RESUMO
INTRODUCTION: Tobacco smoking leads to changes in hemodynamic parameters such as heart rate and systolic or diastolic blood pressure. It has a direct influence on the elasticity of blood vessels and increases arterial stiffness, which can result in development of atherosclerosis. Data show that the nicotine in tobacco smoke probably is responsible for these changes. Electronic cigarettes (e-cigarettes) were supposedly a healthier alternative to combustible cigarettes because they imitate a process of cigarettes smoking but generate nicotine aerosol without the toxic substances from tobacco combustion. However, the use of e-cigarettes is still controversial because their toxicity, safety and long term use health impact have not been sufficiently studied. AIM: The aim of this study was to evaluate changes in arterial stiffness parameters after smoking a cigarette or e-cigarette use. METHODS: Fifteen healthy women, aged 19-25 years old, smoking ≥5 cigarettes per day for at least two years participated in the study. A non-invasive measurement of arterial stiffness parameters - Stiffness Index (SI) and Reflection Index (RI) - was conducted and systolic and diastolic blood pressure and heart rate were measured before and after smoking a conventional cigarette as well as use of an e-cigarette. RESULTS: Statistically significant changes in the SI and RI were observed before and after smoking of a conventional cigarette [SI: 6.75m/s (6.66 - 6.85, 95% CI) vs 6.56m/s (6.46 - 6.65. 95% CI), p=0.0056; RI: 54.0% (51.5 - 56.7, 95% CI) vs 49.6% (47.5 - 51.8, 95% CI), p=0.010]. The use of e-cigarettes resulted in no statistically significant changes in the SI and RI. After both product use systolic and diastolic blood pressure and heart rate increased but the changes were not statistically significant. CONCLUSIONS: In contrast to conventional cigarette use, the use of electronic cigarettes causes no changes in arterial stiffness. This may indicate lower bioavailability of nicotine from the e-cigarette or an additional effect of other substances present in cigarette smoke but absent in an e-cigarette aerosol.
Assuntos
Artérias/efeitos dos fármacos , Nicotina/administração & dosagem , Fumar/efeitos adversos , Rigidez Vascular/efeitos dos fármacos , Administração por Inalação , Adulto , Artérias/fisiopatologia , Pressão Sanguínea/efeitos dos fármacos , Estudos Cross-Over , Sistemas Eletrônicos de Liberação de Nicotina , Feminino , Frequência Cardíaca/efeitos dos fármacos , Humanos , Fumaça/efeitos adversos , Poluição por Fumaça de Tabaco/efeitos adversos , Adulto JovemRESUMO
Iron is a transition metal that plays a crucial role in several physiological processes. It can also exhibit toxic effects on cells, due to its role in the formation of free radicals. Iron deficiency and anemia, as well as iron overload, are the result of impaired iron metabolism, in which a number of proteins, such as hepcidin, hemojuvelin and transferrin, take part. Iron deficiency is common in individuals with renal and cardiac transplants, while iron overload is more common in patients with hepatic transplantation. The current knowledge about iron metabolism in lung graft recipients and donors is limited. The problem is even more complex when we consider the fact that iron metabolism may be also driven by certain drugs used by graft recipients and donors. In this work, we overview the available literature reports on iron turnover in the human body, with particular emphasis on transplant patients, and we also attempt to assess the drugs' impact on iron metabolism, which may be useful in perioperative treatment in transplantology.
Assuntos
Anemia , Deficiências de Ferro , Sobrecarga de Ferro , Humanos , Ferro/metabolismo , Hepcidinas/metabolismo , Transferrina , Sobrecarga de Ferro/tratamento farmacológicoRESUMO
Enzymes of the cytochrome P-450 (CYP 450) which belong to the family of oxidase enzymes, are present in cells of all organisms and play a major role in the first phase of xenobiotic metabolism. There are several isoenzymes of CYP 450 that show differences in the speed of metabolism: poor-, extensive- and ultra-rapid. Nicotine undergoes biotransformation in the liver mainly by the CYP2A6 isoform of CYP 450. There are many polymorphic isoforms of CYP2A6 affecting the metabolism of nicotine. There are also several CYP2A6 activity inhibitors and inducers among commonly used drugs. The ability of CYP2A6 isozymes to activate certain procancerogenic substances present in cigarette smoke makes their polymorphism more significant. Moreover, some isoforms may have also influence on the risk of lung cancer development by affecting the enzymatic activation of tobacco-specific nitrosamines. Metabolism of nicotine, mainly through CYP2A6, has also many clinical implications, such as efficacy and safety of the nicotine replacement therapy (NRT) or occurrence of several diseases. In summary, type of the nicotine metabolism may be a potential predictor of the clinical outcomes in patients with cardiovascular disease, addicted to nicotine and in those using NRT. The purpose of this work is to summarize current knowledge on variation in genetically determined metabolism of nicotine and its clinical significance.