Microdialysis Assessment of Cerebral Perfusion during Cardiac Arrest, Extracorporeal Life Support and Cardiopulmonary Resuscitation in Rats – A Pilot Trial

Schober, Andreas; Warenits, Alexandra-Maria; Testori, Christoph; Weihs, Wolfgang; Hosmann, Arthur; Högler, Sandra; Sterz, Fritz; Janata, Andreas; Scherer, Thomas; Magnet, Ingrid Anna Maria; Ettl, Florian; Laggner, Anton N.; Herkner, Harald; Zeitlinger, Markus

doi:10.1371/journal.pone.0155303

Cited by 12 publications

(10 citation statements)

References 27 publications

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“…Excessive neuronal depolarization after a brain injury results in intracellular Ca 2+ overload and sustained glutamate release (excitotoxicity) (Chamoun et al , 2010 ; Schober et al , 2016 ). Moreover, extracellular glutamate levels are further increased by pathological reversal of astrocytic glutamate transporters (Gouix et al , 2009 ).…”

Section: Classic Mechanisms Mediating Neuroprotective Hypothermiamentioning

confidence: 99%

A New Vision for Therapeutic Hypothermia in the Era of Targeted Temperature Management: A Speculative Synthesis

Jackson

Kochanek

2019

Therapeutic Hypothermia and Temperature Management

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Three decades of animal studies have reproducibly shown that hypothermia is profoundly cerebroprotective during or after a central nervous system (CNS) insult. The success of hypothermia in preclinical acute brain injury has not only fostered continued interest in research on the classic secondary injury mechanisms that are prevented or blunted by hypothermia but has also sparked a surge of new interest in elucidating beneficial signaling molecules that are increased by cooling. Ironically, while research into cold-induced neuroprotection is enjoying newfound interest in chronic neurodegenerative disease, conversely, the scope of the utility of therapeutic hypothermia (TH) across the field of acute brain injury is somewhat controversial and remains to be fully defined. This has led to the era of Targeted Temperature Management, which emphasizes a wider range of temperatures (33–36°C) showing benefit in acute brain injury. In this comprehensive review, we focus on our current understandings of the novel neuroprotective mechanisms activated by TH, and discuss the critical importance of developmental age germane to its clinical efficacy. We review emerging data on four cold stress hormones and three cold shock proteins that have generated new interest in hypothermia in the field of CNS injury, to create a framework for new frontiers in TH research. We make the case that further elucidation of novel cold responsive pathways might lead to major breakthroughs in the treatment of acute brain injury, chronic neurological diseases, and have broad potential implications for medicines of the distant future, including scenarios such as the prevention of adverse effects of long-duration spaceflight, among others. Finally, we introduce several new phrases that readily summarize the essence of the major concepts outlined by this review—namely, Ultramild Hypothermia, the “Responsivity of Cold Stress Pathways,” and “Hypothermia in a Syringe.”

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Section: Classic Mechanisms Mediating Neuroprotective Hypothermiamentioning

confidence: 99%

A New Vision for Therapeutic Hypothermia in the Era of Targeted Temperature Management: A Speculative Synthesis

Jackson

Kochanek

2019

Therapeutic Hypothermia and Temperature Management

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“…LPR had a five-fold increase from baseline levels, and peaked 8 min after return of spontaneous circulation. Glutamate also had a marked increase (3.5-fold) after CA [ 116 ].…”

Section: Microdialysismentioning

confidence: 99%

“…Overall, microdialysis has proven useful in clinical settings to monitor cerebral metabolism in critically ill neurological and neurosurgical patients, enabling physicians to provide more effective treatment depending on which biochemical signals are present [ 117 ]. However, recent studies have demonstrated the growing applications for this tool, used not only for detection of ischemia and distinguishing ischemia from mitochondrial dysfunction, but also detection of successful reperfusion, even comparing different methods of resuscitation [ 116 ]. The growing trend of extended neuromonitoring including devices such as microdialysis is used to gain more personalized information about the patient and their specific brain injury, and thus facilitating the physicians’ decision making in terms of which treatments to pursue [ 118 ].…”

Section: Microdialysismentioning

confidence: 99%

Pathophysiology and the Monitoring Methods for Cardiac Arrest Associated Brain Injury

Reis

Akyol

Araujo

et al. 2017

IJMS

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Cardiac arrest (CA) is a well-known cause of global brain ischemia. After CA and subsequent loss of consciousness, oxygen tension starts to decline and leads to a series of cellular changes that will lead to cellular death, if not reversed immediately, with brain edema as a result. The electroencephalographic activity starts to change as well. Although increased intracranial pressure (ICP) is not a direct result of cardiac arrest, it can still occur due to hypoxic-ischemic encephalopathy induced changes in brain tissue, and is a measure of brain edema after CA and ischemic brain injury. In this review, we will discuss the pathophysiology of brain edema after CA, some available techniques, and methods to monitor brain oxygen, electroencephalography (EEG), ICP (intracranial pressure), and microdialysis on its measurement of cerebral metabolism and its usefulness both in clinical practice and possible basic science research in development. With this review, we hope to gain knowledge of the more personalized information about patient status and specifics of their brain injury, and thus facilitating the physicians’ decision making in terms of which treatments to pursue.

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“…Except for Hc, our model revealed absence of histological signs for neurodegeneration or gliosis at this late time point (7,9,74). It has been shown, that the duration and the depth of the ischemic insult affect the chronology of the manifestation of neuronal damage in the different brain regions (75).…”

Section: Discussionmentioning

confidence: 63%

Motor Cortex and Hippocampus Display Decreased Heme Oxygenase Activity 2 Weeks After Ventricular Fibrillation Cardiac Arrest in Rats

et al. 2020

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Microdialysis Assessment of Cerebral Perfusion during Cardiac Arrest, Extracorporeal Life Support and Cardiopulmonary Resuscitation in Rats – A Pilot Trial

Cited by 12 publications

References 27 publications

A New Vision for Therapeutic Hypothermia in the Era of Targeted Temperature Management: A Speculative Synthesis

A New Vision for Therapeutic Hypothermia in the Era of Targeted Temperature Management: A Speculative Synthesis

Pathophysiology and the Monitoring Methods for Cardiac Arrest Associated Brain Injury

Motor Cortex and Hippocampus Display Decreased Heme Oxygenase Activity 2 Weeks After Ventricular Fibrillation Cardiac Arrest in Rats

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