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Introduction: In the dentistry practice, dentists are exposed to harmful effects caused by several factors, such as the noise produced by their work instruments. In 1959, the American Dental Association recommended periodical hearing assessments and the use of ear protectors. Aquiring more information regarding dentists', dental nurses', and prosthodontists' hearing abilities is necessary to propose prevention measures and early treatment strategies. Objective: To investigate the auditory thresholds of dentists, dental nurses, and prosthodontists. Method: In this clinical and experimental study, 44 dentists (Group I; GI), 36 dental nurses (Group II; GII), and 28 prosthodontists (Group III; GIII) were included, , with a total of 108 professionals. The procedures that were performed included a specific interview, ear canal inspection, conventional and high-frequency threshold audiometry, a speech reception threshold test, and an acoustic impedance test. Results: In the 3 groups that were tested, the comparison between the mean hearing thresholds provided evidence of worsened hearing ability relative to the increase in frequency. For the tritonal mean at 500 to 2,000 Hz and 3,000 to 6,000 Hz, GIII presented the worst thresholds. For the mean of the high frequencies (9,000 and 16,000 Hz), GII presented the worst thresholds. Conclusion: The conventional hearing threshold evaluation did not demonstrate alterations in the 3 groups that were tested; however, the complementary tests such as high-frequency audiometry provided greater efficacy in the early detection of hearing problems, since this population's hearing loss impaired hearing ability at frequencies that are not tested by the conventional tests. Therefore, we emphasize the need of utilizing high-frequency threshold audiometry in the hearing assessment routine in combination with other audiological tests.

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Contractile depression due to stunning has no effect on the inotropic stimulation generated by the Bowditch phenomenon. Immediate and time-dependent enhancements of contraction evoked by sudden VD are proportionally reduced and the slow response time course is unaffected in the stunned myocardium.

ObjectivesTo characterize an experimental model of pulmonary embolism by studying hemodynamics, lung mechanics and histopathologic derangements caused by pulmonary microembolism in pigs. To identify lung alterations after embolism that may be similar to those evidenced in pulmonary inflammatory conditions. Materials and methods Ten Large White pigs (weight 35-42 kg) were instrumented with arterial and pulmonary catheters, and pulmonary embolism was induced in five pigs by injection of polystyrene microspheres (diameter ~300 µM), in order to obtain a pulmonary mean arterial pressure of twice the baseline value. Five other animals injected with saline served as controls. Hemodynamic and respiratory data were collected and pressure x volume curves of the respiratory system were performed by a quasi-static low flow method. Animals were followed for 12 hours, and after death lung fragments were dissected and sent to pathology. Results Pulmonary embolism induced a significant reduction in stroke volume (71 ± 18 ml/min/bpm pre vs 36 ± 9 ml/min/bpm post, P < 0.05), an increase in pulmonary mean arterial pressure (27 ± 4 mmHg pre vs 39 ± 6 mmHg post, P < 0.05) and pulmonary vascular resistance (193 ± 122 mmHg/l/min pre vs 451 ± 149 mmHg/l/min post, P < 0.05). Respiratory dysfunction was evidenced by significant reductions in the PaO 2 /FiO 2 ratio (480 ± 50 pre vs 159 ± 55 post, P < 0.05), the dynamic lung compliance (27 ± 6 ml/cmH 2 O pre vs 19 ± 5 ml/cmH 2 O post, P < 0.05), the increase in dead space ventilation (20 ± 4 pre vs 47 ± 20 post, P < 0.05) and, the shift of pressure x volume curves to the right, with reduction in pulmonary hysteresis. Pathology depicted inflammatory neutrophil infiltrates, alveolar edema, collapse and hemorrhagic infarctions. Conclusion This model of embolism is associated with cardiovascular dysfunction, as well as respiratory injury characterized by a decrease in oxygenation, lung compliance and hysteresis. Pathology findings were similar to those verified in inflammatory pulmonary injury conditions. This model may be useful to study pathophysiology, as well as pharmacologic and ventilatory interventions useful to treat pulmonary embolism. P6 Hemodynamic and metabolic features of a porcine systemic low flow state modelObjective To describe a new experimental systemic low flow state model induced by cardiac tamponade. Methods Ten Large White pigs (43 ± 5 kg) were instrumented with arterial and pulmonary catheters, cystostomy and splenectomy, and a latex balloon was inserted anterior to the heart. Pigs were randomized to a shock group or a control group. The shock group had the balloon inflated with 620 ± 344 ml to keep the mean arterial blood pressure at 45-55 mmHg (mean = 49 ± 4 mmHg) for 1 hour. Hemodynamic data were collected and shown as the mean ± SD. Two-way ANOVA was used with Bonferroni's correction. Results During shock, the SvO 2 was 34 ± 8%, the heart rate was 173 ± 36 bpm, and the stroke volume was 18 ± 12 ml/min/beat. After shock, see Table 1. Conclusion In our model, transient...