Cardiorespiratory fitness as a mediator in the relationship between lung function and blood pressure in adults.

It is unclear whether physical activity and cardiorespiratory fitness (CRF) are pathways that link low pulmonary function (LPF) to increased blood pressure (BP). Therefore, we investigated the extent to which CRF and moderate-to-vigorous physical activity (MVPA) mediate the relationship between LPF and high BP in adults. We conducted a cross-sectional study with 1,362 participants that underwent cardiopulmonary exercise testing (CPET), spirometry, and wore an accelerometer to determine physical activity patterns. We performed mediation analyses using structural equations considering peak oxygen uptake (V̇O2) and MVPA as mediators, forced vital capacity (FVC) and forced expiratory volume in the first second (FEV1) as independent variables, and systolic and diastolic blood pressure (SBP, DBP) as dependent variables. The probability of alpha error was set at 5%. We found a significant total effect of FVC on SBP and DBP considering V̇O2 as mediator (P<0.01). Indirect effects were also significant, with 42.6% of the total effect of FVC on SBP and 77% on DBP mediated by V̇O2 (P<0.01). We did not observe a direct effect of FVC on SBP and DBP. Considering FEV1 as an independent variable, the total effect on SBP was also significant, as were the indirect effects, mediated by V̇O2 at 14.8% for SBP and 7.6% for DBP (P<0.01). We did not find an indirect effect of FVC or FEV1 considering the MVPA as a mediator. CRF mediates the pathway that links LPF and elevated BP. Therefore, CRF is more sensitive to variations in FVC and FEV1 than MVPA.

Cardiorespiratory fitness as a mediator in the relationship between lung function and blood pressure in adults

It is unclear whether physical activity and cardiorespiratory fitness (CRF) are pathways that link low pulmonary function (LPF) to increased blood pressure (BP). Therefore, we investigated the extent to which CRF and moderate-to-vigorous physical activity (MVPA) mediate the relationship between LPF and high BP in adults. We conducted a cross-sectional study with 1,362 participants that underwent cardiopulmonary exercise testing (CPET), spirometry, and wore an accelerometer to determine physical activity patterns. We performed mediation analyses using structural equations considering peak oxygen uptake (V̇O2) and MVPA as mediators, forced vital capacity (FVC) and forced expiratory volume in the first second (FEV1) as independent variables, and systolic and diastolic blood pressure (SBP, DBP) as dependent variables. The probability of alpha error was set at 5%. We found a significant total effect of FVC on SBP and DBP considering V̇O2 as mediator (P<0.01). Indirect effects were also significant, with 42.6% of the total effect of FVC on SBP and 77% on DBP mediated by V̇O2 (P<0.01). We did not observe a direct effect of FVC on SBP and DBP. Considering FEV1 as an independent variable, the total effect on SBP was also significant, as were the indirect effects, mediated by V̇O2 at 14.8% for SBP and 7.6% for DBP (P<0.01). We did not find an indirect effect of FVC or FEV1 considering the MVPA as a mediator. CRF mediates the pathway that links LPF and elevated BP. Therefore, CRF is more sensitive to variations in FVC and FEV1 than MVPA.

In ovo injection of ascorbic acid and higher incubation temperature modulate blood parameters in response to heat exposure in broilers.

1. This study analysed whether in ovo injection of ascorbic acid before incubation and at high incubation temperature influenced blood characteristics and performance in broilers reared in different temperature conditions. 2. A total of 3,000 fertile eggs from broiler breeders (Cobb®) were randomly divided into three incubation treatments: no ascorbic acid injection and egg incubation at 37.5°C (control); no ascorbic acid injection and egg incubation at 39°C; in ovo ascorbic acid injection prior to incubation (6 µg AA/100 µl water) and egg incubation at 39°C. 3. Male chicks hatched from the three incubation treatments were submitted to three distinct rearing temperatures (control, cold and hot) from the third week of age onwards (540 chicks were divided into 6 treatments with 5 replicates per treatment). 4. Measurements at 42 d showed that, after egg incubation at 39°C, the haematocrit, haemoglobin values, ionised calcium and glucose concentrations were increased and base excess values were reduced. However, in ovo injection of ascorbic acid normalised all these parameters. 5. Partial CO2 and O2 pressure were higher with increased rearing temperature. Blood pH was lower when eggs were incubated at 39°C and injected with ascorbic acid. In ovo injection of ascorbic acid induced leucocytosis due to lymphocytosis and heterophilia, restored basophils rate and led to monocytopoenia. Leucocytosis was triggered by hot rearing temperature due to lymphocytosis, eosinophilia and heterophilia. 6. The results obtained in this study showed that in ovo injection of ascorbic acid before incubation may serve as a long-term stimulator and modulator of the broiler immune system, and that high incubation temperatures induce adaptations in the electrolytic balance, minimising or avoiding the occurrence of respiratory alkalosis under hot rearing temperature.

Use of cardiopulmonary exercise testing to assess early ventilatory changes related to occupational particulate matter.

