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SUMMARY: The different embryological origins of striated muscle tissue make it an interesting tissue but at the same time difficult to understand, this is how the musculature of the face comes from the first pharyngeal arch, on the other hand. The muscles of the tongue derive from the somites. The muscles of the larynx come from the pharyngeal arches. The muscles of the spine come from the medial or internal myotome of the somite, while the muscles of the limbs and body wall come from the external myotome. The cardiac musculature originates from the lateral splanchnic mesoderm. In this work, the development of myoblasts in human, mouse and chicken fetuses was studied in the facial region, tongue, and spine, limbs, body wall and cardiac muscles using histological histochemical techniques and immunohistochemical technique. The objective of the work is to compare the histogenesis of striated muscle (skeletal, visceral and cardiac), indicating the differences in origin, evolution of the morphological characteristics in each of them and the signaling routes that are involved in its development.

Los distintos origenes embriológicos del tejido muscular estriado lo hace un tejido interesante, pero a la vez difícil de entender, es así como la musculatura de la cara proviene del primer arco faríngeo, en cambio, la musculatura de la lengua deriva de los somitos. La musculatura de la laringe proviene de los arcos faríngeos. La musculatura de la columna vertebral proviene del miotomo medial o interno del somito, en cambio la musculatura de los miembros y pared del cuerpo proviene del miotomo externo. La musculatura cardiaca se origina del mesoderma lateral esplácnico. En este trabajo se estudió el desarrollo de mioblastos en fetos humanos, de ratón y pollo, en la región facial, lengua, columna vertebral, miembros, pared del cuerpo y musculatura cardíaca mediante técnicas histológicas histoquímicas y técnica inmunohistoquímica. El objetivo del trabajo fue comparar la histogénesis del músculo estriado (esquelético, visceral y cardíaco), indicando las diferencias de origen, evolución de las características morfológicas en cada una de ellas y las rutas de señalización que se ven involucradas en el desarrollo del mismo.

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Chronic Non-Communicable Diseases (NCDs) have been considered a global health problem, characterized as diseases of multiple factors, which are developed throughout life, and regardless of genetics as a risk factor of important relevance, the increase in mortality attributed to the disease to environmental factors and the lifestyle one leads. Although the reactive species (ROS/RNS) are necessary for several physiological processes, their overproduction is directly related to the pathogenesis and aggravation of NCDs. In contrast, dietary polyphenols have been widely associated with minimizing oxidative stress and inflammation. In addition to their antioxidant power, polyphenols have also drawn attention for being able to modulate both gene expression and modify epigenetic alterations, suggesting an essential involvement in the prevention and/or development of some pathologies. Therefore, this review briefly explained the mechanisms in the development of some NCDs, followed by a summary of some evidence related to the interaction of polyphenols in oxidative stress, as well as the modulation of epigenetic mechanisms involved in the management of NCDs.

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Thermal ablation is a well-established successful treatment for cardiac arrhythmia, but it still presents limitations that require further studies and developments. In the rotor-driven functional re-entry arrhythmia, tissue heterogeneity results on the generation of spiral/scroll waves and wave break dynamics that may cause dangerous sustainable fibrillation. The selection of the target region to perform thermal ablation to mitigate this type of arrhythmia is challenging, since it considerably affects the local electrophysiology dynamics. This work deals with the numerical simulation of the thermal ablation of a cardiac muscle tissue and its effects on the dynamics of rotor-driven functional re-entry arrhythmia. A non-homogeneous two-dimensional rectangular region is used in the present numerical analysis, where radiofrequency ablation is performed. The electrophysiology problem for the propagation of the action potential in the cardiac tissue is simulated with the Fenton-Karma model. Thermal damage caused to the tissue by the radiofrequency heating is modeled by the Arrhenius equation. The effects of size and position of a heterogeneous region in the original muscle tissue were first analyzed, in order to verify the possible existence of the functional re-entry arrhythmia during the time period considered in the simulations. For each case that exhibited re-entry arrhythmia, six different ablation procedures were analyzed, depending on the position of the radiofrequency electrode and heating time. The obtained results revealed the effects of different model parameters on the existence and possible mitigation of the functional re-entry arrhythmia.

