Brazilian normal static bone histomorphometry: effects of age, sex, and race.

Bone histomorphometry values for normal individuals within different populations have been well established. We studied iliac crest bone samples from 125 healthy Brazilian subjects. The effect of sex, race, and age variables on histomorphometric parameters was evaluated. Bone volume showed a trend to decrease with age in both sexes, being significantly higher in black females and Caucasian males. Interactions among sex, race, and age had no effect on trabecular thickness (Tb.Th) and trabecular separation (Tb.Sp). However, age had a significant effect on Tb.Th and Tb.Sp, and sex had an impact on Tb.Sp. Trabecular number (Tb.N) was higher in black females than in males and was higher in Asian males than in females. Among females, Tb.N was lower in Asians than in other races and was higher in blacks than in Caucasians and or in those of mulattos. In addition, Tb.N was higher in males under 10 than in males over 50 years old, was higher in females under 10 than in females in any other age bracket, and was lower in females in the 41-50 age bracket than in younger females. Osteoid volume and osteoid surface were significantly higher in males than in females, and a significant age-related difference in osteoid thickness was observed. No significant sex-related or race-related differences were found in terms of resorption, although eroded surface decreased with age. In conclusion, sex, race, and age, as well as interactions among these three variables, were found to affect some static histomorphometric indexes in healthy Brazilian subjects.

Effects of ambient particles and carbon monoxide on supraventricular arrhythmias in a rat model of myocardial infarction.

The association between short-term increases in particulate air pollution and increased cardiovascular morbidity and mortality is well documented. Recent studies suggest an association between particulate matter with aerodynamic diameter < 2.5 microm (PM2.5) and supraventricular arrhythmias (SVA), but the results have been inconsistent. We evaluated this hypothesis in a rat model of acute myocardial infarction (AMI). Diazepam-sedated Sprague-Dawley rats with AMI were exposed (1 h) to either filtered air (n = 16), concentrated ambient fine particles (CAPS; mean = 645.7 microg/m3; n = 23), carbon monoxide (CO; 35 ppm; n = 19), or CAPs and CO (n = 24). Each exposure was immediately preceded and followed by a 1-h exposure to filtered air (baseline and postexposure periods, respectively). Surface electrocardiograms were recorded and the frequency of supraventricular premature beats was quantified. Among rats in the CAPS group, the probability of observing any SVA decreased from baseline to the exposure and postexposure periods. This pattern was significantly different than that observed for the filtered air group during the exposure period (p = .048) only. In the subset of rats with one or more SVA during the baseline period, the change in SVA rate from baseline to exposure period was significantly lower in the CAPS (p = .04) and CO (p = .007) groups only, as compared to the filtered air group. No significant effects were observed in the group simultaneously exposed to CAPS and CO. Thus, the results of this study do not support the hypothesis that exposure to ambient air pollution increases the risk or frequency of supraventricular arrhythmias.

Cardiac effects of carbon monoxide and ambient particles in a rat model of myocardial infarction.

Ambient air pollution is a complex mixture of particulate matter (PM) and gaseous pollutants such as carbon monoxide (CO). The effect of exposure to CO, alone or in combination with ambient PM, on arrhythmia incidence is unclear. To evaluate these effects, left-ventricular myocardial infarction was induced in Sprague-Dawley rats by thermocoagulation. Diazepam-sedated rats were exposed (1 h) to either filtered air (n = 40), CO (35 ppm, n = 19), concentrated air particles (CAPs, median concentration = 350.5 microg/m(3), n = 53), or CAPs and CO (CAPs median concentration = 318.2 microg/m(3), n = 23), 12-18 h after surgery. Each exposure was immediately preceded and followed by a 1 h exposure to filtered air (pre-exposure and post-exposure periods, respectively). The CO target dose of 35 ppm is related to the 1 h U.S. National Ambient Air Quality Standard. Surface electrocardiograms were recorded and heart rate and arrhythmia incidence were quantified. CO exposure reduced ventricular premature beat (VPB) frequency by 60.4% (p = 0.012) during the exposure period compared to controls. This effect was modified by both infarct type and the number of pre-exposure VPBs, and was not mediated through changes in heart rate. Overall, CAPs exposure increased VPB frequency during the exposure period, but this effect did not reach statistical significance. This effect was modified by the number of pre-exposure VPBs. Overall, neither CAPs nor CO had any effect on heart rate, but CAPs increased heart rate in specific subgroups. No significant interactions were observed between the effects of CO and CAPs. In this animal model, the responses to CO and CAPs are distinctly different.

