Chronic experimental myocardial infarction produces antinatriuresis by a renal nerve-dependent mechanism

The present study focused on the role of sympathetic renal nerve activity, in mediating congestive heart failure-induced sodium retention following experimental chronic myocardial infarction. Groups of male Wistar rats (240-260 g) were studied: sham-operated coronary ligation (CON3W, N = 11), coronary ligation and sham-operated renal denervation (INF3W, N = 19), 3 weeks of coronary ligation and sympathetic renal nerve denervation (INF3WDX, N = 6), sham-operated coronary ligation (N = 7), and 16 weeks of coronary ligation (INF16W, N = 7). An acute experimental protocol was used in which the volume overload (VO; 5% of body weight) was applied for 30 min after the equilibration period of continuous iv infusion of saline. Compared to control levels, VO produced an increase (P < 0.01, ANOVA) in urine flow rate (UFR; 570%) and urinary sodium excretion (USE; 1117%) in CON3W. VO induced a smaller increase (P < 0.01) in USE (684%) in INF3W. A similar response was also observed in INF16W. In INF3WDX, VO produced an immediate and large increase (P < 0.01) in UFR (547%) and USE (1211%). Similarly, in INF3W VO increased (P < 0.01) UFR (394%) and USE (894%). Compared with INF3W, VO induced a higher (P < 0.01) USE in INF3WDX, whose values were similar to those for CON3W. These results suggest that renal sympathetic activity may be involved in sodium retention induced by congestive heart failure. This premise is supported by the observation that in bilaterally renal denervated INF3WDX rats myocardial infarction was unable to reduce volume expansion-induced natriuresis. However, the mechanism involved in urinary volume regulation seems to be insensitive to the factors that alter natriuresis.

The decreased oxygen uptake during progressive exercise in ischemia-induced heart failure is due to reduced cardiac output rate

We tested the hypothesis that the inability to increase cardiac output during exercise would explain the decreased rate of oxygen uptake (VO2) in recent onset, ischemia-induced heart failure rats. Nine normal control rats and 6 rats with ischemic heart failure were studied. Myocardial infarction was induced by coronary ligation. VO2 was measured during a ramp protocol test on a treadmill using a metabolic mask. Cardiac output was measured with a flow probe placed around the ascending aorta. Left ventricular end-diastolic pressure was higher in ischemic heart failure rats compared with normal control rats (17 ± 0.4 vs 8 ± 0.8 mmHg, P = 0.0001). Resting cardiac index (CI) tended to be lower in ischemic heart failure rats (P = 0.07). Resting heart rate (HR) and stroke volume index (SVI) did not differ significantly between ischemic heart failure rats and normal control rats. Peak VO2 was lower in ischemic heart failure rats (73.72 ± 7.37 vs 109.02 ± 27.87 mL min-1 kg-1, P = 0.005). The VO2 and CI responses during exercise were significantly lower in ischemic heart failure rats than in normal control rats. The temporal response of SVI, but not of HR, was significantly lower in ischemic heart failure rats than in normal control rats. Peak CI, HR, and SVI were lower in ischemic heart failure rats. The reduction in VO2 response during incremental exercise in an ischemic model of heart failure is due to the decreased cardiac output response, largely caused by depressed stroke volume kinetics.

