Correction: Testosterone deficiency reduces the effects of late cardiac remodeling after acute myocardial infarction in rats.

[This corrects the article DOI: 10.1371/journal.pone.0213351.].

Testosterone deficiency reduces the effects of late cardiac remodeling after acute myocardial infarction in rats.

Testosterone is associated with an increased risk of coronary heart disease. This study evaluated cardiac remodeling 60 days after myocardial infarction (MI) in rats with testosterone deficiency. One week after castration, the animals underwent myocardial infarction. Rats were divided into four groups: orchidectomized (OCT); orchidectomized and infarcted (OCT+MI), MI and control (Sham). The myocyte cross-sectional area and the papillary muscle contractility were evaluated 8 weeks after MI. The coronary bed was perfused with Biodur E20 resin to evaluate the neovascularization after MI. Data were expressed as mean ± SEM followed by ANOVA. Castration reduced myocyte hypertrophy when compared to Sham and myocardial infarction alone as well as preserved the contraction force and activation time after myocardial infarction. After beta-adrenergic stimulation, activation and relaxation kinetics were less impaired in the OCT+MI group than in the MI group. Contraction force was preserved in the OCT+MI group after beta-adrenergic stimulation. Multiple scanning electronic microscope images were obtained to characterize changes in the coronary arteries. Capillary density index was increased in the MI and OCT+MI groups compared with control. The MI and OCT+MI groups were characterized by irregular vessel arrangements with distorted shape, abrupt changes in vessel direction, as well as abrupt changes in diameter after bifurcations when compared to Sham and OCT. The results indicated that testosterone deficiency attenuates adverse cardiac remodeling after MI. Novel findings in this study were that testosterone deficiency in rats, induced by castration, changes the later remodeling after MI, when compared with non castrated rats. The absence of this androgenous hormone seems to be benefic against pathological hypertrophy.

Treatment with high dose of atorvastatin reduces vascular injury in diabetic rats.

BACKGROUND: Previous reports showed conflicting results regarding the treatment effects of statin on Diabetes mellitus (DM). We investigated how treatment with high dose of atorvastatin affects the impaired vascular function in diabetic rats. METHODS: Atorvastatin (80mg/kg/day, oral gavage, 4 weeks) or its vehicle was administered to male control or streptozotocin (STZ)-induced diabetic rats. Aortic segments were used to investigate the vascular reactivity, protein expression of cyclooxygenase-2 (COX-2) and nicotinamide adenine dinucleotide phosphate oxidase (NADPH oxidase) 1 (NOX1) and superoxide anions levels. RESULTS: Atorvastatin treatment did not affect glycemia levels. In diabetic rats, the vascular reactivity to phenylephrine increased compared with controls and the atorvastatin treatment reduced this response. Removal of the endothelium increased the response to phenylephrine in control rats, but not in the diabetic group. Atorvastatin increased the endothelial modulation in diabetic rats. L-NAME (100µM) increased the reactivity in all groups, but this effect was greater in atorvastatin-treated diabetic rats. Indomethacin (10µM) and NS398 (1µM) decreased the contractile response in diabetic rats and atorvastatin reversed these effects, without changing COX-2 expression. Apocynin (30µM) decreased the phenylephrine response in diabetic rats, which also showed increased NOX1 and superoxide anions; these effects were prevented by atorvastatin treatment. CONCLUSIONS: The results suggest that treatment with high dose of atorvastatin, independent of glycemia, improves endothelial function in aortas from diabetic rats by reducing the constrictor prostanoids derived from COX-2 and by reducing the oxidative stress by NADPH oxidase, as well as a possible increasing of nitric oxide participation.

Bone mineral density estimated by osteorisk in patients with adolescent idiopathic scoliosis.

OBJECTIVE: The prevalence of osteoporosis in patients with Adolescent Idiopathic Scoliosis (AIS) is believed to be higher than in the general adolescent population. An alternative to radiology for the characterization of bone mineral density may be through correlative indexes like the Osteorisk index, which is easy to access and low in cost, and which helps the doctor in the request for Bone Densitometry. Our belief that osteoporosis can affect the evolution and treatment of AIS was what motivated us to conduct this study. Our objective was to subjectively evaluate bone mineral density by the Osteorisk index in patients with AIS. METHODS: Healthy patients (control group, n=30) and patients with AIS (n = 30) were evaluated, documenting age, weight and height, and establishing the Osteorisk. The unpaired Student t test was performed, with a level of significance of p <0.05. RESULTS: The mean Osteorisk found for the patients with AIS was 6.38 ± 2.2 while in the control group, it was 8.27 ± 2.14, which represents a low risk of developing osteoporosis in both groups. Comparing these means between the groups, a lower Osteorisk was observed in the AIS group. CONCLUSION: Our study showed that there is low risk of developing osteoporosis in patients with AIS. Level of Evidence I, Prospective study.