Pulmonary arterial hypertension (PAH) is a chronic disease which causes overload to the right ventricle. The effect of preventive training on cardiac remodelling in this condition is still unknown. This study aimed to evaluate the influence of preventive training on hypertrophy, heart function and gene expression of calcium transport proteins in rats with monocrotaline-induced PAH. Thirty-two male Wistar rats were randomly divided into four groups: S, sedentary control; T, trained control; SM, sedentary monocrotaline; and TM, trained monocrotaline. The preventive training protocol was performed on a treadmill for 13 weeks, five times/week. The first two weeks were adopted for adaptation to training with gradual increases in speed/time. The speed of the physical training from the third to tenth weeks was gradually increased from 0.9 to 1.1 km/h for 60 min. Next, monocrotaline was applied (60 mg/kg) to induce PAH and lactate threshold analysis performed to determine the training speeds. The training speed of the TM group in the following two weeks was 0.8 km/h for 60 min and the T = 0.9 km/h for 60 min; in the final two weeks, both groups trained at the same speed and duration 0.9 km/h, 60 min. Cardiac function was assessed through echocardiography, ventricular hypertrophy through histomorphometric analysis and gene expression through RT-qPCR. Right cardiac function assessed through the peak flow velocity was SM = 75.5 cm/s vs. TM = 92.0 cm/s (P = 0.001), and ventricular hypertrophy was SM = 106.4 μm² vs. TM = 77.7 μm² (P = 0.004). There was a decrease in the gene expression of ryanodine S = 1.12 au vs. SM = 0.60 au (P = 0.02) without alterations due to training. Thus, we conclude that prior physical training exerts a cardioprotective effect on the right ventricle in the monocrotaline rat model.

BackgroundRight-sided heart failure has high morbidity and mortality, and may be caused by pulmonary arterial hypertension. Fractal dimension is a differentiated and innovative method used in histological evaluations that allows the characterization of irregular and complex structures and the quantification of structural tissue changes.ObjectiveTo assess the use of fractal dimension in cardiomyocytes of rats with monocrotaline-induced pulmonary arterial hypertension, in addition to providing histological and functional analysis.MethodsMale Wistar rats were divided into 2 groups: control (C; n = 8) and monocrotaline-induced pulmonary arterial hypertension (M; n = 8). Five weeks after pulmonary arterial hypertension induction with monocrotaline, echocardiography was performed and the animals were euthanized. The heart was dissected, the ventricles weighed to assess anatomical parameters, and histological slides were prepared and stained with hematoxylin/eosin for fractal dimension analysis, performed using box-counting method. Data normality was tested (Shapiro-Wilk test), and the groups were compared with non-paired Student t test or Mann Whitney test (p < 0.05).ResultsHigher fractal dimension values were observed in group M as compared to group C (1.39 ± 0.05 vs. 1.37 ± 0.04; p < 0.05). Echocardiography showed lower pulmonary artery flow velocity, pulmonary acceleration time and ejection time values in group M, suggesting function worsening in those animals.ConclusionThe changes observed confirm pulmonary-arterial-hypertension-induced cardiac dysfunction, and point to fractal dimension as an effective method to evaluate cardiac morphological changes induced by ventricular dysfunction.

The aim of this study was to determine the effects of gallium arsenide (GaAs) laser on IGF-I, MyoD, MAFbx, and TNF-α gene expression during the intermediate phase of muscle regeneration after cryoinjury 21 Wistar rats were divided into three groups (n = 7 per group): untreated with no injury (control group), cryoinjury without GaAs (injured group), and cryoinjury with GaAs (GaAs-injured group). The cryoinjury was induced in the central region of the tibialis anterior muscle (TA). The region injured was irradiated once a day during 14 days using GaAs laser (904 nm; spot size 0.035 cm, output power 50 mW; energy density 69 J cm; exposure time 4 s per point; final energy 4.8 J). Twenty-four hours after the last application, the right and left TA muscles were collected for histological (collagen content) and molecular (gene expression of IGF-I, MyoD, MAFbx, and TNF-α) analyses, respectively. Data were analyzed using one-way ANOVA at P < 0.05. There were no significant (P > 0.05) differences in collagen density and IGF-I gene expression in all experimental groups. There were similar (P < 0.05) decreases in MAFbx and TNF-α gene expression in the injured and GaAs-injured groups, compared to control group. The MyoD gene expression increased (P = 0.008) in the GaAs-injured group, but not in the injured group (P = 0.338), compared to control group. GaAs laser therapy had a positive effect on MyoD gene expression, but not IGF-I, MAFbx, and TNF-α, during intermediary phases (14 days post-injury) of muscle repair.

