991 resultados para HYPERTENSIVE ENCEPHALOPATHY
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OBJETIVO: Avaliar as prevalências de excesso de peso (EP), hipertensão arterial (HA) e fatores associados em trabalhadores de empresas beneficiadas pelo Programa de Alimentação do Trabalhador (PAT) da cidade de São Paulo. MÉTODOS: Estudo transversal com 1.339 trabalhadores de 30 empresas. A coleta de dados envolveu a aplicação de um questionário com dados de caracterização dos trabalhadores e peso e altura auto-referidos. Foi realizada a aferição da pressão arterial e o estado nutricional foi classificado segundo o Índice de Massa Corporal (IMC). Odds ratios foram estimadas na avaliação dos fatores de risco associados a HA e EP. RESULTADOS: Os trabalhadores apresentaram, em média, 36,4 anos (dp = 10,3) e 9,9 anos de estudo (dp = 2,3), sendo 60% da amostra pertencente ao sexo masculino. Na comparação com homens, mulheres apresentaram valores significativamente menores de idade, pressão arterial sistólica (PAS) e diastólica (PAD) e IMC e maior escolaridade. As prevalências em homens de EP (25 kg/m2) (56%) e de HA (PAS > 140 mmHg e/ou PAD > 90 mmHg ou uso de medicações anti-hipertensivas) (38%), foram aproximadamente o dobro da registrada em mulheres (30% e 19%), respectivamente. Idade foi fator de risco para a ocorrência de EP e HA em ambos os sexos, enquanto que a escolaridade foi fator de proteção para EP e HA em mulheres e fator de risco para o desenvolvimento de EP em homens. CONCLUSÃO: Os trabalhadores do sexo masculino constituíram uma população de maior risco para ocorrência de HA e EP e devem ser priorizados nos programas que visam a prevenção dessas doenças. Neste sentido, o PAT pode representar um lugar de destaque nas ações de saúde e nutrição no ambiente de trabalho.
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FUNDAMENTO: Em razão das controvérsias existentes na literatura quanto aos possíveis benefícios do treinamento resistido (TR) sobre a pressão arterial de repouso (PA) e por causa da escassez de estudos com indivíduos idosos e hipertensos, o TR é pouco recomendado como forma de tratamento não-farmacológico da hipertensão arterial. OBJETIVO: Verificar os efeitos do TR progressivo sobre a pressão arterial de repouso (PA), a freqüência cardíaca (FC) e o duplo produto (DP) em idosas hipertensas controladas. MÉTODOS: Vinte mulheres idosas (66,8 ± 5,6 anos de idade) sedentárias, controladas com medicação anti-hipertensiva, realizaram 12 semanas de TR, compondo o grupo do treinamento resistido (GTR). Vinte e seis idosas (65,3 ± 3,4 anos de idade) hipertensas controladas não realizaram exercícios físicos durante a pesquisa, constituindo o grupo-controle. RESULTADOS: Houve redução significativa nos valores de repouso da pressão arterial sistólica (PAS), da pressão arterial média (PAM) e do DP após o TR. Não foram encontradas reduções significativas na pressão arterial diastólica (PAD) e na FC de repouso após o TR em ambos os grupos. A magnitude da queda no GTR foi de 10,5 mmHg, 6,2 mmHg e 2.218,6 mmHg x bpm para a PAS, PAM e o DP, respectivamente. CONCLUSÃO: O TR progressivo reduziu a PAS, PAM e o DP de repouso de idosas hipertensas, controladas com medicação anti-hipertensiva.
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A Meningoencefalite Necrotizante (MEN) é uma encefalopatia causada por uma disfunção inflamatória de característica necrotizante. O objetivo deste relato é descrever os aspectos clínicos e anatomopatológicos da Meningoencefalite Necrotizante (MEN) em um cão Maltês. A doença tem um caráter necrótico único e está relacionada intimamente à Encefalite do Cão Pug (ECP) devido a suas semelhanças, bem como à Leucoencefalite Necrotizante (LEN). Embora o primeiro relato de caso de ECP tenha mais de 15 anos e o primeiro relato de caso de MEN em Maltês tenha 11 anos, há muito a ser revelado sobre a etiologia e os mecanismos imunopatológicos da doença. Neste trabalho, relata-se o caso de um cão Maltês com sinais que foram compatíveis com a MEN. Foram detectadas nas imagens macroscópicas, cavitação cerebral, e na microscopia, perda de células do parênquima em certas regiões do córtex cerebral. A partir dessas descobertas descreve-se o primeiro caso de MEN em cão Maltês no Brasil.
