Inflammatory mediators of neuropathic pain / Mediadores inflamatórios na dor neuropática

ABSTRACT BACKGROUND AND OBJECTIVES: Pro-inflammatory chemical mediators and algogenic substances seem to be confused by the sharing of their actions and by interactions in painful and inflammatory presentation. This study aimed at presenting a review of major inflammatory chemical mediators and place them in neuropathic pain pathophysiology. CONTENTS: Inflammation is the homeostatic response of vascularized tissues to remove harmful agents and restore their normal functions. Nervous system (central and/or peripheral) diseases and injuries may induce neuropathic pain and may also modify inflammatory process nervous mediation. In such pathological conditions, there might be pain without restrict link with admitedly harmful or painful stimuli, as well as there might be inflammation without restrict link with the presence of harmful agents and the need to remove them. Chemical mediators involved in neuropathic pain and inflammation pathophysiology modulate the presentation of both. CONCLUSION: Studies on inflammation offer evidences to support the important role of their chemical mediators in neuropathic pain pathogenesis. In peripheral and central sensitization, a thin borderline between reversibility or not of neuropathic pain may be respected or exceeded by inflammatory mediators actions.

RESUMO JUSTIFICATIVA E OBJETIVOS: Mediadores químicos pró-inflamatórios e substâncias algogênicas parecem se confundir pelo compartilhamento de suas ações e pelas interações no quadro doloroso e inflamatório. O objetivo deste estudo foi apresentar uma revisão sobre os principais mediadores químicos inflamatórios e situá-los na fisiopatologia da dor neuropática. CONTEÚDO: A inflamação é a resposta homeostática de tecidos vascularizados no sentido de remoção de agentes lesivos e restauro de suas funções normais. Doenças e lesões no sistema nervoso (central e/ou periférico) podem causar dor neuropática, e, também modificar a mediação nervosa do processo inflamatório. Nessas condições patológicas a dor pode ocorrer sem o vínculo restrito com estímulo reconhecidamente nocivo ou doloroso, assim como ocorrer quadro inflamatório sem o vínculo restrito com a presença de agentes lesivos e a necessidade de removê-los. Os mediadores químicos envolvidos na fisiopatologia da dor neuropática e da inflamação modulam o quadro de ambas. CONCLUSÃO: Os estudos sobre inflamação oferecem evidências para embasar a importância do papel dos seus mediadores químicos na patogênese da dor neuropática. Na sensibilização periférica e, também na central uma fronteira tênue entre a reversibilidade ou não do quadro neuropático pode ser respeitada ou ultrapassada pelas ações de mediadores inflamatórios.

Importancia de las medidas analgésicas en pacientes sometidos a operaciones bucales / Importance of the analgesic measures In subjected patients to buccal operations

Introducción: el dolor lo experimentan todos aquellos seres vivos que disponen de un sistema nervioso y su función es señalar al mismo la zona del organismo expuesta a un daño tisular. Esta señal de alarma desencadena una serie de mecanismos que evita o limita los daños y hace frente al estrés. Objetivo: profundizar en el conocimiento del bloqueo del dolor, tanto periférico como central, que fármacos como los analgésicos pueden ocasionar en tejidos dañados por actos quirúrgicos severos. Material y Método: se realizó una revisión bibliográfica sobre estos aspectos, con un enfoque multidisciplinario y básico-clínico. Se utilizó el método documental para el análisis y tratamiento de la información ofrecida por las fuentes teóricas. PubMed fue utilizada como fundamental fuente de búsqueda y otras bases de datos también consultadas fueron Lilacs, Hinari y Medline. Desarrollo: los neurotransmisores vinculados a la nocicepción son de dos tipos: glutamato y neuropéptidos. En las lesiones severas o persistentes, las fibras C descargan de manera continua y la respuesta de las neuronas nociceptoras del núcleo caudal del trigémino aumenta progresivamente con el tiempo (este fenómeno se denomina wind-up o "de dar cuerda"). Esto es consecuencia de un cambio en la eficacia de las sinapsis glutamatérgicas entre los axones de los nociceptores periféricos y las neuronas del núcleo caudal. Medicamentos como la dipirona y el acetominofen inhiben la generación de la señal dolorosa y la sensibilización concomitante en la terminación nerviosa mediante la interrupción de la síntesis de prostaglandinas. Conclusión: el uso de analgésicos en los primeros estadios de iniciarse la inflamación evita la acumulación de mediadores químicos en la zona dañada y la activación (perpetuación) de la señal nociceptiva.

Introduction: the pain experiences it all those alive beings that have a nervous system and its function is to point out to the same one the area of the organism exposed to a tissular damage. This alarm sign unchains a series of mechanisms that they avoid or they limit the damages and they make in front of the stress. Objective: to deepen in the knowledge of the blockade of the pain, so much outlying as central that drugs like the analgesic ones can cause in tissues damaged by severe surgical acts. Material and Method: was carried out a bibliographical review on these aspects, with a multidisciplinary and basic-clinical focus. The documental method was used for the analysis and treatment of the information offered by the theoretical sources. PubMed was also used as fundamental search source, and other databases consulted they were Lilacs, Hinari and Medline. Development: the tied neurotransmisores to the nocicepción is of two types: glutamate and neuropéptidos. In the severe or persistent lesions, the fibers C discharges in a continuous way and the answer of the neurons nociceptoras of the nucleus flow of the trigémino increases progressively with the time (this phenomenon is denominated wind-up or "of giving sensible"). This is consequence of a change in the effectiveness of the synapses glutamatérgicas between the axones of the outlying nociceptores and the neurons of the nucleus flow. Medications like the dipirona and the acetominofen inhibit the generation of the painful sign and the concomitant sensitization in the nervous termination by means of the interruption of the synthesis of prostaglandins. Conclusion: the use of analgesic in the first stadiums of beginning the inflammation avoids the accumulation of chemical mediators in the damaged area and the activation (perpetuation) of the sign nociceptiva.

Mast Cells and Allergic Rhinitis

That mast cells play a role in acute allergic inflammation by releasing various inflammatory mediators, including histamine, leukotrienes (LT), such as LTC4 and LTD4, and prostaglandins (PG), such as PGD2, is well known. Additionally, mast cells contribute to the development of allergic inflammation also through the release of multifunctional cytokines. The incidence of intraepithelial mast cells (IEMC) is found to be greater in nasal mucosa exposed to an allergen, and the cells are thought to play an important role in producing the immediate allergic reaction. Lamina propira mast cells (LPMC) are known to be the dominant source of TH2 cytokine and are responsible for development of the late phases of an allergic reaction They may upregulate the expression of adhesion molecules on the endothelial cells and induce basophil and eosinophil recruitment. Based on these consideration it can be proposed that mast cell is a initiating cell of allergic reaction in target organ and IEMC and LPMC have capacity to make major contribution to both immediate or late phase reaction of allergic rhinitis.

Segundos mensajeros / Second messengers

En esta revision se describen, de manera esquematica, los mecanismos de accion empleados por los Segundos Mensajeros comenzando por el estimulo del receptor y continuando con las reacciones en cadena que conducen finalmente a una respuesta celular.

This review schematically describes the different mechanisms of action that Second Messengers employ to stimulate receptors and then Initiate a chain of reactions that finally lead to appropriate cellular responses.