In vitro mucus transportability, cytogenotoxicity, and hematological changes as non-destructive physiological biomarkers in fish chronically exposed to metals.

The biomonitoring of fish using biomarkers represents a useful tool for the assessment of aquatic pollution. This study evaluated the sublethal toxic effects of aquatic pollution on fish collected from a site contaminated by metals. Water and fish (Oreochromis niloticus) samples were collected from a pond in the Parque Ecológico do Tietê (PET) that lies along the Tietê River (São Paulo, Brazil), and from a control site (an experimental fish farm). The metal content of the water was evaluated, and fish were used to examine the properties of gill mucus and blood. The PET fish were evaluated for alterations in the in vitro transportability of mucus and changes in blood properties (e.g., cell volume, hemoglobin concentration, red blood cells, and white blood cell count). The results of the water analyzes indicated metal levels above the legal standards for Fe (0.71 mg/L), Ni (0.06 mg/L), Mn (0.11 mg/L), and Pb (0.48 mg/L). Compared to the controls, the hematologic parameter analyzes of PET fish revealed significantly higher numbers of erythrocytes (RBC), leukocytes (WBC), lymphocytes, erythroblasts, and Mean Corpuscular Volume (MCV); however, the hemoglobin content and Mean Corpuscular Hemoglobin Concentration (MCHC) values were significantly lower. The frequencies of nuclear abnormalities and micronuclei were significantly higher and the mucociliary transport was significantly lower in PET fish than in the controls. These results suggest that fish from the contaminated site exhibit a series of physiological responses, which probably indicate health disturbances. Furthermore, the results suggest that blood and mucus are promising, non-destructive targets for use in the monitoring of pollution.

Acute cardiovascular and inflammatory toxicity induced by inhalation of diesel and biodiesel exhaust particles.

Analysis of fuel emissions is crucial for understanding the pathogenesis of mortality because of air pollution. The objective of this study is to assess cardiovascular and inflammatory toxicity of diesel and biodiesel particles. Mice were exposed to fuels for 1 h. Heart rate (HR), heart rate variability, and blood pressure were obtained before exposure, as well as 30 and 60 min after exposure. After 24 h, bronchoalveolar lavage, blood, and bone marrow were collected to evaluate inflammation. B100 decreased the following emission parameters: mass, black carbon, metals, CO, polycyclic aromatic hydrocarbons, and volatile organic compounds compared with B50 and diesel; root mean square of successive differences in the heart beat interval increased with diesel (p < 0.05) compared with control; low frequency increased with diesel (p < 0.01) and B100 (p < 0.05) compared with control; HR increased with B100 (p < 0.05) compared with control; mean corpuscular volume increased with B100 compared with diesel (p < 0.01), B50, and control (p < 0.001); mean corpuscular hemoglobin concentration decreased with B100 compared with B50 (p < 0.001) and control (p < 0.05); leucocytes increased with B50 compared with diesel (p < 0.05); platelets increased with B100 compared with diesel and control (p < 0.05); reticulocytes increased with B50 compared with diesel, control (p < 0.01), and B100 (p < 0.05); metamyelocytes increased with B50 and B100 compared with diesel (p < 0.05); neutrophils increased with diesel and B50 compared with control (p < 0.05); and macrophages increased with diesel (p < 0.01), B50, and B100 (p < 0.05) compared with control. Biodiesel was more toxic than diesel because it promoted cardiovascular alterations as well as pulmonary and systemic inflammation.

Effects of positive end-expiratory pressure in an experimental model of acute myocardial infarct in wistar rats.