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The systemic aspect of vascular damage induced by angiotensin II (ANG II) has been poorly explored in the literature. Considering the presence of ANG II and its specific receptor AT1, in several organs, all tissues might be potentially affected by its effects. The aims of this study were: To evaluate the early histological changes in the heart, liver and kidneys, produced by ANG II infusion, to evaluate the protective effect of losartan. Wistar rats were distributed into three groups: control (no treatment), treated with ANG II, and treated with ANG II + losartan. ANG II was continuously infused over 72 hours by subcutaneous osmotic pumps. Histological sections of the myocardium, kidneys and liver were stained and observed for the presence of necrosis. There were ANG II-induced perivascular inflammation and necrosis of the arteriolar wall in the myocardium, kidney, and liver by, which were partially prevented by losartan. There was no significant correlation between heart and kidney damage. Tissue lesion severity was lower than that of vascular lesions, without statistical difference between groups. ANG II causes vascular injury in the heart, kidneys and liver, indicating a systemic vasculotoxic effect; the mechanisms of damage/protection vary depending on the target organ; perivascular lesions may occur even when anti-hypertensive doses of losartan are used.
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Background: Atherosclerosis and its complications remain the most common cause of death in postmenopausal women. But there are few studies evaluating in hormonal theraphy can affect the autoimmune response involved in atherosclerosis. Objective to evaluate the effects to soy germ isoflavones and hormone replacement theraphy on antibodies against heat shock proteins (HPSP60, HPSP70 and HSC70) in moderately hypertensive hypercholesterolemic postmenopausal women. Methods: Women were treated with soy germ (2g/day) 17'beta'-estradiol(2 mg/day) or 17'beta'-estradiol (2mg/day)+noretisterone acetate (1mg/day), for 3 months after taking placebo for 1 month. The plasma autoantibodies to HSP60, HSP70 and HSC70 were determined by ELISA. Results: Data showed a reduction of autoantibodies against HSC70 after treatment in the 3 studies groups in relation to the placebo. The antibodies reactive to HSP70 were reduced only in women receiving soy germ. No significant differences were found for antibodies against HSP60. Conclusion: The soy germ isoflavones and 17'beta'-estradiol, alone or associated with noretisterone acetate, had similar effects on reduction of antibodies reactive to HSP70 in moderately hypertensive hypercholesterolemic postmenopausal women after 3 months of treatment. Thus, there results indicate that soy isoflavnes and hormone theraphy may modulate some pathways of the immune-inflammatory process in postmenopausal women at high risk for atherosclerosis.
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Continued assessment of temporal trends in mortality and epidemiology of specific cardiovascular diseases in South America is needed to provide a scientific basis for rational allocation of the limited healthcare resources and introduction of strategies to reduce risk and predict the future burden of cardiovascular disease. The epidemiology of cardiomyopathies, adult valve disease and heart failure (HF) in South America is reviewed here. Diseases of the circulatory system are the main cause of death based on data from about 50% of the South American population. Among the cardiovascular causes of death, cerebrovascular disease is predominant followed by ischaemic heart disease, other heart diseases and hypertensive disease. Of note, cerebrovascular disease is the main cause of death in women, and race also influenced cardiovascular mortality rates. HF is the most important cardiovascular reason for admission to hospital due to cardiovascular disease of ischaemic, idiopathic dilated cardiomyopathic, valvular, hypertensive and chagasic aetiologies. Also, mortality due to HF is high, especially owing to Chagas' disease. HF and aetiologies associated with HF are responsible for 6.3% of deaths. Rheumatic fever is the leading cause of valvular heart disease. The findings have important public health implications because the allocation of healthcare resources, and strategies to reduce the risk of HF should also consider controlling Chagas' disease and rheumatic fever in South American countries.
