Ischemic cortical lesions after permanent occlusion of individual middle cerebral artery branches in rats.

Rubino, Gregory; Young, Wise

doi:10.1161/01.str.19.7.870

Cited by 55 publications

(28 citation statements)

References 21 publications

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“…2A). Both naturally occurring (23,44) and genetically induced (19) changes in the nature of these anastomoses lead to a detrimental ischemic outcome following occlusion of the MCA. At the lowest level, described in this article, redundancy is attained by means of loops formed by pial anastomoses between the branches of the MCA.…”

Section: Discussionmentioning

confidence: 99%

“…First, from the perspective of static resource management, when a single surface vessel suffers a targeted occlusion, blood flow in downstream vessels does not cease but rather is maintained in the surface network through the reversal of flow in the nearest downstream vessel (14). This process implies that the interconnections robustly reroute blood, an effect also seen when a major tributary to the middle cerebral artery (MCA) is occluded (23). Second, the recruitment of collateral flow has been shown to improve cerebral blood flow and clinical outcomes in stroke patients (24,25).…”

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confidence: 99%

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Topological basis for the robust distribution of blood to rodent neocortex

Blinder¹,

Shih²,

Rafie³

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

169

224

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The maintenance of robust blood flow to the brain is crucial to the health of brain tissue. We examined the pial network of the middle cerebral artery, which distributes blood from the cerebral arteries to the penetrating arterioles that source neocortical microvasculature, to characterize how vascular topology may support such robustness. For both mice and rats, two features dominate the topology. First, interconnected loops span the entire territory sourced by the middle cerebral artery. Although the loops comprise <10% of all branches, they maintain the overall connectivity of the network after multiple breaks. Second, >80% of offshoots from the loops are stubs that end in a single penetrating arteriole, as opposed to trees with multiple penetrating arterioles. We hypothesize that the loops and stubs protect blood flow to the parenchyma from an occlusion in a surface vessel. To test this, we assayed the viability of tissue that was sourced by an individual penetrating arteriole following occlusion of a proximal branch in the surface loop. We observed that neurons remained healthy, even when occlusion led to a reduction in the local blood flow. In contrast, direct blockage of a single penetrating arteriole invariably led to neuronal death and formation of a cyst. Our results show that the surface vasculature functions as a grid for the robust allocation of blood in the event of vascular dysfunction. The combined results of the present and prior studies imply that the pial network reallocates blood in response to changing metabolic needs.anastomoses | imaging | networks | stroke | vasculature

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Section: Discussionmentioning

confidence: 99%

mentioning

confidence: 99%

Topological basis for the robust distribution of blood to rodent neocortex

Blinder¹,

Shih²,

Rafie³

et al. 2010

Proc. Natl. Acad. Sci. U.S.A.

169

224

View full text Add to dashboard Cite

show abstract

“…For a consistent infarction in normotensive animals (i.e., not the spontaneously hypertensive stain of rat), there needs to be a period of at least 60 min in the rat in which the MCA on the surface of the brain and both common carotids are occluded. [91][92][93][94] In the rat, variations on the three-vessel occlusion model relate to whether the MCA and ipsilateral carotid arteries are permanently or transiently occluded. These variations include permanent occlusion of the ipsilateral common and middle cerebral carotid arteries, 92 permanent occlusion of the ipsilateral common carotid artery alone, 95 permanent occlusion of the middle cerebral artery alone, 94 and temporary occlusion of all three vessels.…”

Section: Other Models Of Mcao: Distal Mcao and Embolic Mcaomentioning

confidence: 99%

Rodent models of focal stroke: Size, mechanism, and purpose

2005

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Summary: Rodent stroke models provide the experimental backbone for the in vivo determination of the mechanisms of cell death and neural repair, and for the initial testing of neuroprotective compounds. Less than 10 rodent models of focal stroke are routinely used in experimental study. These vary widely in their ability to model the human disease, and in their application to the study of cell death or neural repair. Many rodent focal stroke models produce large infarcts that more closely resemble malignant and fatal human infarction than the average sized human stroke. This review focuses on the mechanisms of ischemic damage in rat and mouse stroke models, the relative size of stroke generated in each model, and the purpose with which focal stroke models are applied to the study of ischemic cell death and to neural repair after stroke.