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Cachexia is a multifactorial syndrome that presents with, among other characteristics, progressive loss of muscle mass and anti-cardiac remodeling effect that may lead to heart failure. This condition affects about 80% of patients with advanced cancer and contributes to worsening patients' tolerance to anticancer treatments and to their premature death. Its pathogenesis involves an imbalance in metabolic homeostasis, with increased catabolism and inflammatory cytokines levels, leading to proteolysis and lipolysis, with insufficient food intake. A multimodal approach is indicated for patients with cachexia, with the aim of reducing the speed of muscle wasting and improving their quality of life, which may include nutritional, physical, pharmacologic, and psychological support. This review aims to outline the mechanisms of muscle loss, as well as to evaluate the current clinical evidence of the use of physical exercise in patients with cachexia.

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Histidine-containing dipeptides (HCDs) are abundantly expressed in striated muscles. Although important properties have been ascribed to HCDs, including H+ buffering, regulation of Ca2+ transients and protection against oxidative stress, it remains unknown whether they play relevant functions in vivo. To investigate the in vivo roles of HCDs, we developed the first carnosine synthase knockout (CARNS1-/-) rat strain to investigate the impact of an absence of HCDs on skeletal and cardiac muscle function. Male wild-type (WT) and knockout rats (4 months-old) were used. Skeletal muscle function was assessed by an exercise tolerance test, contractile function in situ and muscle buffering capacity in vitro. Cardiac function was assessed in vivo by echocardiography and cardiac electrical activity by electrocardiography. Cardiomyocyte contractile function was assessed in isolated cardiomyocytes by measuring sarcomere contractility, along with the determination of Ca2+ transient. Markers of oxidative stress, mitochondrial function and expression of proteins were also evaluated in cardiac muscle. Animals were supplemented with carnosine (1.8% in drinking water for 12 weeks) in an attempt to rescue tissue HCDs levels and function. CARNS1-/- resulted in the complete absence of carnosine and anserine, but it did not affect exercise capacity, skeletal muscle force production, fatigability or buffering capacity in vitro, indicating that these are not essential for pH regulation and function in skeletal muscle. In cardiac muscle, however, CARNS1-/- resulted in a significant impairment of contractile function, which was confirmed both in vivo and ex vivo in isolated sarcomeres. Impaired systolic and diastolic dysfunction were accompanied by reduced intracellular Ca2+ peaks and slowed Ca2+ removal, but not by increased markers of oxidative stress or impaired mitochondrial respiration. No relevant increases in muscle carnosine content were observed after carnosine supplementation. Results show that a primary function of HCDs in cardiac muscle is the regulation of Ca2+ handling and excitation-contraction coupling.

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Exhaustive and chronic physical exercise leads to peripheral inflammation, which is one of the molecular mechanisms responsible for the impairment of the insulin signaling pathway in the heart. Recently, 3 different running overtraining models performed downhill (OTR/down), uphill (OTR/up), and without inclination (OTR) increased the serum levels of proinflammatory cytokines. This proinflammatory status induced insulin signaling impairment in the skeletal muscle; however, the response of this signaling pathway in the cardiac muscle of overtrained mice was still unknown. Thus, we investigated the effects of OTR/down, OTR/up, and OTR protocols on the protein levels of phosphorylation of insulin receptor ß (pIRß) (Tyr), phosphorylation of protein kinase B (pAkt) (Ser473), plasma membrane glucose transporter-1 (GLUT1) and GLUT4, phosphorylation of insulin receptor substrate-1 (pIRS-1) (Ser307), phosphorylation of IκB kinase α/ß) (pIKKα/ß (Ser180/181), phosphorylation of p38 mitogen-activated protein kinase (p-p38MAPK) (Thr180/Tyr182), phosphorylation of stress-activated protein kinases-Jun amino-terminal kinases (pSAPK-JNK) (Thr183/Tyr185), and glycogen content in mice hearts. The rodents were divided into naïve (N, sedentary mice), control (CT, sedentary mice submitted to performance evaluations), trained (TR, performed the training protocol), OTR/down, OTR/up, and OTR groups. After the grip force test, the cardiac muscles (ie, left ventricle) were removed and used for immunoblotting and histology. Although the OTR/up and OTR groups exhibited higher cardiac levels of pIRß (Tyr), only the OTR group exhibited higher cardiac levels of pAkt (Ser473) and plasma membrane GLUT4. On the contrary, the OTR/down group exhibited higher cardiac levels of pIRS-1 (Ser307). The OTR model enhanced the cardiac insulin signaling pathway. All overtraining models increased the left ventricle glycogen content, with this probably acting as a compensatory organ in response to skeletal muscle insulin signaling impairment.

