Óxido nítrico: inibição das plaquetas e participação na formação do trombo Nitric oxide: inhibition of platelets and participation in thrombus formation

Neste artigo faremos uma revisão bibliográfica de modo que entendamos como o óxido nítrico (NO) atua sobre as plaquetas, compreendendo assim mais um mecanismo antiplaquetário. Nos últimos 25 anos a função do NO na biologia evoluiu do seu reconhecimento como poluente ambiental para substância endógena envolvida em comunicação intracelular e intercelular e na transdução de sinais. O NO é uma molécula polivalente que exerce um papel na regulação da hemostasia, sendo responsável pela inibição das plaquetas em todos os seus níveis de atuação, desde adesão até agregação, impedindo, dessa forma, posterior formação de trombo. Inúmeras desordens clínicas têm sido reportadas em que a insuficiência da produção de NO endógeno e, portanto, a ausência de inibição de ação plaquetária, parece contribuir para os eventos trombóticos.<br>In this article we make a review above the way that nitric oxide (NO) influence platelets over the past 25 years. The role of NO in biology has evolved from being recognized as an environmental pollutant to an endogenously produced substance involved in intracellular and intercellular communication and signal transduction. NO is a multifunctional molecule that plays a role in the regulation of hemostasis. It is responsible for platelets inhibition in all levels of its action, from adhesion to aggregation, preventing in this manner, thrombus formation. Several clinical disorders have been reported in which endogenous NO production insufficiency and, as a consequence, the absence of platelets action inhibition, seems to contribute to thrombotic events

Dexmedetomidine Use in the Setting of Cocaine-Induced Hypertensive Emergency and Aortic Dissection: A Novel Indication

Aortic dissection is a potentially fatal but rare disease characterized by an aortic intimal tear with blood passing into the media creating a false lumen and with resultant high mortality depending on the location of dissection if not aggressively treated. Cocaine users are known to have a higher incidence of aortic dissection. We report here aortic dissection in a patient with cocaine abuse which did not respond to traditional medication regimes used currently in this setting. Worth mentioning is the use of an alpha-2 receptor selective agonist named Dexmedetomidine as a treatment modality to control hypertension in this patient, which is approved only for sedation of intubated and mechanically ventilated patients in the intensive care settings and for sedation during invasive procedures. This paper illustrates the practical beneficial role of Dexmedetomidine in controling blood pressure in the settings of cocaine-induced sympathetic surge when other treatment modalities fail