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Background: Structural myocardial abnormalities have been extensively documented in hypothyroidism. Experimental studies in animal models have also shown involvement of thyroid hormones in gene expression of myocardial collagen. This study was planned to investigate the ability of ultrasonic tissue characterization, as evaluated by integrated backscatter (IBS), to early identify myocardial involvement in thyroid dysfunction. Patients and Methods: We studied 15 patients with hyperthyroidism (HYPER), 8 patients with hypothyroidism (HYPO), 14 patients with subclinical hypothyroidism (SCH) and 19 normal (N) subjects, who had normal LV systolic function. After treatment, 10 HYPER, 6 HYPO, and 8 SCH patients were reevaluated. IBS images were obtained and analyzed in parasternal short axis (papillary muscle level) view, at left ventricular (LV) posterior wall. The following IBS variables were analyzed: 1) the corrected coefficient (CC) of IBS, obtained by dividing IBS intensity by IBS intensity measured in a rubber phantom, using the same equipment adjustments, at the same depth; 2) cardiac cyclic variation (CV) of IBS - peak-to-peak difference between maximal and minimal values of IBS during cardiac cycle; 3) cardiac cyclic variation index (CVI) of IBS - percentual relationship between the cyclic variation (CV) and the mean value of IBS intensity. Results: CC of IBS was significantly larger (p < 0.05) in HYPER (1.57 +/- 0.6) and HYPO (1.53 +/- 0.3) as compared to SCH (1.32 +/- 0.3) or N (1.15 +/- 0.27). The CV (dB) (HYPO: 7.5 +/- 2.4; SCH: 8.2 +/- 3.1; HYPER: 8.2 +/- 2.0) and the CVI (HYPO: 35.6 +/- 19.7%; SCH: 34.7 +/- 17.5%; HYPER: 37.8 +/- 11.6%) were not significantly different in patients with thyroid dysfunction as compared to N (7.0 +/- 2.0 and 44.5 +/- 15.1%). Conclusions: CC of IBS was able to differentiate cardiac involvement in patients with overt HYPO and HYPER who had normal LV systolic function. These early myocardial structural abnormalities were partially reversed by drug therapy in HYPER group. On the other hand, although mean IBS intensity tended to be slightly larger in patients with SCH as compared to N, this difference was not statistical significant.
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Interethnic differences exist in disease prevalence, especially with regard to cancer and cardiovascular diseases, which involve altered expression or activity of matrix metalloproteinases (MMPs). The hypothesis being tested in this study is that interethnic differences exist between blacks and whites with regard to the distribution of genetic variants of MMP polymorphisms and haplotypes. We examined the distribution of polymorphisms of MMP-2 and MMP-9 genes in 177 black and 140 white subjects. We studied the following polymorphisms: the C(-1306)T in the promoter of the MMP-2 gene, the C(-1562)T and a microsatellite -90(CA)(14-24) in the promoter, and the Q279R in exon 6 of the MMP-9 gene. We have also compared our results with those from Hapmap or Seattle SNPs Projects and estimated the haplotype frequency in these two ethnic groups. The ""C'' allele for the C(-1306)T polymorphism was more common in blacks (91.5%) than in whites (80.4%; p<0.0001). The ""T'' allele for the C(-1562)T polymorphism was more common in blacks (15.0%) than in whites (8.9%; p=0.0279), as well as the alleles with >21 repeats for the -90(CA)(14-24) were more common in blacks than in whites (61.9% in blacks and 49.3% in whites; p=0.0017). We found no interethnic differences for the Q279R polymorphism. Moreover, two haplotypes that combine ""detrimental'' alleles were found at higher frequencies in blacks than in whites (31% vs. 16.4%, respectively; p<0.05). The interethnic differences being reported here replicate those previously found with smaller number of subjects in the Hapmap or Seattle SNPs data and may help explain the higher prevalence of cancer and cardiovascular diseases in blacks compared with whites. Our findings suggest a proportional significance of these polymorphisms in each ethnic group.
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Left ventricular hypertrophy (LVH) is a complication that may result from chronic hypertension. While nitric oxide (NO) deficiency has been associated with LVH, inconsistent results have been reported with regards to the association of endothelial NO synthase (eNOS) polymorphisms and LVH in hypertensive patients. This study aims to assess whether eNOS haplotypes are associated with LVH in hypertensive patients. This study included 101 healthy controls and 173 hypertensive patients submitted to echocardiography examination. Genotypes for three eNOS polymorphisms were determined: a single-nucleotide polymorphism in the promoter region (T-786C) and in exon 7 (Glu298Asp), and variable number of tandem repeats in intron 4. We found no significant association between eNOS genotypes and hypertension or with LVH (all p>0.05). However, while we found two eNOS haplotypes associated with variable risk of hypertension (all p<0.05), we found no significant associations between eNOS haplotypes and LVH (all p>0.05), even after adjustment in multiple linear regression analysis. These findings suggest that eNOS haplotypes that have been associated with variable susceptibility to hypertension were not associated with LVH in hypertensive patients. Further studies are necessary to examine whether other genes downstream may interact with eNOS polymorphisms and predispose to LVH in hypertensive patients.