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“…89 MCAO 1-2 mm below the rhinal fissure typically causes an infarct in the frontopyriform cortex, with variable extension into the frontoparietal cortex and the temporal cortex, 10 and large regional changes of brain water, Na + ,K + , and Ca 2+ concentrations. 2 -3 This MCAO model spares the lenticulostriate branches of the middle cerebral artery (MCA) 89 and causes infarcts largely localized to the cerebral cortex.…”

Section: Iddle Cerebral Artery Occlusion (Mcao) Inmentioning

confidence: 99%

Somatosensory evoked potentials in rat cerebral cortex before and after middle cerebral artery occlusion.

Sakatani

Iizuka

Young

1990

Stroke

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We recorded somatosensory evoked potentials in pentobarbital-anesthetized rats before and after middle cerebral artery occlusion. Trigeminal (vibrissae), median (forelimb), and sciatic (bind limb) nerve stimuli produced consistent, robust, and sharply localized responses in the trigeminal, forelimb, and hind limb regions of the somatosensory cortex of 18 rats. These regions are situated at sequentially greater distances from the center of infarcts produced by middle cerebral artery occlusion. In eight rats, occlusion 1-2 mm below the rhinal fissure abolished somatosensory evoked potentials in all three cortical region within minutes. Positive wavelets preceding the primary cortical response were also diminished by the occlusion, suggesting that ischemia affected the thalamocortical white matter. Four of these eight rats did not show histologically apparent ischemic involvement of the hind limb cortical region at 3 hours after occlusion; sciatic nerve evoked potentials recovered substantially in all four rats, and the amplitudes exceeded baseline (129±30% at 1 hour, 173±33% at 3 hours) in three of the four rats. Three of the eight rats did not have gross ischemic involvement of the forelimb cortical region; median nerve evoked potentials recovered fully in all eight rats, but the amplitudes did not exceed baseline. All eight rats had evidence of ischemic damage in the trigeminal cortex; no rat showed full recovery in this region, and all but one had trigeminal evoked potentials that were <20% of baseline amplitudes by 3 hours after occlusion. Two rats had large infarcts involving the hind limb and forelimb cortical regions and were studied for 24 hours; these rats did not recover evoked potentials in the three regions at 24 hours, although one rat transiently recovered hind limb evoked potentials to 83% of baseline amplitude at 3 hours. Amplitude of the hind limb somatosensory evoked potentials recorded in the contralateral hemisphere doubled after occlusion. Thus, middle cerebral artery occlusion causes widespread loss of somatosensory evoked potentials in the hind limb, forelimb, and trigeminal cortical regions of the ischemic hemisphere of rats. These regions show distinctly different temporal patterns of recovery. Our findings suggest that cortical evoked potentials may be useful for monitoring ischemic damage in these cortical regions after middle cerebral artery occlusion (Stroke 1990^1 89 and causes infarcts largely localized to the cerebral cortex.:The rat primary somatosensory cortex has three anatomically and physiologically distinct regions: the hind limb area (HL), the forelimb area (FL), and the parietal 1 area (Parl).1112 Parl is situated most laterally and receives projections mainly from the cutaneous mechanoreceptors of the mystacial vibrissae, the head, and the neck. HL is located most medially, and FL lies between HL and Parl. Peripheral nerve stimulation produces localized field potentials in the somatosensory cortex. The typical ischemic infarct produced by MCAO encroaches on these regions....

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Ischemic cortical lesions after permanent occlusion of individual middle cerebral artery branches in rats.

Cited by 55 publications

References 21 publications

Topological basis for the robust distribution of blood to rodent neocortex

Topological basis for the robust distribution of blood to rodent neocortex

Rodent models of focal stroke: Size, mechanism, and purpose

Somatosensory evoked potentials in rat cerebral cortex before and after middle cerebral artery occlusion.

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