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The purpose of the present study was to compare the influence of aerobic exercise (AE) lasting 12 weeks to that of resistance exercise (RE) of the same duration on endoplasmic reticulum (ER) stress and mitochondrial biogenesis in the cardiac muscle of middle-aged obese rats. Obesity was induced in thirty 50-week-old male Sprague Dawley rats over 6 weeks by administration of a high-fat diet. The rats were then subjected to treadmill-running (AE) and ladder-climbing (RE) exercises 3 times per week for 12 weeks. Rats in the AE group showed significantly lower increases in body weight and intraperitoneal fat than those in the sedentary control (SC) group (P<0.05). The 12-week exercise regimes resulted in a significant increase in expression of mitochondrial biogenesis markers and levels of peroxisome proliferator-activated receptor gamma coactivator 1α in the cardiac muscle (P<0.05). Phosphorylation of PKR-like ER kinase, an ER stress marker, decreased significantly (P<0.05) after the exercise training. Although a trend for decreased C/EBP homologous protein (CHOP) expression was observed in both exercise groups, only the AE group had a statistically significant decrease (P<0.05). Levels of GRP78, an ER stress marker that protects cardiac muscle, did not significantly differ among the groups. Although only the AE group decreased body weight and fat mass, the two exercise regimes had similar effects on cardiac muscle with the exception of CHOP. Therefore, we suggest that both AE, which results in weight loss, and high-intensity RE, though not accompanied by weight loss, protect obese cardiac muscle effectively.

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Cardiomyopathy related to the absence of dystrophin is an important feature in Duchenne muscular dystrophy (DMD) and in the mdx mouse. Doxycycline (DOX) could be a potential therapy for mdx skeletal muscles dystrophy. We investigated whether the corticoid deflazacort (DFZ) plus DOX could improve cardiac mdx dystrophy better than DFZ alone, later (17 months) in dystrophy. Mdx mice (8 months old) received DFZ/DOX or DFZ for 9 months. The combined therapy was greater than DFZ in reducing fibrosis (60% decrease with DFZ/DOX and 40% with DFZ alone) in the right ventricle and transforming growth factor ß levels (6.8 ± 3.2 in untreated mdx mice, 2.8 ± 1.4 in combined therapy, and 4.6 ± 1.7 in DFZ; P < .05). Combined therapy more effectively ameliorated cardiac dysfunction (electrocardiogram [ECG]) than DFZ. Improvements were seen in the cardiomyopathy index (0.8 ± 0.1 in combined therapy and 1.0 ± 0.2 in DFZ), heart rate (418 ± 46 bpm in combined therapy and 457 ± 29 bpm in DFZ), QRS interval (11.3 ± 2 in combined therapy and 13.6 ± 1 in DFZ), and Q wave amplitude (-40.7 ± 21 in combined therapy and -90.9 ± 36 in DFZ). Both therapies decreased markers of inflammation (tumor necrosis factor α, nuclear factor κB, and metalloproteinase 9). DFZ/DOX improved mdx cardiomyopathy at this stage of the disease, supporting further clinical investigations.

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This study reports the effects of dietary Salba (chia) seeds on the mechanisms underlying impaired glucose metabolism in the heart of dyslipemic insulin-resistant rats fed a sucrose-rich diet (SRD). Wistar rats were fed a SRD for 3 months. Afterwards, half the animals continued with the SRD; in the other half's diet chia seeds replaced corn oil (CO) for three months (SRD+chia). In the control group, corn starch replaced sucrose. The replacement of CO by chia seeds in the SRD restored the activities of key enzymes involved in heart glucose metabolism decreasing fatty acid oxidation. Chia seeds normalized insulin stimulated GLUT-4 transporter, the abundance of IRS-1 and pAMPK, changed the profile of fatty acid phospholipids, reduced left-ventricle collagen deposition and normalized hypertension and dyslipidemia. New evidence is provided concerning the effects of dietary chia seeds in improving the altered metabolic fate of glucose in the heart of dyslipemic insulin-resistant rats.