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Background: The effects of renal denervation on cardiovascular reflexes and markers of nephropathy in diabetic-hypertensive rats have not yet been explored. Methods: Aim: To evaluate the effects of renal denervation on nephropathy development mechanisms (blood pressure, cardiovascular autonomic changes, renal GLUT2) in diabetic-hypertensive rats. Forty-one male spontaneously hypertensive rats (SHR) similar to 250 g were injected with STZ or not; 30 days later, surgical renal denervation (RD) or sham procedure was performed; 15 days later, glycemia and albuminuria (ELISA) were evaluated. Catheters were implanted into the femoral artery to evaluate arterial pressure (AP) and heart rate variability (spectral analysis) one day later in conscious animals. Animals were killed, kidneys removed, and cortical renal GLUT2 quantified (Western blotting). Results: Higher glycemia (p < 0.05) and lower mean AP were observed in diabetics vs. nondiabetics (p < 0.05). Heart rate was higher in renal-denervated hypertensive and lower in diabetic-hypertensive rats (384.8 +/- 37, 431.3 +/- 36, 316.2 +/- 5, 363.8 +/- 12 bpm in SHR, RD-SHR, STZ-SHR and RD-STZ-SHR, respectively). Heart rate variability was higher in renal-denervated diabetic-hypertensive rats (55.75 +/- 25.21, 73.40 +/- 53.30, 148.4 +/- 93 in RD-SHR, STZ-SHR-and RD-STZ-SHR, respectively, p < 0.05), as well as the LF component of AP variability (1.62 +/- 0.9, 2.12 +/- 0.9, 7.38 +/- 6.5 in RD-SHR, STZ-SHR and RD-STZ-SHR, respectively, p < 0.05). GLUT2 renal content was higher in all groups vs. SHR. Conclusions: Renal denervation in diabetic-hypertensive rats improved previously reduced heart rate variability. The GLUT2 equally overexpressed by diabetes and renal denervation may represent a maximal derangement effect of each condition.
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Background: Although exercise training has well-known cardiorespiratory and metabolic benefits, low compliance with exercise training programs is a fact, and the harmful effects of physical detraining regarding these adaptations usually go unnoticed. We investigated the effects of exercise detraining on blood pressure, insulin sensitivity, and GLUT4 expression in spontaneously hypertensive rats (SHR) and normotensive Wistar Kyoto rats (WKY). Methods: Studied animals were randomized into sedentary, trained (treadmill running/5 days a week, 60 min/day for 10 weeks), 1 week of detraining, and 2 weeks of detraining. Blood pressure (tail-cuff system), insulin sensitivity (kITT), and GLUT4 (Western blot) in heart, gastrocnemius and white fat tissue were measured. Results: Exercise training reduced blood pressure (19%), improved insulin sensitivity (24%), and increased GLUT4 in the heart (+34%); gastrocnemius (+36%) and fat (+22%) in SHR. In WKY no change in either blood pressure or insulin sensitivity were observed, but there was an increase in GLUT4 in the heart (+25%), gastrocnemius (+45%) and fat (+36%) induced by training. Both periods of detraining did not induce any change in neither blood pressure nor insulin sensitivity in SHR and WKY. One-week detraining reduced GLUT4 in SHR (heart: -28%; fat: -23%) and WKY (heart: -19%; fat: -22%); GLUT4 in the gastrocnemius was reduced after a 2-week detraining (SHR: -35%; WKY: -25%). There was a positive correlation between GLUT4 (gastrocnemius) and the maximal velocity in the exercise test (r = 0.60, p = 0.004). Conclusions: The study findings show that in detraining, despite reversion of the enhanced GLUT4 expression, cardiorespiratory and metabolic beneficial effects of exercise are preserved.
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Liquid-liquid microextraction without phase segmentation was implemented in a multicommuted flow system for determination of the anti-hypertensive diltiazem. The procedure was based on ion pair formation between the drug and the dye bromothymol blue at pH 3.5. The detection was performed without phase separation in a glass tube coupled to a fiber-optics spectrophotometer. The total volume of chloroform was reduced to 50 mu L in comparison with 10 mL consumed in batch. A linear response was observed between 9 and 120 mu mol L(-1), with a detection limit of 0.9 mu mol L(-1) (99.7% confidence level). The coefficient of variation (n = 10), sampling rate and extraction efficiency were estimated as 0.6%, 78 determinations per hour and 61%, respectively. About 30 mu g of bromothymol blue was consumed and the waste volume was 380 mu L per determination. The results for pharmaceutical samples agreed with those obtained by the reference procedure at the 95% confidence level. (C) 2011 Elsevier B.V. All rights reserved.