Concentrated ambient air particles induce vasoconstriction of small pulmonary arteries in rats.

The objective of this study was to determine whether short-term exposures to concentrated ambient particles (CAPs) alter the morphology of small pulmonary arteries in normal rats and rats with chronic bronchitis (CB). Sprague-Dawley male rats were exposed to CAPs, using the Harvard Ambient Particle Concentrator, or to particle-free air (sham) under identical conditions during 3 consecutive days (5 hr/day) in six experimental sets. CB was induced by exposure to 276 +/- 9 ppm of sulfur dioxide (5 hr/day, 5 days/week, 6 weeks). Physicochemical characterization of CAPs included measurements of particle mass, size distribution, and composition. Rats were sacrificed 24 hr after the last CAPs exposure. Histologic slides were prepared from random sections of lung lobes and coded for blinded analysis. The lumen/wall area (L/W) ratio was determined morphometrically on transverse sections of small pulmonary arteries. When all animal data (normal and CB) were analyzed together, the L/W ratios decreased as concentrations of fine particle mass, silicon, lead, sulfate, elemental carbon, and organic carbon increased. In separate univariate analyses of animal data, the association for sulfate was significant only in normal rats, whereas silicon was significantly associated in both CB and normal rats. In multivariate analyses including all particle factors, the association with silicon remained significant. Our results indicate that short-term CAPs exposures (median, 182.75 micro g/m3; range, 73.50-733.00 micro g/m3) can induce vasoconstriction of small pulmonary arteries in normal and CB rats. This effect was correlated with specific particle components and suggests that the pulmonary vasculature might be an important target for ambient air particle toxicity.

Electrocardiographic changes during exposure to residual oil fly ash (ROFA) particles in a rat model of myocardial infarction.

Epidemiological studies have reported a positive association of short-term increases in ambient particulate matter (PM) with daily mortality and hospital admissions for cardiovascular disease. Although patients with cardiopulmonary disease appear to be most at risk, particulate-related cardiac effects following myocardial infarction (MI) have not been examined. To improve understanding of mechanisms, we developed and tested a model for investigating the effects of inhaled PM on arrhythmias and heart rate variability (HRV), a measure of autonomic nervous system activity, in rats with acute MI. Left-ventricular MI was induced in 31 Sprague-Dawley rats by thermocoagulation of the left coronary artery; 32 additional rats served as sham-operated controls. Diazepam-sedated rats were exposed (1 h) to residual oil fly ash (ROFA), carbon black, or room air at 12-18 h after surgery. Each exposure was immediately preceded and followed by a 1-h exposure to room air (baseline and recovery periods, respectively). Lead-II electrocardiograms were recorded. In the MI group, 41% of rats exhibited one or more premature ventricular complexes (PVCs) during the baseline period. Exposure to ROFA, but not to carbon black or room air, increased arrhythmia frequency in animals with preexisting PVCs. Furthermore, MI rats exposed to ROFA, but not to carbon black or room air, decreased HRV. There was no difference in arrhythmia frequency or HRV among sham-operated animals. These results underscore the usefulness of this model for elucidating the physiologic mechanisms of pollution-induced cardiovascular arrhythmias and contribute to defining the specific constituents of ambient particles responsible for arrhythmias.

Papel da histomorfometria óssea no diagnóstico diferencial da osteomalacia / Role of bone histomorphometry in the differential diagnosis of osteomalacia

A osteomalacia é uma doença ósteo-metabólica em que há deficiente mineralização do osso, e é definida pela histomorfometria óssea por apre-sentar espessura do rebordo osteóide (O.Th) maior do que 15µm, e inter-valo de tempo para mineralização (MLT) maior do que 100 dias. As princi-pais etiologias de osteomalacia são a deficiência de ação da vitamina D e a hipofosfatemia. Neste trabalho, 14 pacientes com osteomalacia diag-nosticados clínica e laboratorialmente foram divididos em dois grupos: 6 pacientes com deficiente ação de vitamina D e 8 hipofosfatêmicos. Todos os pacientes apresentaram ao exame histomorfométrico aumento do O.Th e do MLT compatível com o diagnóstico de osteomalacia. A superfície de reabsorção óssea estava aumentada no grupo com defi-ciência de ação da vitamina D. Em seis pacientes hipofosfatêmicos, a superfície de reabsorção óssea estava ausente, em um paciente dentro da normalidade mas em um paciente encontrava se aumentada. Con-clusão: a histomorfometria dinâmica óssea através da análise dos parâmetros de formação confirmam o diagnóstico de osteomalacia, enquanto que os parâmetros de reabsorção permitem uma orientação etiológica.