Background: Brazil is the worldwide leader in the long-term use of pesticides and herbicides. This compromises the health of handlers by causing harmful neurological, respiratory, and cardiovascular changes. The herbicide 2.4D has been shown to cause cardiac overload with subsequent pathological remodeling. Objective: To analyze the cardiac morphological repercussions on the left ventricle (LV) of mice submitted to nebulization by the herbicide 2.4D. Methods: Fifteen mice were divided into three groups: control group (CG; n = 5) exposed to nebulization with sodium chloride solution; low concentration group (LCG; n = 5) exposed to nebulization of the herbicide 2.4D with 3.71 x 10-3 grams; and high concentration group (HCG; n = 5) exposed to nebulization of the herbicide 2.4D with 9.28 x 10-3 grams for 15 minutes. The fractal dimension analysis was performed through the box-counting method. Later, the ImageJ program was used to calculate the fractal dimension of each group. To evaluate cardiac remodeling, histological slides were prepared and stained with Hematoxylin-Eosin (HE). Fifty areas of cardiomyocytes were analyzed per animal. The comparisons between groups were performed by ANOVA One-Way with Tukey's posttest (p < 0.05). Results: There was no change in fractal dimension values between the CG = 1.37 ± 0.02, LCG = 1.33 ± 0.04 and the HCG = 1.33 ± 0.07 groups. However, cardiac hypertrophy occurred in the HCG = 303.9 ± 38.80 μm 2 when compared to the CG group = 236.9 ± 61.71 μm 2 (p = 0.034). Conclusion: The herbicide 2.4D used for 72 hours did not promote cardiotoxicity when evaluated by fractal dimension. However, cardiomyocyte hypertrophy was observed in the LV.

This study aimed to evaluate the effect of High-Intensity Interval Training (HIIT) on the skeletal muscle of Spontaneously Hypertensive Rats (SHR). Method: In total, 20 male rats, SHR, 12 months old, were used, distributed into 2 groups: Control Group (C) and Training Group (HIIT). The training lasted approximately 50 minutes/day, 5 days/week, for 8 weeks. Systolic blood pressure (BP) was measured at the beginning and end of the study. Analysis: The medial gastrocnemius muscle was used to measure the smallest fiber diameter, after which the Shapiro-Wilk normality test was performed, followed by the Mann Whitney test to compare the medians and interquartile intervals (IQI) of the muscle fibers and Student t-test for performance. For analysis of BP, Analysis of Variance -ANOVA was used, followed by Tukey's post-test. All procedures adopted a significance value of 5% (p < 0.05). Results: The median values for the variable "smallest diameter" of muscle fibers were 29.48 (IQI: 9.96) µm in the C group and 33.45 (IQI: 9.44) µm in the HIIT group (p < 0.05). Also, the performance was increased in the trained animal group and blood pressure values decreased significantly at the end of the experiment (p < 0.05). Conclusion: The HIIT intensity promoted an increase in the median values of the muscle fibers and performance. Finally, a significant decrease was observed in blood pressure variation values.

No abstract

Funding Acknowledgements Type of funding sources: None. Introduction Pulmonary hypertension (PH) is a progressive disease characterized by elevated right ventricular afterload, vascular remodeling, right ventricular hypertrophy and dysfunction, and ultimately heart failure. Physical exercise has been recognized as a treatment for this condition. Although different mechanisms have been proposed to explain PH development, the influence of preventive exercise training interventions onset of pulmonary hypertension in right ventricular hypertrophy is underexplored. Purpose Analyze the effect of preventive training in global gene expression profiling of right ventricular in PH from rats. Methods Twenty-four male Wistar rats (206-220 g) were divided into three four groups (n=8/group): S, sedentary control; SPH, sedentary pulmonary hypertension; and TPH, trained pulmonary hypertension group. The preventive training protocol was performed on a treadmill for 13 weeks, five times/week. Cardiac hypertrophy by PH was experimentally induced by a single intraperitoneal injection (60 mg/kg) of monocrotaline after the protocol training. The S were injected with saline solution. The rats were evaluated 28 days after monocrotaline administration, in the early stage of the PH. Left ventricle weight, right ventricle weight, and atrium weight normalized by body weight were used as indexes of heart hypertrophy. Gene expression profiling was performed using the Rat Gene ST Array platform. To further understand the biological relevance of differential expressed genes, we performed a functional enrichment analysis in the context of the gene ontology (biological process, molecular function, and cellular component) and interaction networks (KEGG, Reactome, Wikipathways and BioPlanet). Results Through the analysis, the HP group had cardiac hypertrophy, and the training mitigated this change p&lt; 0.05. Global gene expression profiling identified 687 differentially expressed genes (S vs. SPH), in the hypertrophy right ventricular during PH, and when compared to preventive training, 91 genes were dysregulated (SPH vs TPH). Gene ontology analysis on expression profiling data revealed alteration on genes that regulate the inflammatory process, muscle growth, metabolic processes, cell death, and ion regulation comparison between SPH vs. TPH The genes that were altered in the hypertrophy phase of PH and modified by the exercise were platelet alpha granule lumen (genes Fgg and Qsox1), NAD + binding (gene Cryl1), positive regulation of cAMP-mediated signaling (gene Cxcl11), positive regulation of macrophage differentiation (Il34 gene), mRNA cleavage (Cstf3 gene), negative regulation of transporter activity (Wwp2 gene), regulation of respiratory system process (Mtg2 gene) p&lt; 0.05. Conclusion Preventive training influences changes in cardiac gene expression profile in the hypertrophy stage of PH. New genes have been identified, and these could be biomarkers and potential therapeutic targets in the early stage of PH.

No abstract