Endotoxemia induces lung-brain coupling and multi-organ injury following cerebral ischemia-reperfusion.

Endotoxemia induces lung-brain coupling and multi-organ injury following cerebral ischemia-reperfusion.
Exp Neurol. 2017 Jul 27;:
Authors: Mai N, Prifti L, Rininger A, Bazarian H, Halterman MW
Abstract
Post-ischemic neurodegeneration remains the principal cause of mortality following cardiac resuscitation. Recent studies have implicated gastrointestinal ischemia in the sepsis-like response associated with the post-cardiac arrest syndrome (PCAS). However, the extent to which the resulting low-grade endotoxemia present in up to 86% of resuscitated patients affects cerebral ischemia-reperfusion injury has not been investigated. Here we report that a single injection of low-dose lipopolysaccharide (50μg/kg, IP) delivered after global cerebral ischemia (GCI) induces blood-brain barrier permeability, microglial activation, cortical injury, and functional decline in vivo, compared to ischemia alone. And while GCI was sufficient to induce neutrophil (PMN) activation and recruitment to the post-ischemic CNS, minimal endotoxemia exhibited synergistic effects on markers of systemic inflammation including PMN priming, lung damage, and PMN burden within the lung and other non-ischemic organs including the kidney and liver. Our findings predict that acute interventions geared towards blocking the effects of serologically occult endotoxemia in survivors of cardiac arrest will limit delayed neurodegeneration, multi-organ dysfunction and potentially...

Source: Experimental Neurology - July 27, 2017 Category: Neurology Authors: Mai N, Prifti L, Rininger A, Bazarian H, Halterman MW Tags: Exp Neurol Source Type: research