P57 Effective combination treatments for cerebral resuscitation from cardiac arrest in dogs. Exploratory studies

Ebmeyer, Uwe; Šafář, Peter; Radovsky, Ann; Sharma, Cordelia; Tanigawa, Keiichiro; Wang, Y.; Capone, Antonio; Xiao, Feng; Bircher, N.; Stezoski, William; Alexander, Henry

doi:10.1016/0300-9572(94)90181-3

Cited by 12 publications

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“…Based on the postulated hypothesis that the pathophysiologic mechanisms of brain damage caused by CA and resuscitation are complicated and multifactorial, multifaceted mechanism-orientated and outcome-targeted combination treatment strategies are needed. 2,154 Secondary to the evidence that mild hypothermia (34ЊC) significantly improves overall and neurologic outcome in CA patients, 143,144 in dogs after 11 minutes of ventricular fibrillation (VF)-induced CA, 155 and in rats after 8 minutes of asphyxiationinduced CA, 156 and attenuates brain edema formation induced by asphyxial CA, 9 we postulate that an optimal approach to maximize neurologic protection and resuscitation after CA will be mild hypothermia combined with the effective, mechanism-orientated and outcome-targeted agents. A clinically feasible cooling method, namely, peritoneal lavage, was initiated by the author of this paper in 1993 and has been effectively used in dog CA models.…”

Section: Brain Edema-mitigating Interventions In Experimental and CLImentioning

confidence: 99%

Bench to Bedside: Brain Edema and Cerebral Resuscitation: The Present and Future

Xiao

2002

Acad Emergency Med

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Sudden cardiac arrest (CA) claims approximately 1,200 lives daily in the United States. Cardiopulmonary resuscitation attempts have so far achieved suboptimal results, and even when restoration of spontaneous circulation (ROSC) is achieved, about 30% of survivors suffer permanent brain damage. This illustrates the need for an improved basic scientific understanding of the pathophysiology of global cerebral injury caused by whole-body ischemia/reperfusion (I/R) injury following CA. Brain edema has been recently documented in experimental CA followed by one hour of ROSC. Brain edema has also been documented in CA and stroke patients by computed tomography or magnetic resonance imaging scanning, and has been shown to predict a poor neurologic outcome. The mechanisms underlying brain edema formation elicited by CA are unclear. New scientific findings of the roles of blood-brain barrier (BBB) permeability, matrix metalloproteinases (MMPs) of a family of proteases, aquaporin 4 (AQP4) of a family of membrane water-channel proteins, and the N-methyl-D-aspartate (NMDA) receptors in the mechanisms underlying CA-elicited brain edema were reviewed. By defining the roles of BBB permeability, MMPs, AQP4, and NMDA receptors in CA-induced brain edema formation, effective new therapeutic strategies to extend cellular and tissue survival, and preserve neurologic function following CA may be feasible.

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