Incidence of heart failure in infarcted rats that die spontaneously

The present study reports for the first time the incidence of congestive heart failure (CHF) in previously infarcted rats that died spontaneously. Previously, pulmonary (PWC) and hepatic (HWC) water contents were determined in normal rats: 14 control animals were evaluated immediately after sacrifice, 8 placed in a refrigerator for 24 h, and 10 left at room temperature for 24 h. In the infarcted group, 9 rats died before (acute) and 28 died 48 h after (chronic) myocardial infarction. Thirteen chronic animals were submitted only to autopsy (N = 13), whereas PWC and HWC were also determined in the others (N = 15). Seven rats survived 48 h and died during anesthesia. Notably, PWC differed in normal rats: ambient (75.7 ± 1.3%) < control (77.5 ± 0.7%) < refrigerator (79.1 ± 1.4%) and there were no differences with respect to HWC. No clinical signs of CHF (dyspnea, lethargy or foot edema) were observed in infarcted rats before death. PWC was elevated in all chronic and anesthetized rats. HWC was increased in 48% of chronic and in all anesthetized rats. Our data showed that PWC needs to be evaluated before 24 h post mortem and that CHF is the rule in chronic infarcted rats suffering natural death. The congestive syndrome cannot be diagnosed correctly in rats by clinical signs alone, as previously proposed.

Rats with high left ventricular end-diastolic pressure can be identified by Doppler echocardiography one week after myocardial infarction

The severity of left ventricular (LV) dysfunction in rats with myocardial infarction (MI) varies widely. Because homogeneity in baseline parameters is essential for experimental investigations, a study was conducted to establish whether Doppler echocardiography (DE) could accurately identify animals with high LV end-diastolic pressure as a marker of LV dysfunction soon after MI. Direct measurements of LV end-diastolic pressure were made and DE was performed simultaneously 1 week after surgically induced MI (N = 16) or sham-operation (N = 17) in female Wistar rats (200 to 250 g). The ratio of peak early (E) to late (A) diastolic LV filling velocities and the ratio of E velocity to peak early (Em) diastolic myocardial velocity were the best predictors of high LV end-diastolic pressure (>12 mmHg) soon after MI. Cut-off values of 1.77 for the E/A ratio (P = 0.001) identified rats with elevated LV end-diastolic pressure with 90% sensitivity and 80% specificity. Cut-off values of 20.4 for the E/Em ratio (P = 0.0001) identified rats with elevated LV end-diastolic pressure with 81.8% sensitivity and 80% specificity. Moreover, E/A and E/Em ratios were the only echocardiographic parameters independently associated with LV end-diastolic pressure in multiple linear regression analysis. Therefore, DE identifies rats with high LV end-diastolic pressure soon after MI. These findings have implications for using serial DE in animal selection and in the assessment of their response to experimental therapies.

Ventricular performance and Na+-K+ ATPase activity are reduced early and late after myocardial infarction in rats

Myocardial infarction leads to compensatory ventricular remodeling. Disturbances in myocardial contractility depend on the active transport of Ca2+ and Na+, which are regulated by Na+-K+ ATPase. Inappropriate regulation of Na+-K+ ATPase activity leads to excessive loss of K+ and gain of Na+ by the cell. We determined the participation of Na+-K+ ATPase in ventricular performance early and late after myocardial infarction. Wistar rats (8-10 per group) underwent left coronary artery ligation (infarcted, Inf) or sham-operation (Sham). Ventricular performance was measured at 3 and 30 days after surgery using the Langendorff technique. Left ventricular systolic pressure was obtained under different ventricular diastolic pressures and increased extracellular Ca2+ concentrations (Ca2+e) and after low and high ouabain concentrations. The baseline coronary perfusion pressure increased 3 days after myocardial infarction and normalized by 30 days (Sham 3 = 88 ± 6; Inf 3 = 130 ± 9; Inf 30 = 92 ± 7 mmHg; P < 0.05). The inotropic response to Ca2+e and ouabain was reduced at 3 and 30 days after myocardial infarction (Ca2+ = 1.25 mM; Sham 3 = 70 ± 3; Inf 3 = 45 ± 2; Inf 30 = 29 ± 3 mmHg; P < 0.05), while the Frank-Starling mechanism was preserved. At 3 and 30 days after myocardial infarction, ventricular Na+-K+ ATPase activity and contractility were reduced. This Na+-K+ ATPase hypoactivity may modify the Na+, K+ and Ca2+ transport across the sarcolemma resulting in ventricular dysfunction.

