The natural course of lesion development in brain ischemia

Back, Tobias; Schüler, Olaf G.

doi:10.1007/978-3-7091-0603-7_7

Cited by 19 publications

(15 citation statements)

References 45 publications

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“…It is well established that histological evidence of ischemia becomes more pronounced after 24 hours and progressively gets worse up to 48-hours. 29 The observed differences in total cerebral histological score therefore are very likely to be an underestimation since there was significantly more time in the intervention groups to develop the observed ischemic changes.…”

Section: Discussionmentioning

confidence: 98%

Ischemic post-conditioning and vasodilator therapy during standard cardiopulmonary resuscitation to reduce cardiac and brain injury after prolonged untreated ventricular fibrillation

et al. 2013

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Aim of the study We investigated the effects of ischemic postconditioning (IPC) with and without cardioprotective vasodilatory therapy (CVT) at the initiation of cardiopulmonary resuscitation (CPR) on cardio-cerebral function and 48-hour survival. Methods Prospective randomized animal study. Following 15 minutes of ventricular fibrillation, 42 Yorkshire farm pigs weighing an average of 34±2 kg were randomized to receive standard CPR (SCPR, n=12), SCPR+IPC (n=10), SCPR+IPC+CVT (n=10), or SCPR+CVT (n=10). IPC was delivered during the first 3 minutes of CPR with 4 cycles of 20 seconds of chest compressions followed by 20-second pauses. CVT consisted of intravenous sodium nitroprusside (2 mg) and adenosine (24 mg) during the first minute of CPR. Epinephrine was given in all groups per standard protocol. A transthoracic echocardiogram was obtained on all survivors 1 and 4 hours post-ROSC. The brains were extracted after euthanasia at least 24 hours later to assess ischemic injury in 7 regions. Ischemic injury was graded on a 0–4 scale with (0=no injury to 4= >50% neural injury). The sum of the regional scores was reported as cerebral histological score (CHS). 48 hours survival was reported. Results Post-resuscitation left ventricular ejection (LVEF) fraction improved in SCPR+CVT, SCPR+IPC+CVT and SCPR+IPC groups compared to SCPR (59%±9%, 52%±14%, 52%±14% vs. 35%±11%, respectively, p<0.05). Only SCPR+IPC and SCPR+IPC+CVT, but not SCPR+CVT, had lower mean CHS compared to SCPR (5.8±2.6, 2.8±1.8 vs. 10±2.1, respectively, p<0.01). The 48-hour survival among SCPR+IPC, SCPR+CVT, SCPR+IPC+CVT and SCPR was 6/10, 3/10, 5/10 and 1/12, respectively (Cox regression p<0.01). Conclusions IPC and CVT during standard CPR improved post-resuscitation LVEF but only IPC was independently neuroprotective and improved 48-hour survival after 15min of untreated cardiac arrest in pigs.

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Section: Discussionmentioning

confidence: 98%

Ischemic post-conditioning and vasodilator therapy during standard cardiopulmonary resuscitation to reduce cardiac and brain injury after prolonged untreated ventricular fibrillation

et al. 2013

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“…stroke, traumatic brain injury or neurodegenerative maladies like Alzheimer's disease and multiple sclerosis (MS), includes loss of neural tissue (for details see Back and Schüler 2004;Pantano et al 2006;Aktas et al 2007). In MS, microglia are activated by auto-reactive T cells that peak during the acute disease causing a collapse of the blood-brain barrier and introducing an invasion of all the members of a full-scale immune response (Rasmussen et al 2007).…”

mentioning

confidence: 99%

Effects of dissolucytotic gold ions on recovering brain lesions

Danscher

2010

Histochem Cell Biol

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“…Animal models of stroke can be divided into two main categories, depending on whether they achieve global or focal brain ischemia. In humans, global brain ischemia occurs following cardiac arrest, but the most common strokes are due to localized infarcts (Back and Schuler, 2004). In the present report we implemented a lacunae ischemic cerebral vasoconstriction model following local ET-1 administration into the SN.…”

Section: Discussionmentioning

confidence: 99%

Neural differentiation of transplanted neural stem cells in a rat model of striatal lacunar infarction: light and electron microscopic observations

Muñetón-Gómez¹,

Doncel‐Pérez²,

Fernández³

et al. 2012

Front. Cell. Neurosci.

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The increased risk and prevalence of lacunar stroke and Parkinson's disease (PD) makes the search for better experimental models an important requirement for translational research. In this study we assess ischemic damage of the nigrostriatal pathway in a model of lacunar stroke evoked by damaging the perforating arteries in the territory of the substantia nigra (SN) of the rat after stereotaxic administration of endothelin-1 (ET-1), a potent vasoconstrictor peptide. We hypothesized that transplantation of neural stem cells (NSCs) with the capacity of differentiating into diverse cell types such as neurons and glia, but with limited proliferation potential, would constitute an alternative and/or adjuvant therapy for lacunar stroke. These cells showed neuritogenic activity in vitro and a high potential for neural differentiation. Light and electron microscopy immunocytochemistry was used to characterize GFP-positive neurons derived from the transplants. 48 h after ET-1 injection, we characterized an area of selective degeneration of dopaminergic neurons within the nigrostriatal pathway characterized with tissue necrosis and glial scar formation, with subsequent behavioral signs of Parkinsonism. Light microscopy showed that grafted cells within the striatal infarction zone differentiated with a high yield into mature glial cells (GFAP-positive) and neuron types present in the normal striatum. Electron microscopy revealed that NSCs-derived neurons integrated into the host circuitry establishing synaptic contacts, mostly of the asymmetric type. Astrocytes were closely associated with normal small-sized blood vessels in the area of infarct, suggesting a possible role in the regulation of the blood brain barrier and angiogenesis. Our results encourage the use of NSCs as a cell-replacement therapy for the treatment of human vascular Parkinsonism.

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The natural course of lesion development in brain ischemia

Cited by 19 publications

References 45 publications

Ischemic post-conditioning and vasodilator therapy during standard cardiopulmonary resuscitation to reduce cardiac and brain injury after prolonged untreated ventricular fibrillation

Ischemic post-conditioning and vasodilator therapy during standard cardiopulmonary resuscitation to reduce cardiac and brain injury after prolonged untreated ventricular fibrillation

Effects of dissolucytotic gold ions on recovering brain lesions

Neural differentiation of transplanted neural stem cells in a rat model of striatal lacunar infarction: light and electron microscopic observations

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