Spirometry has been used as the main strategy for assessing ventilatory changes related to occupational exposure to particulate matter (OEPM). However, in some cases, as one of its limitations, it may not be sensitive enough to show abnormalities before extensive damage, as seen in restrictive lung diseases. Therefore, we hypothesized that cardiopulmonary exercise testing (CPET) may be better than spirometry to detect early ventilatory impairment caused by OEPM. We selected 135 male workers with at least one year of exposure. After collection of self-reported socioeconomic status, educational level, and cardiovascular risk data, participants underwent spirometry, CPET, body composition assessment (bioelectrical impedance), and triaxial accelerometry (for level of physical activity in daily life). CPET was performed using a ramp protocol on a treadmill. Metabolic, cardiovascular, ventilatory, and submaximal relationships were measured. We compared 52 exposed to 83 non-exposed workers. Multiple linear regressions were developed using spirometry and CPET variables as outcomes and OEPM as the main predictor, and adjusted by the main covariates. Our results showed that OEPM was associated with significant reductions in peak minute ventilation, peak tidal volume, and breathing reserve index. Exposed participants presented shallower slope of ΔVT/ΔlnV̇E (breathing pattern), i.e., increased tachypneic breathing pattern. The OEPM explained 7.4% of the ΔVT/ΔlnV̇E variability. We found no significant influence of spirometric indices after multiple linear regressions. We conclude that CPET might be a more sensitive feature of assessing early pulmonary impairment related to OEPM. Our cross-sectional results suggested that CPET is a promising tool for the screening of asymptomatic male workers.

Incubation temperature alters thermal preference and response to heat stress of broiler chickens along the rearing phase.

The current study aimed to investigate whether embryonic temperature manipulation may alter thermal preference throughout the rearing phase of broiler chickens and how this manipulation may affect response to thermal challenge, metabolism, growth rate and feed intake rate. Eggs were exposed to a constant incubation temperature [machine temperatures: 36°C (Low), 37.5°C (Control), and 39°C (High); eggshell temperature of 37.4 ± 0.08°C, 37.8 ± 0.15°C, and 38.8 ± 0.33°C, respectively] from d 13 till hatching. Low treatment chickens showed lower plasma T3 and GH levels at d 1 of age and lower T3 level at d 42 of age compared to the Control treatment. Preferred ambient, rectal temperature, T4 level, growth rate, food intake rate, and response to thermal challenge were not altered in these chickens. On the other hand, High-treatment chickens exhibited high preferred ambient temperature and rectal temperature during the first 2 wk post-hatch, lower plasma T3 level at d 21 and 42 and a delayed increase in respiratory movement in response to thermal challenge compared to the Control treatment. However, chickens subjected to the Control and High treatments did not differ in T4 and GH level and performance. We conclude that exposure to high temperature during late embryonic development has long-lasting effects on the thermoregulatory system of broiler chickens by affecting the heat tolerance of these chickens. Moreover, the preferred ambient temperature of the chickens from heat-treated eggs correspond to those recommended for the strain under study, whereas for the cold-treated and control-chickens it was 1°C below, indicating that incubation temperature might have consequences on the ambient temperature chickens require during the rearing phase.

Incubation temperature manipulation during fetal development reduces adiposity of broiler hatchlings.

Broilers are known as an efficient source of lean meat. Genetic selection resulted in broiler strains with large body size and fast growth, but a concomitant increase in fat deposition also occurred. Other than reducing nutrient intake, there is a lack of alternative methods to control body fat composition of broilers. The present study assessed whether incubation temperature (machine temperatures: 36ºC, 37.5ºC, and 39ºC; eggshell temperatures: 37.4 ± 0.08°C, 37.8 ± 0.15ºC, and 38.8 ± 0.33°C, respectively.) from d 13 affects broiler hatchling fat deposition. We analyzed adipocyte hypertrophy and proliferation in 3 body regions; weight and chemical composition of yolk-free chicks and yolk sacs; and serum lipid profile. Increased incubation temperature reduced abdominal and cervical adipocyte size. Independently of temperature, cervical adipocytes were smaller and showed higher proliferation than adipocytes in the abdominal and thigh regions. Smaller cervical adipocytes were observed in birds from eggs incubated at 36ºC and 39ºC. With regard to weight and composition of chicks, ash content as a percentage of dry matter was the only variable affected by temperature; it was higher in chicks from eggs incubated at 36ºC than at 39ºC and showed no significant difference between chicks incubated at 39ºC and 37.5ºC. Absolute and relative weights of yolk sacs were higher from eggs incubated at 39ºC than at 36ºC, and these two treatments did not differ from the 37.5ºC control. Absolute measures of yolk sac lipids, moisture, dry matter, and crude protein content were lower in chicks from eggs incubated at 36ºC, and no significant differences were found for these variables between chicks from eggs incubated at 37.5ºC and 39ºC. Hatchlings from eggs incubated at 36°C had significantly higher cholesterol levels than chicks incubated at the other 2 temperatures, but no additional effects on blood lipids were detected. Incubation temperature manipulation during fetal development altered cervical and abdominal adipocyte size in broiler hatchlings and could become a tool in hatcheries to manipulate chick quality, although further studies are needed to evaluate its long-term effects.

