Objetivo Avaliar os efeitos do tabagismo sobre o sistema cardiovascular, através de metodologia não invasiva, analisando as alterações hemodinâmicas clínicas e propriedades elásticas arteriais, após exposição ao fumo. Métodos Estudo realizado em 45 voluntários sendo 18 (F) e 27 (M), fumantes T (n = 25, idade 40 ± 9 anos) e não fumantes NT (n = 20, idade 39 ± 9 anos), que foram submetidos a determinação do monóxido de carbono (CO) e avaliação das propriedades elásticas arteriais por ultrassonografia e teste de função endotelial (hiperemia reativa - HR) antes (B1) e após (B2) a exposição por 20 minutos a um cigarro ou à degustação de uma bala. Resultados Os grupos NT e T mostraram-se homogêneos. A concentração de CO no grupo T era maior do que no grupo NT em condições basais. A concentração de CO no grupo NT não variou antes e após à exposição proposta (bala) mas no grupo T aumentou de maneira significante após o cigarro. A pressão arterial sistólica (PAS) foi igual no B1 nos dois grupos, mas significativamente maior no B2 para o Gr T. A pressão arterial diastólica (PAD) no B1 e B2 não mostrou variação estatísticamente significante nos dois grupos. A freqüência cardíaca (FC) apresentou comportamento estatisticamente diferente nos dois grupos (NT apresentou redução e T apresentou aumento). Em relação às propriedades elásticas arteriais e resposta do fluxo regional: a complacência e a distensibilidade já se mostraram diferentes (p < 0,001) no período basal sendo maior no grupo NT comparado ao grupo T; mas após a HR 1 e 2, o grupo T mostrou elevação estatísticamente significante destas duas propriedades, sendo que o grupo NT não mostrou tais achados. O diâmetro máximo da artéria braquial mostrou-se aumentado em relação ao basal tanto após HR1 como após HR2 apenas no grupo T. O índice de fluxo total (IFT) não era diferente nos dois grupos no B1 e B2, mas após HR 1 e 2 ambos mostraram aumentos significantes (p < 0,001). Houve correlação positiva entre variáveis CO com PAD e FC no grupo T. No grupo NT não houve correlação do CO com PAS, PAD ou FC. Conclusão O tabagismo altera as propriedades elásticas das artérias e tem papel na hemodinâmica com provável participação do monóxido de carbono. / Objective to evaluate the effects of cigarette smoking on cardiovascular system, with non-invasive methodology, analysing hemodynamic disturbs and arterial elastic properties after being exposed to tobacco. METHODS This study was realized in 45 volunteers, 18 female and 27 male smokers T (n=25, age 40 ± 9 years) and non-smokers NT (n=20, age 39 ± 9 years), who were submitted to the determination of carbon monoxide (CO) to the evaluation of the arterial elastic properties by ultrassonography and test endotelial function (reactive hyperemia - HR) before (B1) and after (B2) the exposition for 20 minutes to a cigarette or a candy. RESULTS Both NT and T groups were similar.The CO concentration in the T group was higher than in the NT group on basal conditions. The CO concentration in the NT group have not changed before and after the proposed exposition (candy) but in the T group it was significant in creased after the cigarette exposition.The systolic blood pressure (PAS) was similar on B1 for both groups, but it was significantly higher on B2 for the T group. The diastolic blood pressure (PAD) on B1 and B2 didn´t exposition significant statistical variation on both groups. The cardiac frequency (FC) presented a different result for both groups with statistical significance ( NT had decrease and T had improved). Regarding the arterial elastic properties and the regional flux response: the complacence and the distensibility were different (p < 0,001) in the basal period and they were higher in the NT group compared to the T group. After HR 1 and 2, the T group showed a significant statistical increase of those two properties and the NT group didn´t show those results. The righest diameter of the brachial artery was increased in relation to the basal diameter after HR1 as well as after HR2 only in the T group. The total flux index (IFT) were not different in both groups in B1 and B2, but after HR1 and 2 both showed significant increase (p < 0,001). There was a positive correlation between the CO variations in relation to PAD and FC in the T group. In the NT group there was a no correlation of CO with PAS, PAD or FC. CONCLUSION Cigarette smoking changes the arterial elastic properties and it has a role in the hemodynamic with possible participation of the carbon monoxide

Indiana University-Purdue University Indianapolis (IUPUI) / Streptococcus mutans is a key contributor to dental caries. Smokers have increased caries, but the association between tobacco, nicotine, caries and S. mutans growth is little investigated. In the first section, seven S. mutans strains were used for screening. The minimum inhibitory concentration (MIC), minimum bactericidal concentration (MBC), and minimum biofilm inhibitory concentration (MBIC) were 16 mg/ml (0.1 M), 32 mg/ml (0.2 M), and 16 mg/ml (0.1 M), respectively, for most of the S. mutans strains. Growth of planktonic S. mutans cells was significantly repressed by 2.0-8.0 mg/ml nicotine concentrations. Biofilm formation and metabolic activity of S. mutans was increased in a nicotine-dependent manner up to 16.0 mg/ml. Scanning electron microscopy (SEM) revealed higher nicotine-treated S. mutans had thicker biofilm and more spherical bacterial cells than lower concentrations of nicotine. In the second section, confocal laser scanning microscopy (CLSM) results demonstrated that both biofilm bacterial cell numbers and extracellular polysaccharide (EPS) synthesis were increased by nicotine. Glucosyltransferase (Gtf) and glucan binding protein A (GbpA) protein expression of S. mutans planktonic cells were upregulated, while GbpB protein expression of biofilm cells were downregulated by nicotine. The mRNA expression of those genes were mostly consistent with their protein results. Nicotine was not directly involved in S. mutans LDH activity. However, since it increased the total number of bacterial cells in biofilm; total LDH activity of S. mutans biofilm was increased. In the third section, a PCR-based multiple species cell counting (PCR-MSCC) method was designed to investigate the effect of nicotine on S. mutans in a ten mixed species culture. The absolute S. mutans number in mixed biofilm culture was increased but the percentage of S. mutans in the total number of bacterial cells was not changed. In conclusion, nicotine enhanced biofilm formation and biofilm metabolism of S. mutans, through stimulating S. mutans planktonic cell Gtfs and Gbps expression. This leads to more planktonic cells attaching to dental biofilm. Increased S. mutans cell numbers, in biofilms of single species or ten mixed species, resulted in higher overall LDH activity. More lactic acid may be generated and contribute to caries development in smokers.