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Malaria remains one of the most important infectious diseases in the world, being a significant public health problem associated with poverty and it is one of the main obstacles to the economy of an endemic country. Among the several complications, the effects of malaria seem to target the skeletal muscle system, leading to symptoms, such as muscle aches, muscle contractures, muscle fatigue, muscle pain, and muscle weakness. Malaria cause also parasitic coronary artery occlusion. This article reviews the current knowledge regarding the effect of malaria disease and the anti-malarial drugs on skeletal and cardiac muscles. Research articles and case report publications that addressed aspects that are important for understanding the involvement of malaria parasites and anti-malarial therapies affecting skeletal and cardiac muscles were analysed and their findings summarized. Sequestration of red blood cells, increased levels of serum creatine kinase and reduced muscle content of essential contractile proteins are some of the potential biomarkers of the damage levels of skeletal and cardiac muscles. These biomarkers might be useful for prevention of complications and determining the effectiveness of interventions designed to protect cardiac and skeletal muscles from malaria-induced damage.

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This study explores the mechanisms underlying the altered lipid metabolism in the heart of dyslipemic insulin-resistant (IR) rats fed a sucrose-rich diet (SRD) and investigates if chia seeds (rich in α-linolenic acid 18:3, n-3 ALA) improve/reverse cardiac lipotoxicity. Wistar rats received an SRD-diet for three months. Half of the animals continued with the SRD up to month 6. The other half was fed an SRD in which the fat source, corn oil (CO), was replaced by chia seeds from month 3 to 6 (SRD+chia). A reference group consumed a control diet (CD) all the time. Triglyceride, long-chain acyl CoA (LC ACoA) and diacylglycerol (DAG) contents, pyruvate dehydrogenase complex (PDHc) and muscle-type carnitine palmitoyltransferase 1 (M-CPT1) activities and protein mass levels of M-CPT1, membrane fatty acid transporter (FAT/CD36), peroxisome proliferator activated receptor α (PPARα) and uncoupling protein 2 (UCP2) were analyzed. Results show that: (a) the hearts of SRD-fed rats display lipotoxicity suggesting impaired myocardial lipid utilization; (b) Compared with the SRD group, dietary chia normalizes blood pressure; reverses/improves heart lipotoxicity, glucose oxidation, the increased protein mass level of FAT/CD36, and the impaired insulin stimulated FAT/CD36 translocation to the plasma membrane. The enhanced M-CPT1 activity is markedly reduced without similar changes in protein mass. PPARα slightly decreases, while the UCP2 protein level remains unchanged in all groups. Normalization of dyslipidemia and IR by chia reduces plasma fatty acids (FAs) availability, suggesting that a different milieu prevents the robust translocation of FAT/CD36. This could reduce the influx of FAs, decreasing the elevated M-CPT1 activity and lipid storage and improving glucose oxidation in cardiac muscles of SRD-fed rats.

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The aim of this study was to investigate the activities of important enzymes involved in the phosphoryl transfer network (adenylate kinase and creatine kinase (CK)), lactate dehydrogenase (LDH), respiratory chain complexes and biomarkers of cardiac function in rat experimentally infected by Trypanosoma evansi. Rat heart samples were evaluated at 5 and 15 days post-infection (PI). At 5 day PI, there was an increase in LDH and CK activities, and a decrease in respiratory chain complexes II, IV and succinate dehydrogenase activities. In addition, on day 15 PI, a decrease in the respiratory chain complex IV activity was observed. Biomarkers of cardiac function were higher in infected animals on days 5 and 15 PI. Considering the importance of the energy metabolism for heart function, it is possible that the changes in the enzymatic activities involved in the cardiac phosphotransfer network and the decrease in respiratory chain might be involved partially in the role of biomarkers of cardiac function of T. evansi-infected rats.

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The phylum Myxozoa Grassé, 1970, consists of a heterogenous group of around 50 genera that are worldwide disseminated in a wide variety of aquatic media. In the present study, 43 specimens of Pimelodus ornatus were collected from an adjacent area to the Cachoeira do Arari municipality on Marajó Island, in the Brazilian state of Pará, in 2013. Macroscopic analysis showed the presence of whitened plasmodia located in the cardiac muscle and also in the region between the bulbus arteriosus and atrium cordis. Microscopic analysis on the parasitized tissues revealed spores that were typically piriform, with the anterior portion slightly narrower than the posterior end. The spore valves were symmetrical. The present species is placed in the genus Myxobolus Butschli, 1882, because of the presence of a pair of equal polar capsules in each spore. The prevalence of parasitism observed was 13.9% (6/43). This research note reports the first occurrence of Myxobolus as a parasite of the heart in the teleostean fish P. ornatus in the Amazon region and confirms the occurrence of secondary myocarditis in this fish, caused by parasitism by Myxobolus sp. The rarity of this parasitic species of Myxobolus at this tissue site, associated with other spore morphology characteristics in the fish, suggests that it is an undescribed species.