Cardiac gene expression and systemic cytokine profile are complementary in a murine model of post-ischemic heart failure

After myocardial infarction (MI), activation of the immune system and inflammatory mechanisms, among others, can lead to ventricular remodeling and heart failure (HF). The interaction between these systemic alterations and corresponding changes in the heart has not been extensively examined in the setting of chronic ischemia. The main purpose of this study was to investigate alterations in cardiac gene and systemic cytokine profile in mice with post-ischemic HF. Plasma was tested for IgM and IgG anti-heart reactive repertoire and inflammatory cytokines. Heart samples were assayed for gene expression by analyzing hybridization to AECOM 32k mouse microarrays. Ischemic HF significantly increased the levels of total serum IgM (by 5.2-fold) and total IgG (by 3.6-fold) associated with a relatively high content of anti-heart specificity. A comparable increase was observed in the levels of circulating pro-inflammatory cytokines such as IL-1β (3.8X) and TNF-α (6.0X). IFN-γ was also increased by 3.1-fold in the MI group. However, IL-4 and IL-10 were not significantly different between the MI and sham-operated groups. Chemokines such as MCP-1 and IL-8 were 1.4- and 13-fold increased, respectively, in the plasma of infarcted mice. We identified 2079 well annotated unigenes that were significantly regulated by post-ischemic HF. Complement activation and immune response were among the most up-regulated processes. Interestingly, 21 of the 101 quantified unigenes involved in the inflammatory response were significantly up-regulated and none were down-regulated. These data indicate that post-ischemic heart remodeling is accompanied by immune-mediated mechanisms that act both systemically and locally.

Remodeling in the ischemic heart: the stepwise progression for heart

Abstract Coronary artery disease is the leading cause of death in the developed world and in developing countries. Acute mortality from acute myocardial infarction (MI) has decreased in the last decades. However, the incidence of heart failure (HF) in patients with healed infarcted areas is increasing. Therefore, HF prevention is a major challenge to the health system in order to reduce healthcare costs and to provide a better quality of life. Animal models of ischemia and infarction have been essential in providing precise information regarding cardiac remodeling. Several of these changes are maladaptive, and they progressively lead to ventricular dilatation and predispose to the development of arrhythmias, HF and death. These events depend on cell death due to necrosis and apoptosis and on activation of the inflammatory response soon after MI. Systemic and local neurohumoral activation has also been associated with maladaptive cardiac remodeling, predisposing to HF. In this review, we provide a timely description of the cardiovascular alterations that occur after MI at the cellular, neurohumoral and electrical level and discuss the repercussions of these alterations on electrical, mechanical and structural dysfunction of the heart. We also identify several areas where insufficient knowledge limits the adoption of better strategies to prevent HF development in chronically infarcted individuals.

Effects of single-dose atorvastatin on interleukin-6, interferon gamma, and myocardial no-reflow in a rabbit model of acute myocardial infarction and reperfusion

The mechanisms of statins relieving the no-reflow phenomenon and the effects of single-dose statins on it are not well known. This study sought to investigate the effects of inflammation on the no-reflow phenomenon in a rabbit model of acute myocardial infarction and reperfusion (AMI/R) and to evaluate the effects of single-dose atorvastatin on inflammation and myocardial no-reflow. Twenty-four New Zealand white male rabbits (5-6 months old) were randomized to three groups of eight: a sham-operated group, an AMI/R group, and an atorvastatin-treated group (10 mg/kg). Animals in the latter two groups were subjected to 4 h of coronary occlusion followed by 2 h of reperfusion. Serum levels of interleukin (IL)-6 were measured by enzyme-linked immunosorbent assay. The expression of interferon gamma (IFN-γ) in normal and infarcted (reflow and no-reflow) myocardial tissue was determined by immunohistochemical methods. The area of no-reflow and necrosis was evaluated pathologically. Levels of serum IL-6 were significantly lower in the atorvastatin group than in the AMI/R group (P<0.01). Expression of IFN-γ in infarcted reflow and no-reflow myocardial tissue was also significantly lower in the atorvastatin group than in the AMI/R group. The mean area of no-reflow [47.01% of ligation area (LA)] was significantly smaller in the atorvastatin group than in the AMI/R group (85.67% of LA; P<0.01). The necrosis area was also significantly smaller in the atorvastatin group (85.94% of LA) than in the AMI/R group (96.56% of LA; P<0.01). In a secondary analysis, rabbits in the atorvastatin and AMI/R groups were divided into two groups based on necrosis area (90% of LA): a small group (<90% of LA) and a large group (>90% of LA). There was no significant difference in the area of no-reflow between the small (61.40% of LA) and large groups (69.87% of LA; P>0.05). Single-dose atorvastatin protected against inflammation and myocardial no-reflow and reduced infarct size during AMI/R in rabbits. No-reflow was not dependent on the reduction of infarct size.

