Neuronal damage after hypothermic circulatory arrest and retrograde cerebral perfusion in the pig

Ye, Jian; Yang, Luojia; Bigio, Marc R. Del; Filgueiras, Carlos Luiz; Ede, Mauricio; Summers, Randy; Salerno, Tomás A.; Deslauriers, Roxanne

doi:10.1016/0003-4975(96)00076-8

Cited by 66 publications

(9 citation statements)

References 16 publications

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“…The specific domain that may be affected by retrograde cerebral perfusion is memory that is consistent with current concepts of cerebral vulnerability to ischaemic injury in the hippocampus which is the most sensitive region [29]. These reports may explain the presence of a diffuse non-migrainous headache during TGA attacks in 5 of our patients and the absence of other focal neurological symptoms in all patients.…”

Section: Discussionsupporting

confidence: 87%

Transient Global Amnesia: A Clinical and Sonographic Study

Akkawi¹,

Agosti²,

Anzola³

et al. 2003

Eur Neurol

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Background: The aetiology of transient global amnesia (TGA) is still unknown. The aim of this study was to identify potential risk factors for TGA, vascular risk factors, the role of patent foramen ovale (PFO) and of retrograde jugular venous flow. Methods: 138 subjects entered the study, including 48 patients with TGA, 42 age-matched patients with transient ischaemic attack (TIA) and 48 controls. PFO was studied by contrast transcranial duplex sonography. Retrograde jugular venous flow was tested with air contrast ultrasound venography (ACUV). Results: TGA patients and controls showed a lower prevalence for vascular risk factors than TIA patients. No statistical difference was found between the 3 groups with regard to PFO. ACUV detected jugular valve incompetence in 72.9% TGA, 35.7% TIA and 39.5% controls (TGA vs. TIA and TGA vs. controls p < 0.01). Conclusions: TGA patients have fewer vascular risk factors than TIA patients. Paradoxical embolism due to PFO as a cause of TGA is not confirmed in our study. Cerebral venous hypertension due to incompetence of the internal jugular valve may play a role in the pathogenesis of TGA.

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Section: Discussionsupporting

confidence: 87%

Transient Global Amnesia: A Clinical and Sonographic Study

Akkawi¹,

Agosti²,

Anzola³

et al. 2003

Eur Neurol

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“…Age and temperature appear to influence neuronal injury, making certain nerve cell populations more vulnerable to injury 5,8,9,11,12 . In particular, the hippocampus, cerebellum, striatum, thalamus, amygdala, and neocortex have been reported vulnerable in adult normothermic ischemia 19 .…”

Section: Discussionmentioning

confidence: 99%

“…We have previously reported that the sensory and motor neocortex, and hippocampus are selectively vulnerable to injury in an acute model of HCA at 18°C 8 . Neurological damage in these areas may explain, in part, impairment of memory, cognition, and motor function seen in adults after cardiac arrest 3,6,11,12 …”

mentioning

confidence: 99%

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Hypothermia at 10°C Reduces Neurologic Injury After Hypothermic Circulatory Arrest in the Pig

et al. 2008

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“…Ye et al. (1996) demonstrated regional differences in damaged hippocampal pyramidal cells in a porcine model after hypothermic circulatory arrest (120 min, 15°C) or hypothermic circulatory arrest (HCA) with retrograde cerebral perfusion (RCP) (120 min, 15°C) followed by 60 min of reperfusion (37°C normothermic CPB). Thereby, morphological changes of hematoxylin and eosin (HE)‐stained slice cultures after hypoxia/ischemia were significantly more pronounced in CA4 and CA3 than in CA1.…”

Section: Selective Vulnerability Under Cpbmentioning

confidence: 99%

Selective vulnerability of hippocampal CA1 and CA3 pyramidal cells: What are possible pathomechanisms and should more attention be paid to the CA3 region in future studies?

Einenkel,

Salameh

2023

J of Neuroscience Research

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Transient ischemia and reperfusion selectively damage neurons in brain, with hippocampal pyramidal cells being particularly vulnerable. Even within hippocampus, heterogeneous susceptibility is evident, with higher vulnerability of CA1 versus CA3 neurons described for several decades. Therefore, numerous studies have focused exclusively on CA1. Pediatric cardiac surgery is increasingly focusing on studies of hippocampal structures, and a negative impact of cardiopulmonary bypass on the hippocampus cannot be denied. Recent studies show a shift in selective vulnerability from neurons of CA1 to CA3. This review shows that cell damage is increased in CA3, sometimes stronger than in CA1, depending on several factors (method, species, age, observation period). Despite a highly variable pattern, several markers illustrate greater damage to CA3 neurons than previously assumed. Nevertheless, the underlying cellular mechanisms have not been fully deciphered to date. The complexity is reflected in possible pathomechanisms discussed here, with numerous factors (NMDA, kainate and AMPA receptors, intrinsic oxidative stress potential and various radicals, AKT isoforms, differences in vascular architecture, ratio of pro‐ and anti‐apoptotic Bcl‐2 factors, vulnerability of interneurons, mitochondrial dysregulation) contributing to either enhanced CA1 or CA3 vulnerability. Furthermore, differences in expressed genome, proteome, metabolome, and transcriptome in CA1 and CA3 appear to influence differential behavior after damaging stimuli, thus metabolomics‐, transcriptomics‐, and proteomics‐based analyses represent a viable option to identify pathways of selective vulnerability in hippocampal neurons. These results emphasize that future studies should focus on the CA3 field in addition to CA1, especially with regard to improving therapeutic strategies after ischemic/hypoxic brain injury.

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Neuronal damage after hypothermic circulatory arrest and retrograde cerebral perfusion in the pig

Cited by 66 publications

References 16 publications

Transient Global Amnesia: A Clinical and Sonographic Study

Transient Global Amnesia: A Clinical and Sonographic Study

Hypothermia at 10°C Reduces Neurologic Injury After Hypothermic Circulatory Arrest in the Pig

Selective vulnerability of hippocampal CA1 and CA3 pyramidal cells: What are possible pathomechanisms and should more attention be paid to the CA3 region in future studies?

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