No abstract

Physical inactivity, diabetes, hypertension, dyslipidemia, smoking and obesity were associated with imbalance in oxidative stress, leading to endothelial dysfunction. Such dysfunction is present in both cardiovascular disease (CVD) and erectile dysfunction (ED). ED is the persistent inability to achieve or sustain an erection sufficient for satisfactory sexual performance and is one of the first manifestations of endothelial damage in men with CVD risk factors. The purpose of this article is to review the results of studies involving physical activity, CVD, endothelial dysfunction and ED in order to verify its applicability for improving the health and quality of life of men with such disorders. There is consistent evidence that endothelial damage is intimately linked to ED, and this manifestation seems to be associated with the appearance CVDs. On the other hand, physical activity has been pointed out as an important clinical strategy in the prevention and treatment of CVDs and ED mainly associated with improvement of endothelial function. However, further experimental and clinical prospective investigations are needed to test the role of physical exercises in the modulation of endothelial function and their implications on erectile function and the appearance of CVDs.

BackgroundThe increase in fructose consumption is paralleled by a higher incidence of metabolic syndrome, and consequently, cardiovascular disease mortality. We examined the effects of 8 weeks of low intensity exercise training (LET) on metabolic, hemodynamic, ventricular and vascular morphological changes induced by fructose drinking in male rats.MethodsMale Wistar rats were divided into (n = 8 each) control (C), sedentary fructose (F) and ET fructose (FT) groups. Fructose-drinking rats received D-fructose (100 g/l). FT rats were assigned to a treadmill training protocol at low intensity (30% of maximal running speed) during 1 h/day, 5 days/week for 8 weeks. Measurements of triglyceride concentrations, white adipose tissue (WAT) and glycemia were carried out together with insulin tolerance test to evaluate metabolic profile. Arterial pressure (AP) signals were directly recorded. Baroreflex sensitivity (BS) was evaluated by the tachycardic and bradycardic responses. Right atria, left ventricle (LV) and ascending aorta were prepared to morphoquantitative analysis.ResultsLET reduced WAT (−37.7%), triglyceride levels (−33%), systolic AP (−6%), heart weight/body weight (−20.5%), LV (−36%) and aortic (−76%) collagen fibers, aortic intima-media thickness and circumferential wall tension in FT when compared to F rats. Additionally, FT group presented improve of BS, numerical density of atrial natriuretic peptide granules (+42%) and LV capillaries (+25%), as well as the number of elastic lamellae in aorta compared with F group.ConclusionsOur data suggest that LET, a widely recommended practice, seems to be particularly effective for preventing metabolic, hemodynamic and morphological disorders triggered by MS.

Protein deprivation causes a delay in neuronal maturation but postnatal recovery can almost completely restore the normal morphology of myenteric neurons.

Background: The estrogen deficiency, abnormal lipid profile, weight gain and a sedentary lifestyle are factors associated with the increased prevalence of cardiovascular disease in menopausal women. However, physical exercise practice reduces some of these risk factors. Moreover, it has been shown that exercise has an impact on inflammation, in sympathetic activity and improves endothelial function. Aims: The present study aims to evaluate the effects of moderate aerobic training on biochemical, morphological and physiological parameters in LDL Knockout mice with estrogen deprivation, evaluating the components of the ascending aortic wall. Methods: The animals were randomly divided into six groups (n=5): sedentary control (SC), sedentary control ovariectomized (SCO), trained control ovariectomized (TCO), LDL-Knockout sedentary (KS), LDL-Knockout sedentary ovariectomized (KOS) and LDL-Knockout trained ovariectomized (KOT). The trained groups underwent a protocol of moderate training for 4 weeks on a treadmill with speed and progressive load. After training, blood samples were collected for biochemical assessments and the aorta was removed for dissection and histological morphometry study. In addition, the expression of angiotensin-converting enzyme (ACE) and angiotensin II proteins were examined by immunohistochemistry in all groups of animals. Results: Changes of expressions of ACE and angiotensin II were found when the group was subjected to exercise. The concentrations of cholesterol and triglycerides were lower in the groups of animals with estrogen deprivation and dyslipidemia. In animals that performed exercises we found significant increase (p<0.05) in Vv[lam]; decrease in Vv[col] and CWT, and a tendency for decrease both in TS and IMT when compared to the SC groups. The histological morphometry findings showed consistency in the results of the aorta study when the ovariectomized group underwent the exercise protocol. Conclusion: We conclude that physical training contributed to reducing vessel rigidity and to improvements in vascular compliance, with the increase in volume density of elastic lamellae in the estrogen-deprived groups who had normal cholesterol levels.

