Embolic Stroke Models

Wang-Fischer, Yanlin; Divani, Afshin A.; Koetzner, Lee

doi:10.1201/9781420009521-14

Cited by 6 publications

(9 citation statements)

References 1 publication

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“…Given that PAIS occurs mostly during the first 24 h after birth, we chose this P1 time point. The remaining P1 offspring from S or LPS-exposed dams was submitted to a prothrombotic stress: transcutaneous laser photothrombosis (PT; laser intensity: 125 mW for 2 min (min)) applied on both MCA segments located between the ear and the eye [31] following aluminium phthalocyanine tetrasulfonate (AlPcS 4 ) ip exposure. AlPcS 4 (650 µg/kg) is a non-toxic photosensitizer used in animal models [32], which was injected ip 30 min before laser illumination [33].…”

Section: Methodsmentioning

confidence: 99%

Perinatal Arterial Ischemic Stroke Is Associated to Materno-Fetal Immune Activation and Intracranial Arteritis

Guiraut

Cauchon

Lepage

et al. 2016

IJMS

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The medium-size intra-cranial arteries arising from the carotid bifurcation are prone to perinatal arterial ischemic strokes (PAIS). PAIS’ physiopathology needs to be better understood to develop preventive and therapeutic interventions that are currently missing. We hypothesized that materno-fetal inflammation leads to a vasculitis affecting selectively the carotidian tree and promoting a focal thrombosis and subsequent stroke. Dams were injected with saline or lipopolysaccharide (LPS) from Escherichia coli. A prothrombotic stress was applied on LPS-exposed vs. saline (S)-exposed middle cerebral arteries (MCA). Immunolabeling detected the inflammatory markers of interest. In S-exposed newborn pups, a constitutive higher density of macrophages combined to higher expressions of tumor necrosis factor-α (TNF-α), and interleukin 1β (IL-1β) was observed within the wall of intra- vs. extra-cranial cervicocephalic arteries. LPS-induced maternal and placental inflammatory responses mediated by IL-1β, TNF-α and monocyte chemotactic protein 1 (MCP-1) were associated with: (i) increased density of pro-inflammatory macrophages (M1 phenotype); and (ii) pro-inflammatory orientation of the IL-1 system (IL-1β/IL-1 receptor antagonist (IL-1Ra) ratio) within the wall of LPS-, vs. S-exposed, intra-cranial arteries susceptible to PAIS. LPS plus photothrombosis, but not sole photothrombosis, triggered ischemic strokes and subsequent motor impairments. Based on these preclinical results, the combination of pro-thrombotic stress and selective intra-cranial arteritis arising from end gestational maternal immune activation seem to play a role in the pathophysiology of human PAIS.

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Section: Methodsmentioning

confidence: 99%

Perinatal Arterial Ischemic Stroke Is Associated to Materno-Fetal Immune Activation and Intracranial Arteritis

Guiraut

Cauchon

Lepage

et al. 2016

IJMS

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“…Ischemic conditions were achieved via surgical occlusion of the stem of the left proximal middle cerebral artery [ 12 – 14 ]. The skull and dura were carefully removed from a 2×2 mm ‘surgical window’ just anterior and lateral to the imaging window (over MCA’s stem, also known as the M1 segment just distal to MCA’s lenticulostriate branch) and a half-curve reverse cutting suture needle and thread (4-0 silk) was passed through the pial layer of the meninges, below MCA and above the cortical surface.…”

Section: Methodsmentioning

confidence: 99%

Sensory Stimulation-Based Complete Protection from Ischemic Stroke Remains Stable at 4 Months Post-Occlusion of MCA