UNLABELLED: Our purpose in this study was to access the pulmonary effects of mechanical ventilation with positive end-expiratory pressure (PEEP; 10 cmH2O) or without PEEP (zero PEEP-ZEEP) in a rat model of acute myocardial infarction that resulted in hypotension but not in pulmonary congestion. METHODS: Wistar rats were anesthetized (1.5% isoflurane) and myocardial infarct was induced by ligature of the anterior interventricular coronary artery. Rats with myocardial infarct were compared with sham-operated (Sham) and closed thorax groups. RESULTS AND CONCLUSION: There was a significant decrease in MAP in the acute myocardial infarct group (92.5 +/- 4.2 mmHg) when compared with closed chest group (113.0 +/- 4.4 mmHg). There was no significant difference between acute myocardial infarct and Sham groups in PEEP or ZEEP. Mechanical ventilation for 120 min resulted in a significant increase in respiratory system elastance in the groups ventilated with ZEEP (2.59 +/- 0.17 and 2.32 +/- 0.17 cmH2O.mL, Sham and acute myocardial infarct groups, respectively). This effect of mechanical ventilation was not observed in the presence of PEEP in both groups. There was no significant increase in the amount of perivascular pulmonary edema measured in all groups studied. Mean airspace linear intercept and lung tissue distortion index also did not show statistically significant difference between Sham and acute myocardial infarct groups. We conclude that in this experimental model of acute myocardial infarct (12.4 +/- 4.1% area of necrotic tissue and 26.4 +/- 4.0% area of ischemic tissue), there was a protective pulmonary effect of PEEP.

Effects of exercise training on papain-induced pulmonary emphysema in Wistar rats.

The purpose of the present study was to evaluate the role of exercise training on the development of papain-induced emphysema in rats. Our hypothesis was that the increase in pulmonary tissue stretching associated with exercise could increase the severity of a protease-induced emphysema. Wistar rats were randomly assigned to four groups (n = 10 for each group) that received, respectively, intratracheal infusion of papain (6 mg in 1 ml of 0.9% NaCl) or vehicle and were submitted or not to a protocol of exercise on a treadmill. Rats exercised at 13.3 m/min, 6 days/wk, for 9 wk (increasing exercise time, from 10 to 35 min). We measured respiratory system elastance and resistance, the size and weight of the heart, and pulmonary mean linear intercept (Lm). After 9 wk of exercise training, there were no differences in respiratory system resistance and elastance values among the four experimental groups. Volume of the heart was significantly greater in rats submitted to exercise training (P = 0.007) compared with sedentary rats due to increases in volumes of both right and left cardiac chambers. Lm was significantly greater in rats that received papain compared with saline-infused rats (P = 0.025). Surprisingly, this was true, even though there was no significant decrease in elastance, possibly due to connective tissue remodeling. However, Lm was significantly greater in papain + exercise rats compared with rats that received papain and were not submitted to exercise. We conclude that exercise training can increase alveolar damage induced by papain infusion.

Análise da remodelação vascular na isquemia pulmonar experimental, nas fases aguda e crônica / Analysis of acute and chronic vascular remodeling in an experimental model of pulmonary ischemia

INTRODUÇAO: Alterações estruturais da circulação pulmonar traduzem processo de remodelação vascular e têm relação provável com variações locais de fluxo e isquemia. OBJETIVO: Definir as alterações histológicas na circulação pulmonar após obstrução experimental da artéria pulmonar. Correlacioná-las com os padrões de redistribuição sangüínea e remodelação vascular. MÉTODO: Foram submetidos à toracotomia esquerda 48 ratos Wistar, alocados aleatoriamente em dois grupos, com ligadura da artéria pulmonar e controle, e sacrificados com 1, 7, 30 e 60 dias. Nos pulmões retirados avaliou-se presença de sinais de injúria no parênquima e mensurou-se diâmetro externo e espessura da parede das arteríolas de bronquíolos terminais, respiratórios e alveolares. Diâmetro interno e porcentagem de espessura da parede foram calculados. RESULTADOS: Só ocorreu infarto, necrose e hemorragia no pulmão isquêmico. No não isquêmico houve aumento mantido dos diâmetros externo e interno das arteríolas, com redução inicial da espessura no 1º dia e valores semelhantes aos do grupo controle no 60º dia. No pulmão isquêmico houve redução transitória nos diâmetros externo e interno das arteríolas de bronquíolos terminais e respiratórios, com aumento, inicial e transitório, na sua espessura. As arteríolas alveolares apresentaram aumento do diâmetro externo e espessura da parede, com redução do diâmetro interno, mantida e progressiva. CONCLUSAO: Este modelo reproduz arteriopatia distal em pacientes com tromboembolismo pulmonar crônico. A resposta vascular no pulmão não isquêmico é compatível com padrão de remodelação de hiperfluxo; a no pulmão isquêmico com hipofluxo e isquemia. Nas arteríolas de bronquíolos terminais e respiratórios a resposta foi transitória. Nas alveolares foi progressiva e mantida, pela provável ocorrência tardia de hiperfluxo local.