Biochemical Alterations in Cerebrospinal Fluid During Thoracoabdominal Aortic Cross-clamping in Dogs

Real-Time Monitoring of Mitochondrial NADH and Microcirculatory Blood Flow in the Spinal Cord

“…Simultaneously, the levels of Fluorescence and NADH rose, indicating tissue metabolic stress and mitochondrial dysfunction due to the deficit of oxygen, glucose, and other metabolites, shifting the energy equilibrium towards anaerobic metabolism, as was previously reported. 22,33 Once the reperfusion started, all of the fluorometric parameters fully recovered. The observed hyperemia was probably produced by autoregulation mechanisms activated by the sympathetic nervous system, as was previously reported for ischemia models in pigs and mice.…”

Biomarkers in spinal cord injury

“…Twelve studies investigated biomarkers in humans [22][23][24][25][26][27][28][29][30][31][32] and six studies investigated biomarkers in animals. [33][34][35][36][37][38] Relatively few studies have been performed in which biomarkers in serum and/or CSF after SCI were investigated. For those that have been conducted, S-100b and neuron-specific enolase (NSE) have especially received attention.…”

“…Another study simulating ischemic SCI using thoracoabdominal aortic cross-clamping in 10 dogs identified significantly elevated NSE levels in CSF during clamping and reperfusion. 35 Time-dependency of biomarkers Cao et al 38 evaluated the relationship between the protein levels of NSE and S-100b in serum and CSF and the severity of acute SCI in an animal model. Eighty Sprague-Dawley rats were divided into four groups: control group, mild SCI group, moderate SCI group and severe SCI group.…”

Heat shock proteins as biomarkers for the rapid detection of brain and spinal cord ischemia: a review and comparison to other methods of detection in thoracic aneurysm repair

“…Von Reyn examined sodium channel proteolysis from rat brain with calpain activation (von Reyn et al 2009) but again at longer time points. These studies are inconclusive; lactate appeared to correlate best with ischemic injuries (Brock et al 1997;Lindsay et al 1999;Nagy et al 2002). Recently, Sharp and colleagues described microRNA and gene expression profiles from rat brain and serum after ischemic stroke, induced seizures, and intracranial hemorrhage Zhang et al 2010), but again, these markers were not measured until 24 h after injury and are, therefore, not useful for rapid detection.…”

“…CSF bathes the neural tissues of the brain and spinal cord and should allow detection of the biochemical products of acute CNS ischemia more rapidly than in serum, particularly if the blood brain barrier is intact. Specific biochemical markers that have been examined to date include lactate, pCO 2 , neuron-specific enolase (NSE) (Nagy et al 2002), excitatory neurotransmitters such as glutamate, aspartate, glycine (Brock et al 1997), tau, glucose, pH, and S100β. These markers also markedly increase in serum at other times, including during surgical procedures unrelated to acute brain injury (Anderson et al 2001;Routsi et al 2006).…”