Hancock

Lay²,

Davis

et al. 2013

J Neurol Disord

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Previous research from our lab has shown that when using a rodent model of ischemic stroke (permanent middle cerebral artery occlusion), mild sensory stimulation, when delivered within two hours of ischemic onset, completely protects the cortex from impending ischemic stroke damage when assessed 24 hours post-occlusion. However, the long-term stability of this protection remains unclear. Using intrinsic signal optical imaging for assessment of cortical function, laser speckle imaging for assessment of blood flow, a battery of behavioral tests and cresyl violet for histological assessment, the present study examined whether this protection was long-lasting. When assessed 4 months post-occlusion (this length of time being equivalent to 10–15 years in humans), rats receiving sensory stimulation treatment immediately after ischemic onset exhibit normal neuronal and vascular function, and they are behaviorally and histologically equivalent to healthy controls (surgical shams). Thus, the complete neuroprotection due to cortical activation via sensory stimulation remains stable with time. These findings add support to the translational potential of this sensory stimulation-based treatment.

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“…Ischemic conditions were achieved via surgical occlusion and transection of the M1 segment (just distal to lenticulostriate branching) of the left middle cerebral artery such that only MCA cortical branches were affected and thus only cortical infarct (no subcortical damage) was expected (Tamura et al, 1981, Brint et al, 1988, Wang-Fischer, 2009). The skull and dura were carefully removed from a 2×2mm ‘surgical window’ just anterior and lateral to the imaging window (over the occlusion location; the M1 segment just distal to MCA’s lenticulostriate branching) and a half-curve reverse cutting suture needle and thread (4-0 silk) was passed through the pial layer of the meninges, below MCA and above the cortical surface.…”

Section: Methodsmentioning

confidence: 99%

“…Experimental MCA occlusions also lead to loss of function, cortical infarct, and behavioral impairment (Wang-Fischer, 2009). We have previously shown that, if initiated within 1 and in most cases 2 hours of permanent middle cerebral artery occlusion (pMCAO) in a rat model, intermittent single whisker stimulation prevents the expected damage and deficits.…”

Section: Introductionmentioning

confidence: 99%

Mild Sensory Stimulation Reestablishes Cortical Function during the Acute Phase of Ischemia

Lay

Davis²,

Chen-Bee³

et al. 2011

J. Neurosci.

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When delivered within 1 and in most cases 2 hours of permanent middle cerebral artery occlusion (pMCAO), mild sensory stimulation (intermittent single whisker stimulation) was shown to be completely neuroprotective according to assessment with multiple techniques 24 hours after pMCAO in a rodent model of ischemic stroke (Lay et al., 2010). The acute effect of stimulation treatment on the ischemic cortex however, had yet to be reported. Here we characterize cortical function and perfusion during the 120 minute whisker stimulation period in four experimental groups with treatment initiated 0, 1, 2 hours (protected groups) or 3 hours post-pMCAO (unprotected group) using multiple techniques. According to functional imaging, a gradual return of evoked whisker functional representation to baseline levels was initiated with treatment onset and completed within the treatment period. Evoked neuronal activity and reperfusion to the ischemic area also showed a gradual recovery in protected animals. Surprisingly, a similar recovery profile was observed in response to treatment in all protected animals, irrespective of treatment onset time. Non-stimulated pMCAO control group data demonstrate that reperfusion is not spontaneous. This makes the complete protection observed in the majority of animals stimulated at 2 hours post-pMCAO even more surprising as these animals recovered despite having been in this severely ischemic state for two full hours. In summary, when delivered within a 2 hour window post- pMCAO, whisker stimulation treatment initiated reperfusion and a gradual recovery of cortical function that was completed or nearly completed within the treatment period.

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Embolic Stroke Models

Cited by 6 publications

References 1 publication

Perinatal Arterial Ischemic Stroke Is Associated to Materno-Fetal Immune Activation and Intracranial Arteritis

Perinatal Arterial Ischemic Stroke Is Associated to Materno-Fetal Immune Activation and Intracranial Arteritis

Sensory Stimulation-Based Complete Protection from Ischemic Stroke Remains Stable at 4 Months Post-Occlusion of MCA

Mild Sensory Stimulation Reestablishes Cortical Function during the Acute Phase of Ischemia

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