O filo Myxozoa Grassé, 1970, consiste em um grupo heterogêneo de cerca de 50 gêneros que são disseminados em todo o mundo em uma grande variedade de meios aquáticos. No presente estudo, quarenta e três espécimes de Pimelodus ornatus foram coletados a partir de uma área adjacente à cidade de Cachoeira do Arari, na Ilha do Marajó, no Estado do Pará, em 2013. À análise macroscópica verificou-se a presença de plasmódios esbranquiçados, localizados no músculo cardíaco e também na região entre o bulbus arteriosus e o atrium cordis. A análise microscópica dos tecidos parasitados revelou esporos que eram tipicamente piriformes, com a porção anterior um pouco mais estreita do que a extremidade posterior, sendo suas válvulas simétricas. A prevalência do parasitismo observada foi de 13,9% (6/43). Esta nota de pesquisa relata a primeira ocorrência de Myxobolus como um parasita do coração no peixe teleósteo P. ornatus, na Região Amazônica e, confirma a ocorrência de miocardite secundária causada por esse parasitismo. A raridade da ocorrência de Myxobolus sp. neste tecido, associado a outras características morfológicas dos esporos no peixe, sugere que é uma espécie não descrita.

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The phylum Myxozoa Grassé, 1970, consists of a heterogenous group of around 50 genera that are worldwide disseminated in a wide variety of aquatic media. In the present study, 43 specimens of Pimelodus ornatus were collected from an adjacent area to the Cachoeira do Arari municipality on Marajó Island, in the Brazilian state of Pará, in 2013. Macroscopic analysis showed the presence of whitened plasmodia located in the cardiac muscle and also in the region between the bulbus arteriosus and atrium cordis. Microscopic analysis on the parasitized tissues revealed spores that were typically piriform, with the anterior portion slightly narrower than the posterior end. The spore valves were symmetrical. The present species is placed in the genus Myxobolus Butschli, 1882, because of the presence of a pair of equal polar capsules in each spore. The prevalence of parasitism observed was 13.9% (6/43). This research note reports the first occurrence of Myxobolus as a parasite of the heart in the teleostean fish P. ornatus in the Amazon region and confirms the occurrence of secondary myocarditis in this fish, caused by parasitism by Myxobolus sp. The rarity of this parasitic species of Myxobolus at this tissue site, associated with other spore morphology characteristics in the fish, suggests that it is an undescribed species.

O filo Myxozoa Grassé, 1970, consiste em um grupo heterogêneo de cerca de 50 gêneros que são disseminados em todo o mundo em uma grande variedade de meios aquáticos. No presente estudo, quarenta e três espécimes de Pimelodus ornatus foram coletados a partir de uma área adjacente à cidade de Cachoeira do Arari, na Ilha do Marajó, no Estado do Pará, em 2013. À análise macroscópica verificou-se a presença de plasmódios esbranquiçados, localizados no músculo cardíaco e também na região entre o bulbus arteriosus e o atrium cordis. A análise microscópica dos tecidos parasitados revelou esporos que eram tipicamente piriformes, com a porção anterior um pouco mais estreita do que a extremidade posterior, sendo suas válvulas simétricas. A prevalência do parasitismo observada foi de 13,9% (6/43). Esta nota de pesquisa relata a primeira ocorrência de Myxobolus como um parasita do coração no peixe teleósteo P. ornatus, na Região Amazônica e, confirma a ocorrência de miocardite secundária causada por esse parasitismo. A raridade da ocorrência de Myxobolus sp. neste tecido, associado a outras características morfológicas dos esporos no peixe, sugere que é uma espécie não descrita.