Cardiovascular function alterations induced by acute paradoxical sleep deprivation in rats.

Sleep loss has been implicated in triggering the hypertension. The goal of the present study was investigated the possible mechanisms underlying cardiovascular alterations after acute paradoxical sleep deprivation (PSD). Male Wistar rats were assigned in two experimental groups: (1) control and (2) PSD for 24 h using the modified single platform method. Paradoxical sleep deprived rats exhibited higher blood pressure, heart rate (HR) and impaired baroreceptor sensitivity. After pharmacological autonomic double blockade (propranolol and methylatropine administration), intrinsic heart rate was decreased after PSD. The PSD rats showed a reduction in the vagal tone without affecting sympathetic tone. Isoproterenol administration (0.001, 0.01 and 1 µg/kg) induced an increase in ΔHR responses in PSD group. Electrocardiographic analysis in response to ß-adrenergic stimulation indicated that PSD contributed to ventricular cardiac arrhythmias. Our findings suggest that acute paradoxical sleep loss induce cardiovascular alterations, autonomic imbalance accompanied by impaired baroreflex sensitivity and increased arrhythmia susceptibility.

Epidemiological study of myiases in the Hospital do Andaraí, Rio de Janeiro, including reference to an exotic etiological agent.

Myiases are infestations with dipteran larvae in both necrosed and living tissues, the food source of these insects. These illnesses occur in warm humid climates, and are most frequent in developing countries. We assessed the epidemiological aspects and the influence of climate on the occurrence of myiases and the bioagents in patients admitted to the federal Hospital do Andaraí in Rio de Janeiro from February 2007 to 2008. The influence of abiotic factors (temperature, humidity, and rainfall) on the incidence of myiases was investigated by using the Pearson's correlation test. Of the 40 patients studied, the prevalence of myiases was higher in adults, particularly in the 40 to 65 year-old (37.5%) African descent males (57.5%). Most of the injuries were caused by trauma (62.5%). Some patients made use of licit (50%) and illicit drugs (17.2%). The occurrence of myiases was not affected by the abiotic factors investigated. The cases reported here were treated in only one hospital, indicating that the disease is relatively common. The most frequent bioagent was Cochliomyia hominivorax (Coquerel), but Cochliomyia macellaria (Fabricius), Chrysomya albiceps (Wiedemann) and Dermatobia hominis (Wiedemann) (Diptera: Calliphoridae) were also detected causing myiases. Chrysomya albiceps is an exotic etiologic agent of myiases.

Ketamine impairs recognition memory consolidation and prevents learning-induced increase in hippocampal brain-derived neurotrophic factor levels.

The non-competitive N-methyl-d-aspartate (NMDA) glutamate receptor antagonist ketamine has been shown to produce cognitive deficits. However, the effects of ketamine on the consolidation phase of memory remain poorly characterized. Here we show that systemic administration of ketamine immediately after training dose-dependently impairs long-term retention of memory for a novel object recognition (NOR) task in rats. Control experiments showed that the impairing effects of ketamine could not be attributed to an influence on memory retrieval or sensorimotor effects. In addition, ketamine prevented the increase in hippocampal brain-derived neurotrophic factor (BDNF) levels induced by NOR learning. Our results show for the first time that ketamine disrupts the consolidation phase of long-term recognition memory. In addition, the findings suggest that the amnestic effects of ketamine might be at least partially mediated by an influence on BDNF signaling in the hippocampus.

Molecular mechanisms mediating gastrin-releasing peptide receptor modulation of memory consolidation in the hippocampus.

Although the gastrin-releasing peptide-preferring bombesin receptor (GRPR) has been implicated in memory formation, the underlying molecular events are poorly understood. In the present study, we examined interactions between the GRPR and cellular signaling pathways in influencing memory consolidation in the hippocampus. Male Wistar rats received bilateral infusions of bombesin (BB) into the dorsal hippocampus immediately after inhibitory avoidance (IA) training. Intermediate doses of BB enhanced, whereas a higher dose impaired, 24-h IA memory retention. The BB-induced memory enhancement was prevented by pretraining infusions of a GRPR antagonist or inhibitors of protein kinase C (PKC), mitogen-activated protein kinase (MAPK) kinase and protein kinase A (PKA), but not by a neuromedin B receptor (NMBR) antagonist. We next further investigated the interactions between the GRPR and the PKA pathway. BB-induced enhancement of consolidation was potentiated by coinfusion of activators of the dopamine D1/D5 receptor (D1R)/cAMP/PKA pathway and prevented by a PKA inhibitor. We conclude that memory modulation by hippocampal GRPRs is mediated by the PKC, MAPK, and PKA pathways. Furthermore, pretraining infusion of BB prevented beta-amyloid peptide (25-35)-induced memory impairment, supporting the view that the GRPR is a target for the development of cognitive enhancers for dementia.