUH + NALE – 11.26±0.58%, p>0.05). The number of nucleoli in the CMC nuclei of the left and right ventricles in the heart of 7-day old animals in the IUH + NALE group did not differ from the control too. The CML indices of heart homogenates in the IUH + NALE group were significantly lower than those in the IUH group. In 60-day old male rats exposed to IUH, there was a decrease in heart mass by 18.5%, sizes of CMC nuclei by 7.5% and 16.1% in the left and right ventricles, respectively, and in the total nucleoli area in the CMC nuclei of the left ventricle (control – 3.953±0.085; IUH – 3.372±0.078*; p<0.05). In 60-day old male rats subjected to IUH and injections of the NALE peptide from the 2nd to the 6th days of their lives, heart mass (control – 692.73±26.81 mg; IUH + NALE – 631.0±29.79 mg; p>0.05) and the size of the CMC nuclei of the right ventricle (control – 54.25±0.84; IUH + NALE – 55.24±0.94; p>0.05) did not differ significantly from the control. The size of the nuclei, the number and size of the nucleoli in the CMC of the left ventricle, as well as the area of the nucleoli in the CMC of the right ventricle in 60-day old male rats of the IUH + NALE group significantly exceeded control group values. Conclusion ― Administration of the NALE peptide to albino rats subjected to IUH normalized DNA-synthetic activity and the number of nucleoli in the nuclei of CMC in 7-day old animals, and also reduced the severity of oxidative stress in the heart tissue. In 60-day old albino male rats exposed to IUH, injecting NALE from the 2nd to the 6th days of their lives eliminated declines in heart mass and sizes of the CMC nuclei and nucleoli, and also led to an increase in the values of the nucleus-and-nucleolus complex indices compared with the control.


1992 ◽  
Vol 262 (3) ◽  
pp. H868-H874 ◽  
Author(s):  
N. Afzal ◽  
N. S. Dhalla

To examine the status of sarcoplasmic reticulum (SR) with respect to Ca2+ transport in congestive heart failure due to myocardial infarction, the left coronary artery in rats was ligated for 4, 8, and 16 wk. The left heart function was assessed with an intraventricular pressure transducer, and SR membrane fractions from the right ventricle and the viable left ventricle were isolated for measuring the ATP-dependent Ca2+ uptake activities. In comparison to sham-operated controls, SR Ca2+ uptake activity was decreased in viable left ventricle of the experimental animals at 4, 8, and 16 wk. On the other hand, SR Ca2+ uptake activity in the right ventricle was increased at 4 and 8 wk, but no change was apparent at 16 wk of coronary occlusion. The decrease in SR Ca2+ uptake in left ventricle and increase in right ventricle were associated with corresponding changes in maximal velocity values without any alterations in the affinity for Ca2+. These opposite changes in the right and left ventricles were dependent on the scar size as well as time after inducing the myocardial infarction. The SR Ca(2+)-stimulated adenosinetriphosphatase activity was decreased in left ventricle and increased in the right ventricle from 4 wk experimental animals. The results suggest differential remodeling of the SR membranes with respect to Ca(2+)-pump mechanisms in left and right ventricles during the development of congestive heart failure.


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