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Angiotensin I-converting enzyme (ACE) is recognized as one of the main effector molecules involved in blood pressure regulation. In the last few years some polymorphisms of ACE such as the insertion/deletion (I/D) polymorphism have been described, but their physiologic relevance is poorly understood. In addition, few studies investigated if the specific activity of ACE domain is related to the I/D polymorphism and if it can affect other systems. The aim of this study was to establish a biochemical and functional characterization of the I/D polymorphism and correlate this with the corresponding ACE activity. For this purpose, 119 male brazilian army recruits were genotyped and their ACE plasma activities evaluated from the C- and N-terminal catalytic domains using fluorescence resonance energy transfer (FRET) peptides, specific for the C-domain (Abz-LFK(Dnp)OH), N-domain (Abz-SDK(Dnp)P-OH) and both C- and N-domains (Abz-FRK(Dnp)P-OH). Plasma kallikrein activity was measured using Z-Phe-Arg-AMC as substrate and inhibited by selective plasma kallikrein inhibitor (PKSI). Some physiological parameters previously described related to the I/D polymorphism such as handgrip strength, blood pressure, heart rate and BMI were also evaluated. The genotype distribution was II n = 27, ID n = 64 and DD n = 28. Total plasma ACE activity of both domains in II individuals was significantly lower in comparison to ID and DD. This pattern was also observed for C- and N-domain activities. Difference between ID and DD subjects was observed only with the N-domain specific substrate. Blood pressure, heart rate, handgrip strength and BMI were similar among the genotypes. This polymorphism also affected the plasma kallikrein activity and DD group presents high activity level. Thus, our data demonstrate that the I/D ACE polymorphism affects differently both ACE domains without effects on handgrip strength. Moreover, this polymorphism influences the kallikrein-kinin system of normotensive individuals. (C) 2009 Elsevier Ltd. All rights reserved.
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The Kallikrein-Kinin System (KKS) has been associated to inflammatory and immunogenic responses in the peripheral and central nervous system by the activation of two receptors, namely B1 receptor and B2 receptor. The B1 receptor is absent or under-expressed in physiological conditions, being up-regulated during tissue injury or in the presence of cytokines. The B2 receptor is constitutive and mediates most of the biological effects of kinins. Some authors suggest a link between the KKS and the neuroinflammation in Alzheimer`s disease (AD). We have recently described an increase in bradykinin (BK) in the cerebrospinal fluid and in densities of B1 and B2 receptors in brain areas related to memory, after chronic infusion of amyloid-beta (A beta) peptide in rats, which was accompanied by memory disruption and neuronal loss. Mice lacking B1 or B2 receptors presented reduced cognitive deficits related to the learning process, after acute intracerebroventricular (i.c.v). administration of A. Nevertheless, our group showed an early disruption of cognitive function by i.c.v. chronic infusion of A beta after a learned task, in the knock-out B2 mice. This suggests a neuroprotective role for B2 receptors. In knock-out B1 mice the memory disruption was absent, implying the participation of this receptor in neurodegenerative processes. The acute or chronic infusion of A beta can lead to different responses of the brain tissue. In this way, the proper involvement of KKS on neuroinflammation in AD probably depends on the amount of A beta injected. Though, BK applied to neurons can exert inflammatory effects, whereas in glial cells, BK can have a potential protective role for neurons, by inhibiting proinflammatory cytokines. This review discusses this duality concerning the KKS and neuroinflammation in AD in vivo.
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Cardiovascular responses elicited by the stimulation of kinin B2 receptors in the IV cerebral ventricle paratrigeminal nucleus or in the thoracic spinal cord are similar to those observed during an exercise bout Considering that the kalikrein-kinin system (KKS) could act on the cardiovascular modulation during behavioral responses as physical exercise or stress this study evaluated the central B2 receptor densities of Wistar (W) and spontani ously hypertensive rats (SHR) after chronic moderate exercise Animals we re exercise-trained for ten weeks on a treadmill Afterwards systolic blood pressure decreased in both trained strains Animals were killed and the medulla and spinal cord extracted for B2 receptor autoradiography Trained animals were compared to their sedentary controls Sedentary groups showed specific binding sites for Hoe-140 (fmol/mg of tissue) in laminas 1 and 2 of the spinal cord nucleus of the solitary tract (NTS) area postrema (AP) spinal trigeminal tract (sp5) and paratrigeminal nucleus (Pa5) In trained W a significant increase (p<0 05) in specific binding was observed in the Pa5 (31 3%) and NTS (28 2%) Trained SHR showed a significant decrease in n ceptor density in lamina 2 (21 9%) of the thoracic spinal cord and an increase in specific binding in Pa5 (36 1%) We suggest that in the medulla chronic exercise could hyper stimulate the KKS enhancing their efficiency through the increase of B2 receptor density involving this receptor in central cardiovascular control during exercise or stress In the lamina 2 B2 receptor might be involved in the exercise-induced hypotension (C) 2010 Elsevier BV All rights reserved