Spatial variability of particle size fractions of an Oxisol cultivated with conilon coffee

Information on the spatial distribution of particle size fractions is essential for use planning and management of soils. The aim of this work to was to study the spatial variability of particle size fractions of a Typic Hapludox cultivated with conilon coffee. The soil samples were collected at depths of 0-0.20 and 0.20-0.40 m in the coffee canopy projection, totaling 109 georeferentiated points. At the depth of 0.2-0.4 m the clay fraction showed average value significantly higher, while the sand fraction showed was higher in the depth of 0-0.20 m. The silt showed no significant difference between the two depths. The particle size fractions showed medium and high spatial variability. The levels of total sand and clay have positive and negative correlation, respectively, with the altitude of the sampling points, indicating the influence of landscape configuration.

Effect of N and K doses in nutritive solution on growth, production and coffee bean size

An adequate supply of nutrients is essential for obtaining high yields of coffee. The objective of this study was to evaluate the effect of N, K and the N:K ratio on vegetative and reproductive growth of coffee. For this purpose, coffee plants were grown in nutrient solution containing K in the concentrations of 1.08; 2.15; 3.23 and 5.38 mmol L-1 combined with a dose of 6 mmol L-1 N, resulting in the N:K ratios (w/w): 1:0.5; 1:1; 1:1.5 and 1:2.5. The control treatment consisted of the doses 3 and 1.61 mmol L-1 of N and K respectively, resulting in the N:K ratio (w/w) 1.0:1.5. The following variables were evaluated: height, stem diameter, number of nodes of the eighth plagiotrofic branch (index branch), pairs of plagiotrofic branches and number of nodes in the orthotropic branch every three weeks from the beginning of the experiment. Additionally, it was evaluated the chemical composition of processed beans and leaves between the flowering and the rapid expansion stage of the cherry beans, production of cherry beans per plant and classification of beans according to the size. N influenced mainly the characteristics of vegetative growth and K influenced mainly the reproductive growth evaluated by the production. The lowest production resulted in the highest percentages of beans retained on sieves with holes larger than 16/64", while the highest production promoted an increase in the percentage of beans retained on sieves with holes smaller than 16/64".

Shape and size of jatropha beans (Jatropha curcas L.) during drying at different temperatures

This study was carried out to study the physical properties of the jatropha beans over the drying under six air conditions, based on measurements of roundness, sphericity, volume, superficial area, projected area and surface/volume ratio. Jatropha beans with moisture content around 0.61 (decimal d.b.) were subjected to thin-layer drying in oven with forced-air circulation under six temperature conditions (36, 45, 60, 75, 90 and 105 °C) and relative humidity of 31.7; 19.6; 9.4; 4.8; 2.6 and 1.5% respectively, until reaching the moisture content of 0.11 ± 0.006 (decimal d. b.). The results showed that the necessary time for jatropha beans to reach the moisture content of 0.11 ± 0.006 (decimal d.b.) were 1.5; 2.25; 3.0; 4.75; 6.75 and 12.0 h for the drying temperatures of 105, 90, 75, 60, 45 and 36 °C, respectively; and the reduction in the moisture content as well as the drying conditions promoted changes in the shape and reduced the size of the jatropha beans.

