Muerte encefálica: repercusión sobre órganos y tejidos

Domínguez-Roldán, José María; García-Alfaro, C.; Jimenez-Gonzalez, P.I.; Hernandez-Hazañas, F.; Castillo, María Eugenia; Egea-Guerrero, Juan José

doi:10.1016/j.medin.2009.03.008

Cited by 16 publications

(13 citation statements)

References 33 publications

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“…Such factors as polytrauma, hypoxia, and intracranial bleeding can influence the course of the inflammatory process triggered by BD in different organs (1,2). To evaluate the role of BD-associated trauma, matching sham-operated rats were assessed over time.…”

Section: Discussionmentioning

confidence: 99%

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Paradoxical effects of brain death and associated trauma on rat mesenteric microcirculation: an intravital microscopic study

Simas¹,

Sannomiya²,

Cruz³

et al. 2012

Clinics

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OBJECTIVE:Experimental findings support clinical evidence that brain death impairs the viability of organs for transplantation, triggering hemodynamic, hormonal, and inflammatory responses. However, several of these events could be consequences of brain death–associated trauma. This study investigated microcirculatory alterations and systemic inflammatory markers in brain-dead rats and the influence of the associated trauma.METHOD:Brain death was induced using intracranial balloon inflation; sham-operated rats were trepanned only. After 30 or 180 min, the mesenteric microcirculation was observed using intravital microscopy. The expression of P-selectin and ICAM-1 on the endothelium was evaluated using immunohistochemistry. The serum cytokine, chemokine, and corticosterone levels were quantified using enzyme-linked immunosorbent assays. White blood cell counts were also determined.RESULTS:Brain death resulted in a decrease in the mesenteric perfusion to 30%, a 2.6-fold increase in the expression of ICAM-1 and leukocyte migration at the mesentery, a 70% reduction in the serum corticosterone level and pronounced leukopenia. Similar increases in the cytokine and chemokine levels were seen in the both the experimental and control animals.CONCLUSION:The data presented in this study suggest that brain death itself induces hypoperfusion in the mesenteric microcirculation that is associated with a pronounced reduction in the endogenous corticosterone level, thereby leading to increased local inflammation and organ dysfunction. These events are paradoxically associated with induced leukopenia after brain damage.

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Section: Discussionmentioning

confidence: 99%

“…Brain death (BD) triggers a series of hemodynamic, hormonal, and inflammatory effects that have different roles in the organs that may be transplanted (2). The systemic effects of BD include increased expression of adhesion molecules, increased leukocyte infiltration of different organs, and increased serum cytokine levels (1-3).…”

Section: Introductionmentioning

confidence: 99%

Paradoxical effects of brain death and associated trauma on rat mesenteric microcirculation: an intravital microscopic study

Simas¹,

Sannomiya²,

Cruz³

et al. 2012

Clinics

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“…Cerebral injury is correlated to the abundant synthesis of inflammatory cytokines during CA and resuscitation (61,62). In the brain, cytokines are not only produced by the cells of the immune system, but also expressed in resident brain cells, including neurons and glia (63).…”

Section: Role Of Cytokines In Cerebral Injury Following Ca and Resuscmentioning

confidence: 99%

Inflammatory mechanisms involved in brain injury following cardiac arrest and cardiopulmonary resuscitation

et al. 2016

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Abstract. Cardiac arrest (CA) is a leading cause of fatality and long-term disability worldwide. Recent advances in cardiopulmonary resuscitation (CPR) have improved survival rates; however, the survivors are prone to severe neurological injury subsequent to successful CPR following CA. Effective therapeutic options to protect the brain from CA remain limited, due to the complexities of the injury cascades caused by global cerebral ischemia/reperfusion (I/R). Although the precise mechanisms of neurological impairment following CA-initiated I/R injury require further clarification, evidence supports that one of the key cellular pathways of cerebral injury is inflammation. The inflammatory response is orchestrated by activated glial cells in response to I/R injury. Increased release of danger-associated molecular pattern molecules and cellular dysfunction in activated microglia and astrocytes contribute to ischemia-induced cytotoxic and pro-inflammatory cytokines generation, and ultimately to delayed death of neurons. Furthermore, cytokines and adhesion molecules generated within activated microglia, as well as astrocytes, are involved in the innate immune response; modulate influx of peripheral immune and inflammatory cells into the brain, resulting in neurological injury. The present review discusses the molecular aspects of immune and inflammatory mechanisms in global cerebral I/R injury following CA and CPR, and the potential therapeutic strategies that target neuroinflammation and the innate immune system.

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“…(Schrader et al,1985). Imediatamente após a morte encefálica ocorre um pico hipertensivo, com perda da atividade do núcleo vagal, caracterizada pela máxima estimulação da atividade simpática (Barklin, 2009;Domínguez-Roldán et al, 2009). O pico hipertensivo decorre do aumento de catecolaminas séricas, fase denominada de tempestade autonômica ou de catecolaminas, com liberação massiva de substâncias vasoativas que provocam vasoconstrição generalizada e redução do fluxo sanguíneo para os órgãos.…”

Section: Morte Encefálicaunclassified

“…O pico hipertensivo decorre do aumento de catecolaminas séricas, fase denominada de tempestade autonômica ou de catecolaminas, com liberação massiva de substâncias vasoativas que provocam vasoconstrição generalizada e redução do fluxo sanguíneo para os órgãos. A extensa vasoconstrição periférica leva à isquemia; o metabolismo se _______________________________________________________________________________________________________________________________________________________________________ _______________________________________________________________________________________________________________________________________________________________________________________________________________________ altera de aeróbico para anaeróbico; por fim ocorre vasodilatação, hipovolemia e disfunção cardíaca (Barklin, 2009;Domínguez-Roldán et al, 2009). O episódio hipotensivo, que se segue ao pico hipertensivo, ocorre principalmente como consequência da vasodilatação (Chamorro et al, 2009;Skrabal et al, 2005) (Skrabal et al, 2005;Domínguez-Roldán et al, 2009).…”

Section: Morte Encefálicaunclassified

Estudo dos processos de mobilização, ativação e apoptose das células da medula óssea em modelo de morte encefálica em ratos

Menegat¹

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Muerte encefálica: repercusión sobre órganos y tejidos

Abstract: Brain death is accompanied by a series of hemodynamic, hormonal and inflammatory systemic effects that have an important repercussion on the economy of the organs and ARTICLE IN PRESS 0210-5691/$ -see front matter & 2009 Elsevier España, S.L. y SEMICYUC. Todos los derechos reservados.

Cited by 16 publications

References 33 publications

Paradoxical effects of brain death and associated trauma on rat mesenteric microcirculation: an intravital microscopic study

Paradoxical effects of brain death and associated trauma on rat mesenteric microcirculation: an intravital microscopic study

Inflammatory mechanisms involved in brain injury following cardiac arrest and cardiopulmonary resuscitation

Estudo dos processos de mobilização, ativação e apoptose das células da medula óssea em modelo de morte encefálica em ratos

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