RESUMO
Sepsis and septic shock are major causes of mortality among hospitalized patients. The sepsis state is due to dysregulated host response to infection, leading to inflammatory damage to nearly every organ system. Early recognition of sepsis and appropriate treatment with antibiotics, fluids, and vasopressors is essential to reducing organ system injury and mortality. This review summarizes the current understanding of the epidemiology, pathophysiology, diagnosis, and treatment of sepsis and septic shock.
Assuntos
Tomada de Decisão Clínica , Escores de Disfunção Orgânica , Sepse/diagnóstico , Choque Séptico/diagnóstico , Pressão Sanguínea/efeitos dos fármacos , Serviço Hospitalar de Emergência , Mortalidade Hospitalar , Humanos , Classificação Internacional de Doenças , Taxa Respiratória , Sensibilidade e Especificidade , Sepse/fisiopatologia , Sepse/terapia , Choque Séptico/fisiopatologia , Choque Séptico/terapia , Síndrome de Resposta Inflamatória Sistêmica/diagnóstico , Terminologia como Assunto , Vasoconstritores/uso terapêuticoAssuntos
Azoospermia/fisiopatologia , Ductos Ejaculatórios/fisiopatologia , Infertilidade Masculina/fisiopatologia , Glândulas Seminais/fisiopatologia , Azoospermia/etiologia , Dilatação Patológica/diagnóstico por imagem , Dilatação Patológica/fisiopatologia , Ductos Ejaculatórios/diagnóstico por imagem , Humanos , Infertilidade Masculina/etiologia , Imageamento por Ressonância Magnética , Masculino , Pessoa de Meia-Idade , Glândulas Seminais/diagnóstico por imagemRESUMO
Small increases in physiological nitrite concentrations have now been shown to mediate a number of biological responses, including hypoxic vasodilation, cytoprotection after ischemia/reperfusion, and regulation of gene and protein expression. Thus, while nitrite was until recently believed to be biologically inert, it is now recognized as a potentially important hypoxic signaling molecule and therapeutic agent. Nitrite mediates signaling through its reduction to nitric oxide, via reactions with several heme-containing proteins. In this report, we show for the first time that the mitochondrial electron carrier cytochrome c can also effectively reduce nitrite to NO. This nitrite reductase activity is highly regulated as it is dependent on pentacoordination of the heme iron in the protein and occurs under anoxic and acidic conditions. Further, we demonstrate that in the presence of nitrite, pentacoordinate cytochrome c generates bioavailable NO that is able to inhibit mitochondrial respiration. These data suggest an additional role for cytochrome c as a nitrite reductase that may play an important role in regulating mitochondrial function and contributing to hypoxic, redox, and apoptotic signaling within the cell.