Abstract. The myenteric plexus of the proximal colon, midcolon, and distal colon was studied in mice chronically infected with the Y strain of Trypanosoma cruzi by means of histochemical methods for NADH-diaphorase and acetylcholinesterase (AChE) on whole mount preparations. Ganglia of infected mice displayed an irregular distribution, with neurons severely altered in form and were found side by side with slightly degenerated or morphologically normal ones. Significant reductions of at least 36% in the numbers of neurons were recorded in all regions of the colons of infected animals, especially in the distal colon where the neuron number decreased by more than 44%. Measurements of neuron size suggest that the neuronal destruction caused by T. cruzi affected the medium and large neurons. The small neurons apparently were not affected by the infection. The histochemical demonstration of AChE by the direct coloring copper ferrocyanide method showed that in the control animals, most of the neurons of the plexus displayed AChE activity in the cytoplasm although the neurons showed different reaction intensities. The AChE activity was also present, but at a lower intensity, in the myenteric plexus of the colons of infected animals. These results suggest that the T. cruzi infection affects some categories of neurons and implies that some particular enteric neurotransmitter systems could be affected and the potency of their action upon intestinal function consequently reduced.The digestive form of Chagas' disease involves denervation of the myenteric plexus, which influences disturbances of motility and absorption. 1 The extent of the neurolysis will determine the severity of the sequelae and the patient's future degree of clinical adaptation. 2 Studies involving the myenteric plexus of the colon of animals chronically infected with Trypanosoma cruzi have been carried out and have demonstrated a reduction of 34-37% of the neuronal population. 3,4 Okumura 5 found that 65% of the ganglion neurons of the mouse colon may be destroyed in experimentally infected mice. These studies were done in histologic sections made in the plane of the plexus. However, these sections rarely pass through more than a few ganglia simultaneously, while whole mount preparations, in which the muscle layers are stretched on a plane, can display the whole plexus. 6 Furthermore, the use of whole mount preparations presents the myenteric plexus as a monolayer of nerve cells, and it has therefore been possible, in parallel with neuron counts, to make measurements of neuron somata of unsectioned nerve cells. 7 Therefore, in this study, we used laminar preparations of the mouse colon to 1) quantify the loss of myenteric neurons that occurred with T. cruzi infection, 2) see whether any particular size grouping of neurons is affected, and 3) determine the activity of acetylcholinesterase (AChE) in the myenteric plexus of the mouse colon chronically infected with T. cruzi. MATERIALS AND METHODSTwenty male Swiss mice weighing 20-25 g (13-15 weeks old) were ...

AIM:To evaluate the effects of protein deprivation on the myenteric plexus of the esophagus of weanling rats. METHODS:Pregnant female Wistar rats were divided into 2 groups: nourished (N), receiving normal diet, and undernourished (D), receiving a protein-deprived diet, which continued after birth. At twenty-one days of age, 13 esophagi from each group were submitted to light microscopy and morphometrical analysis employing the NADH diaphorase, NADPH diaphorase and acetylcholinesterase techniques. Three other esophagi from each group were evaluated with transmission electron microscopy (TEM). RESULTS:In both the NADH-and the NADPH-reactive mounts, the neurons of the N mounts were more intensely stained, while in the D esophagi only the larger neurons were reactive. Many myenteric neurons of N were intensely reactive for AChE activity but only a few neurons of D exhibited these aspects. Ultrastructural analysis revealed that the granular reticulum of N showed large numbers of ribosomes aligned on the outer surface of its regularly arranged membrane while the ribosomes of D were disposed in clusters. The chromatin was more homogeneously scattered inside the neuron nucleus of N as well as the granular component of the nucleolus was evidently more developed in this group. Statistically significant differences between N and D groups were detected in the total estimated number of neurons stained by the NADPH technique. CONCLUSION:The morphological and quantitative data shows that feeding with protein-deprived diet in 21-d old rats induces a delay in the development of the myenteric neurons of the esophagus.

TANASOV, V. S.; NETO, W. K.; GONÇALVES, L.; MAIFRINO, L. B. M.; DE SOUSA, R. R. & GAMA, E. F. Use of anabolic steroid altered the liver morphology of rats. Int. J. Morphol., 32(3):756-760, 2014. SUMMARY:The aim of this research was to investigate the effect of testosterone propionate administration in the liver of rats. The rats were divided in the following groups: Initial control (SC), Aged control (SE) and Anabolic group (SA). Testosterone propionate was administered three times per week during 16 weeks. Using morphoquantitative techniques, we quantified the volume densities of lobular and non-lobular parenchyma, area and number of nuclei of hepatocytes. The data were analyzed statistically using mean and standard deviation, ANOVA one-way and level of significance about p≤0.05. Our results showed an increase in capillaries, perisinusoidal spaces and biliary ducts in SE group compared to SC. SA group showed a decrease in hepatic cells, non-lobular volume density and hepatocytes nuclei area, but also an increase in capillaries, perisinusoidal spaces, biliary ducts, number of hepatocytes and non-hepatocyte nuclei compared to SC. We conclude that a direct toxicity may have occurred, with consequent loss of the cells.