Temporal Correlation Analysis of Penumbral Dynamics in Focal Cerebral Ischemia

A novel temporal correlation technique was used to map the first-pass transit of iodinated contrast agents through the brain. Transit profiles after bolus injections were measured with dynamic computed tomography (CT) scanning (1 image/s over 50 s). A rabbit model of focal cerebral ischemia (n = 6) was used, and dynamic CT scans were performed at 30, 60, 90, and 120 min postocclusion. Within the ischemic core, no bolus transit was detectable, demonstrating that complete ischemia was present after arterial occlusion. In the periphery of the ischemic distribution, transit dynamics showed smaller peaks, broadened profiles, and overall delay in bolus transit. A cross-correlation method was used to generate maps of delays in ischemic transit profiles compared with normal transit profiles from the contralateral hemisphere. These maps showed that penumbral regions surrounding the ischemic core had significantly delayed bolus transit profiles. Enlargement of the ischemic core over time (from 30 to 120 min postocclusion) was primarily accomplished by the progressive deterioration of the penumbral regions. These results suggest that (a) temporal correlation methods can define regions of abnormal perfusion in focal cerebral ischemia, (b) peripheral regions of focal cerebral ischemia are characterized by delays in bolus transit profiles, and (c) these regions of bolus transit delay deteriorate over time and thus represent a hemodynamic penumbra.

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L-arginine decreases infarct size caused by middle cerebral arterial occlusion in SHR

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1992.263.5.h1632 ◽

1992 ◽

Vol 263 (5) ◽

pp. H1632-H1635 ◽

Cited By ~ 9

Author(s):

E. Morikawa ◽

Z. Huang ◽

M. A. Moskowitz

Keyword(s):

Cerebral Ischemia ◽

Infarct Size ◽

Focal Cerebral Ischemia ◽

Arterial Occlusion ◽

Cerebral Blood Vessels ◽

Hypertensive Rats ◽

Vessel Occlusion ◽

Spontaneously Hypertensive ◽

Cerebral Arterial Occlusion ◽

Carotid Arterial

L-Arginine, but not D-arginine, serves as a precursor for the synthesis of nitric oxide (NO), a potent dilator of cerebral blood vessels. We examined the effects of administering L-arginine (300 mg/kg ip) on the volume of infarction in two models of focal cerebral ischemia in spontaneously hypertensive rats (SHR). L-Arginine was administered before (16 and 3 h) and after (5 min and 2 h) vessel occlusion, and animals were killed 24 h later. L-Arginine treatment decreased infarct size in rats subjected to distal middle cerebral arterial (MCA) plus ipsilateral common carotid arterial (CCA) occlusion by 31% [147 +/- 12 (saline) vs. 101 +/- 9 mm3 (L-arginine), P < 0.05]. D-Arginine, administered according to the same dosage and protocol, was without effect. In the group subjected to proximal MCA occlusion, L-arginine decreased infarction size in the striatum by 28% [47 +/- 5 (saline) vs. 34 +/- 3 mm3 (L-arginine), P < 0.05] and neocortex by 11% [193 +/- 7 (saline) vs. 171 +/- 8 mm3 (L-arginine), P < 0.05]. Changes in blood pressure or other measured physiological parameters did not account for the observed differences. The possible use of L-arginine for the treatment of focal cerebral ischemia merits further investigation.

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Nimodipine Pretreatment Improves Cerebral Blood Flow and Reduces Brain Edema in Conscious Rats Subjected to Focal Cerebral Ischemia

Journal of Cerebral Blood Flow & Metabolism ◽

10.1038/jcbfm.1990.147 ◽

1990 ◽

Vol 10 (6) ◽

pp. 903-913 ◽

Cited By ~ 51

Author(s):

Michael Jacewicz ◽

Steve Brint ◽

Jody Tanabe ◽

Xing-Je Wang ◽

William A. Pulsinelli

Keyword(s):