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Clinical and laboratory changes were evaluated in rabbits after intoxication by Amorimia rigida, a plant that causes sudden death. Nine New Zealand male rabbits, averaging 3.54 kg, were categorized into three groups (n = 3) and received, for eight consecutive days, the equivalent of 30 g/kg dry matter of A. rigida water-soluble (SG) and water-insoluble (IG) extracts via nasoesophageal route. The control group received water. There were no alterations in creatine kinase enzyme (CK), CK myocardial fraction (CKMB) or troponine I (cTnI). None of the animals had clinical or electrocardiographic (conventional and Holter) alterations. There were progressive decreases in the left ventricular ejection fraction and systolic fractional shortening. Doppler echocardiography alterations suggested a systolic dysfunction in the SG and IG groups and diastolic dysfunction in IG group. It was concluded that the soluble and insoluble extracts of A. rigida cause deficit of cardiac function.(AU)

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Clinical and laboratory changes were evaluated in rabbits after intoxication by Amorimia rigida, a plant that causes sudden death. Nine New Zealand male rabbits, averaging 3.54 kg, were categorized into three groups (n = 3) and received, for eight consecutive days, the equivalent of 30 g/kg dry matter of A. rigida water-soluble (SG) and water-insoluble (IG) extracts via nasoesophageal route. The control group received water. There were no alterations in creatine kinase enzyme (CK), CK myocardial fraction (CKMB) or troponine I (cTnI). None of the animals had clinical or electrocardiographic (conventional and Holter) alterations. There were progressive decreases in the left ventricular ejection fraction and systolic fractional shortening. Doppler echocardiography alterations suggested a systolic dysfunction in the SG and IG groups and diastolic dysfunction in IG group. It was concluded that the soluble and insoluble extracts of A. rigida cause deficit of cardiac function.

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Os esteroides anabólicos androgênicos (EAAs) são drogas sintetizadas a partir da testosterona. Sua ação anabólica deve-se principalmente ao aumento da síntese e redução na degradação das proteínas musculares. Este trabalho investiga os efeitos do treinamento de natação associado ao tratamento com decanoato de nandrolona sobre a pressão arterial, as dimensões cardíacas e reatividade vascular. Quarenta ratos Wistar machos, com idade de 60 dias, foram divididos em quatro grupos (n = 10): sedentário (SN), sedentário tratado (ST), treinados (TN) e treinados tratados (TT). Animais TN e TT realizaram um treinamento de natação durante 12 semanas, enquanto os animais ST e TT receberam decanoato de nandrolona semanalmente (15mg/kg). O coração e os testículos foram removidos e pesados. O diâmetro da cavidade do ventrículo esquerdo (DcVE) e a espessura da parede ventricular (EspVE) foram medidos com um paquímetro eletrônico. A pressão arterial sistólica (PAS) e a pressão arterial diastólica (PAD) foram medidas semanalmente; ainda, foi estudada a reatividade vascular das artérias mesentéricas em resposta à noradrenalina. Em nosso trabalho não houve alterações no peso do coração; no entanto, verificamos aumento no DcVE (p < 0,05) em ratos TN, enquanto a EspVE aumentou (p < 0,05) nos ratos ST e TT, ambos em relação ao SN. O peso do testículo diminuiu (p < 0,05) em ST e TT em relação a SN. Tanto a pressão arterial quanto a reatividade vascular não foram alteradas. Concluímos que o treinamento de natação aumentou o diâmetro da cavidade ventricular esquerda, enquanto o tratamento com decanoato de nandrolona aumentou a espessura da parede ventricular esquerda, sugerindo uma hipertrofia concêntrica.

Anabolic androgenic steroids (AASs) are drugs synthesized from testosterone. Their anabolic action is mainly due to increased synthesis and reduced degradation of muscle proteins. The purpose of this study was to investigate the effects of swimming training associated to nandrolone decanoate treatment on the blood pressure, the myocardial dimensions, vascular reactivity. Forty Wistar male rats, aged 60 days, were divided into 4 groups (n = 10): sedentary (SN), sedentary treated (ST), trained (TN) and trained treated (TT). TN and TT animals performed a swimming training during 12 weeks and ST and TT animals received weekly nandrolone decanoate (15mg/ kg). The heart and teste were removed and weighted. The left ventricular diameter (LVD) and left ventricular wall thickness (LVWT) had been measured with an electronic pachymeter. Systolic blood pressure (SBP) and diastolic blood pressure (DBP) was weekly measured, while the mesenteric arteries vascular reactivity was studied for its response to noradrenaline. There were no alterations in the heart weight, but the LVD increased (p < 0,05) in TN rats, while the LVWT increased (p < 0,05) in ST and TT rats, both in relation to SN. Testicle weight decreased (p < 0,05) in the ST and TT animals in relation to SN. There was no alteration in blood pressure, neither vascular reactivity. It was concluded that swimming training increased the left ventricular diameter, while nandrolone decanoate treatment increased mainly the left ventricular wall thickness, suggesting concentric hypertrophy.