Determination of reactivity rates of silicate particle-size fractions

The efficiency of sources used for soil acidity correction depends on reactivity rate (RR) and neutralization power (NP), indicated by effective calcium carbonate (ECC). Few studies establish relative efficiency of reactivity (RER) for silicate particle-size fractions, therefore, the RER applied for lime are used. This study aimed to evaluate the reactivity of silicate materials affected by particle size throughout incubation periods in comparison to lime, and to calculate the RER for silicate particle-size fractions. Six correction sources were evaluated: three slags from distinct origins, dolomitic and calcitic lime separated into four particle-size fractions (2, 0.84, 0.30 and <0.30-mm sieves), and wollastonite, as an additional treatment. The treatments were applied to three soils with different texture classes. The dose of neutralizing material (calcium and magnesium oxides) was applied at equal quantities, and the only variation was the particle-size material. After a 90-day incubation period, the RER was calculated for each particle-size fraction, as well as the RR and ECC of each source. The neutralization of soil acidity of the same particle-size fraction for different sources showed distinct solubility and a distinct reaction between silicates and lime. The RER for slag were higher than the limits established by Brazilian legislation, indicating that the method used for limes should not be used for the slags studied here.

O peso do varejo, o peso no varejo e a identidade: uma análise de consumidoras plus size

Este trabalho estuda o conceito de identidade sob a ótica do consumo feminino de moda plus size. Foram realizadas 14 entrevistas fenomenológicas, observadas por uma perspectiva hermenêutica. Três categorias temáticas emergiram dos dados: a construção da identidade pela moda, o que envolve ser plus size e estratégias criativas para lidar com a configuração do portfólio de produtos no varejo, que não favorece mulheres plus size. Entre os principais resultados, destacam-se a forma pela qual o termo plus size age como estigma, influenciando os projetos identitários das consumidoras, o papel do varejo na estigmatização e a saga quase epopeica das compras, que envolve até um "mercado negro" com as vendedoras.

Rise and fall in ischemic heart disease mortality: it may have happened before

The rise in ischemic heart disease(IHD) mortality occurring mostly during the first half of the 20th century is usually associated with economic development and its consequences for people's lifestyles. On the basis of historical evidence, it is postulated that a previous IHD epidemic cycle may have occurred in England and Wales towards the turn of the nineteenth century. The implications of this on causal theories and current etiological research on atherosclerosis are discussed.

Air pollution effects on myocardial infarction

OBJECTIVE: Myocardial infarction is an acute and severe cardiovascular disease that generally leads to patient admissions to intensive care units and few cases are initially admitted to infirmaries. The objective of the study was to assess whether estimates of air pollution effects on myocardial infarction morbidity are modified by the source of health information. METHODS: The study was carried out in hospitals of the Brazilian Health System in the city of São Paulo, Southern Brazil. A time series study (1998-1999) was performed using two outcomes: infarction admissions to infirmaries and to intensive care units, both for people older than 64 years of age. Generalized linear models controlling for seasonality (long and short-term trends) and weather were used. The eight-day cumulative effects of air pollutants were assessed using third degree polynomial distributed lag models. RESULTS: Almost 70% of daily hospital admissions due to myocardial infarction were to infirmaries. Despite that, the effects of air pollutants on infarction were higher for intensive care units admissions. All pollutants were positively associated with the study outcomes but SO2 presented the strongest statistically significant association. An interquartile range increase on SO2 concentration was associated with increases of 13% (95% CI: 6-19) and 8% (95% CI: 2-13) of intensive care units and infirmary infarction admissions, respectively. CONCLUSIONS: It may be assumed there is a misclassification of myocardial infarction admissions to infirmaries leading to overestimation. Also, despite the absolute number of events, admissions to intensive care units data provides a more adequate estimate of the magnitude of air pollution effects on infarction admissions.