Blood Flow ◽

Cerebral Ischemia ◽

Brain Edema ◽

Focal Cerebral Ischemia ◽

Polyethylene Glycol 400 ◽

Conscious Rats ◽

Ischemic Core ◽

Cortical Ischemia ◽

Vascular Steal ◽

Common Carotid Arteries

The effect of nimodipine pretreatment on CBF and brain edema was studied in conscious rats subjected to 2.5 h of focal cortical ischemia. An infusion of nimodipine (2 μg/kg/min i.v.) or its vehicle, polyethylene glycol 400, was begun 2 h before the ischemic interval and was continued throughout the survival period. Under brief halothane anesthesia, the animals' right middle cerebral and common carotid arteries were permanently occluded, and 2.5 h later, they underwent a quantitative CBF study ([14C]iodoantipyrine autoradiography followed by Quantimet 970 image analysis). Nimodipine treatment improved blood flow to the middle cerebral artery territory without evidence of a “vascular steal” and reduced the volume of the ischemic core (cortex with CBF of < 25 ml/100 g/min) and accompanying edema by ∼50% when compared with controls (p = 0.006 and 0.0004, respectively). Mild hypotension induced by nimodipine did not aggravate the ischemic insult. The ischemic core volumes, however, were 50–75% smaller than the 24-h infarct volumes generated in a similar paradigm that demonstrated 20–30% infarct reduction with continuous nimodipine treatment. These results suggest that nimodipine pretreatment attenuates the severity of early focal cerebral ischemia, but that with persistent ischemia, cortex surrounding the ischemic core undergoes progressive infarction and the early benefit of nimodipine treatment is only partly preserved.

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Selective lenticulostriate arterial occlusion. A reproducible model of primate focal cerebral ischemia

Surgical Neurology ◽

10.1016/0090-3019(86)90180-1 ◽

1986 ◽

Vol 25 (6) ◽

pp. 545-552 ◽

Cited By ~ 6

Author(s):

Howard Yonas ◽

Sidney K. Wolfson ◽

Eugene E. Cook ◽

David Gur

Keyword(s):

Cerebral Ischemia ◽

Focal Cerebral Ischemia ◽

Arterial Occlusion

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Interrupted Arterial Occlusion Reduces Ischemic Damage in a Focal Cerebral Ischemia Model of Rats

Neurosurgery ◽

10.1097/00006123-199510000-00020 ◽

1995 ◽

Vol 37 (4) ◽

pp. 750???757

Author(s):

Yasutaka Kurokawa ◽

Bruce I. Tranmer

Keyword(s):

Cerebral Ischemia ◽

Focal Cerebral Ischemia ◽

Arterial Occlusion ◽

Ischemic Damage

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The Expression of FOXJ1 in Neurogenesis after Transient Focal Cerebral Ischemia

Canadian Journal of Neurological Sciences / Journal Canadien des Sciences Neurologiques ◽

10.1017/s0317167100014372 ◽

2013 ◽

Vol 40 (3) ◽

pp. 403-409 ◽

Cited By ~ 1

Author(s):

Yabo Huang ◽

Zheng Xu ◽

Jie Cao ◽

Haibo Cao ◽

Shiming Zhang

Keyword(s):

Cerebral Ischemia ◽

Expression Pattern ◽

Focal Cerebral Ischemia ◽

Artery Occlusion ◽

Adult Brain ◽

Immunofluorescence Staining ◽

Double Immunofluorescence ◽

Adult Rats ◽

Ischemic Core ◽

The Brain

Objective and Background:FOXJ1 is a member of the Forkhead/winged-helix (Fox) family of transcription factors, which is required for the differentiation of the cells acting as adult neural stem cells which participate in neurogenesis and give rise to neurons, astrocytes, oligodendrocytes. The expression pattern of FOXJ1 in the brain after cerebral ischemia has so far not been described. In the current study, we investigated the expression pattern of FOXJ1 in the rat brain after cerebral ischemia by animal model.Methods:We performed a middle cerebral artery occlusion (MCAO) model in adult rats and investigated the expression of FOXJ1 in the brain by Western blotting and immunochemistry; double immunofluorescence staining was used to analyze FOXJ1's co-expression with Ki67.Results:Western blot analysis showed that the expression of FOXJ1 was lower than normal and sham-operated brain after cerebral ischemia, but the level of FOXJ1 gradually increased from Day 1 to Day 14. Immuohistochemical staining suggested that the immunostaining of FOXJ1 deposited strongly in the ipsilateral and contralateral hemisphere in the cortical penumbra (CP). There was no FOXJ1 expression in the ischemic core (IC). The positive cells in the cortical penumbra might migrat to the ischemic core. In addition, double immunofluorescence staining revealed that FOXJ1 was co-expressed with mAP-2 and gFAP, and Ki67 had the colocalization with NeuN, GFAP, and FOXJ1.Conclusions:All our findings suggest that FOXJ1 plays an important role on neuronal production and neurogenesis in the adult brain after cerebral ischemia.

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