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Background:  :  :  : Trypanosoma evansi is the etiologic agent of the equine trypanosomosis, a disease related to the detriment of the extensive bovine farming in the Venezuelan grasslands. Even though macroscopic pathologies such as anemia, pale mucosa, icteric tissues, generalized edema, splenomegaly, liver and renal hypertrophy, abortion, anoestrus, emaciation, lymphadenopathies, striated muscle atrophy as well as epicardiac and endocardiac hemorrhages have been describedfor infections with the agent, no reports of any heart ultrastructural change in experimental or natural infections induced by Venezuelan T.evansi isolates are available. This, a transmission electron microscopic approach to the problem was needed. This work describes cell features of the cardiac myocyte and the cardiac microvasculature ultrastructure in mice experimentally infected with an equine local isolate of T. evansi, also providing an account of the infection with the mices survival. Material, Methods & Results: NMRI Mus musculus were inoculated with a Venezuelan T. evansi isolate derived from a naturally infected Equus caballus. From day three post-infection, and every other day until the mices death, one rodent was randomly sacrificed, the heart apex was isosmotically removed and cut in symmetrical blocks, which were fixed, post-fixed, dehydrated, infiltrated, included, sectioned, contrasted

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Background:  :  :  : Trypanosoma evansi is the etiologic agent of the equine trypanosomosis, a disease related to the detriment of the extensive bovine farming in the Venezuelan grasslands. Even though macroscopic pathologies such as anemia, pale mucosa, icteric tissues, generalized edema, splenomegaly, liver and renal hypertrophy, abortion, anoestrus, emaciation, lymphadenopathies, striated muscle atrophy as well as epicardiac and endocardiac hemorrhages have been describedfor infections with the agent, no reports of any heart ultrastructural change in experimental or natural infections induced by Venezuelan T.evansi isolates are available. This, a transmission electron microscopic approach to the problem was needed. This work describes cell features of the cardiac myocyte and the cardiac microvasculature ultrastructure in mice experimentally infected with an equine local isolate of T. evansi, also providing an account of the infection with the mices survival. Material, Methods & Results: NMRI Mus musculus were inoculated with a Venezuelan T. evansi isolate derived from a naturally infected Equus caballus. From day three post-infection, and every other day until the mices death, one rodent was randomly sacrificed, the heart apex was isosmotically removed and cut in symmetrical blocks, which were fixed, post-fixed, dehydrated, infiltrated, included, sectioned, contrasted

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Background: Trypanosoma evansi is the etiologic agent of the equine trypanosomosis, a disease related to the detriment of the extensive bovine farming in the Venezuelan grasslands. Even though macroscopic pathologies such as anemia, pale mucosa, icteric tissues, generalized edema, splenomegaly, liver and renal hypertrophy, abortion, anoestrus, emaciation, lymphadenopathies, striated muscle atrophy as well as epicardiac and endocardiac hemorrhages have been described for infections with the agent, no reports of any heart ultrastructural change in experimental or natural infections induced by Venezuelan T. evansi isolates are available. So, a transmission electron microscopic approach to the problem was needed. This work describes cell features of the cardiac myocyte and the cardiac microvasculature ultrastructure in mice experimentally infected with an equine local isolate of T. evansi, also providing an account of the infection with the mice’s survival. Materials, Methods & Results: NMRI Mus musculus were inoculated with a Venezuelan T. evansi isolate derived from a naturally infected Equus caballus. From day three post-infection, and every other day until the mice’s death, one rodent was randomly killed, the heart apex was isosmotically removed and cut in symmetrical blocks, which were fixed, post-fixed, dehydrated, infiltrated, included, sectioned, contrasted and studied by means of transmission electron microscopy, with the subsequent characterization of the cardiac myocyte and the cardiac microvasculature transformations. The evaluation of the micrographs demonstrated ultrastructural time-increasing harmful mitochondrial alterations that included reduction in the number of mitochondria per cell, decrease in mitochondrial dimensions and lessening of the number of cristae per mitochondrion. Myofibrillar destruction, myofilament loss and atrophy were also evident.(...)

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