RESUMO
Introduction: Mortality data make it possible to develop indicators to guide the planning of health promotion and prevention actions in order to reduce mortality from preventable causes. However, there are no publications on physicians' mortality in the state of Espírito Santo, Brazil. Objectives: To describe mortality distribution and potential years of life lost from 2006 to 2015 among physicians who lived in Espírito Santo. Methods: This is a descriptive study of secondary data from the Mortality Information System of the Brazilian Ministry of Health. The distribution of socio-demographic variables and of basic cause of death was studied by absolute and relative frequencies. Potential years of life lost in each death were considered the years remaining from age at death up to the age limit of 70 years. Results: There were 20 deaths of female physicians (14.5%) and 118 (85.5%) of male physicians, with predominance of whites (87.9%) and married (56%) individuals. The main causes of death were neoplasms (39.1%), diseases of the circulatory system (19.6%), and external causes (19.6%). The majority of female and male deaths occurred from 60 to 69 years, but average death was significantly lower among women compared to men (respectively 58.3 and 67.0 years). Potential years of life lost totaled 1,226 years, with a mean of 14.6, which was greater in women (20.4) compared to men (13.4). Conclusions: Mortality trends observed in the general population were also present among physicians in Espírito Santo. However, contrary to the general population pattern, average death age was lower in women. Early mortality caused many lost years of life, especially among women.
RESUMO
Cardiovascular diseases are among the main causes of mortality in the world. There is evidence of cardiovascular harm after exposure to low lead or mercury concentrations, but the effects of chronic exposure to the association of low doses of these toxic metals are still unknown. This work evaluated after 4 weeks, the association effects of low concentrations of lead and mercury on blood pressure and vascular resistance reactivity. Wistar rats were exposed for 28 days to lead acetate (1st dose of 4 µg/100 g and subsequent doses of 0.05 µg /100 g/day to cover daily losses) and mercury chloride (1st dose of 2.17 µg/kg and subsequent doses of 0.03 µg/kg/ day to cover daily losses) and the control group received saline, i.m. Results showed that treatment increased blood pressure and induced left ventricular hypertrophy. The mesenteric vascular reactivity to phenylephrine and the endothelium-dependent vasodilator response assessed by acetylcholine did not change. Additionally, reduced involvement of vasoconstrictor prostanoids derived from cyclooxygenase was observed in the PbHg group. By other regulatory routes, such as potassium channels, the vessel showed a greater participation of BKCa channels, and a reduction in the participation of Kv channels and SKCa channels. The endothelium-independent smooth muscle relaxation was significantly impaired by reducing cGMP, possibly through the hyperstimulation of Phosphodiesterase-5 (PDE5). Our results suggested that exposure to low doses of lead and mercury triggers this compensatory mechanism, in response to the augment of arterial pressure.
