scholarly journals Hyperglycemia Accelerates Apparent Diffusion Coefficient-Defined Lesion Growth after Focal Cerebral Ischemia in Rats with and Without Features of Metabolic Syndrome

2013 ◽  
Vol 33 (10) ◽  
pp. 1556-1563 ◽  
Author(s):  
David Tarr ◽  
Delyth Graham ◽  
Lisa A Roy ◽  
William M Holmes ◽  
Christopher McCabe ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Metabolic Syndrome ◽  
Diffusion Coefficient ◽  
Apparent Diffusion Coefficient ◽  
Middle Cerebral Artery ◽  
Infarct Volume ◽  
Artery Occlusion ◽  
Ischemic Damage ◽  
Apparent Diffusion ◽  
Cerebral Artery Occlusion

Poststroke hyperglycemia is associated with a poor outcome yet clinical management is inadequately informed. We sought to determine whether clinically relevant levels of hyperglycemia exert detrimental effects on the early evolution of focal ischemic brain damage, as determined by magnetic resonance imaging, in normal rats and in those modeling the ‘metabolic syndrome’. Wistar Kyoto (WKY) or fructose-fed spontaneously hypertensive stroke-prone (ffSHRSP) rats were randomly allocated to groups for glucose or vehicle administration before permanent middle cerebral artery occlusion. Diffusion-weighted imaging was carried out over the first 4 hours after middle cerebral artery occlusion and lesion volume calculated from apparent diffusion coefficient maps. Infarct volume and immunostaining for markers of oxidative stress were measured in the fixed brain sections at 24 hours. Hyperglycemia rapidly exacerbated early ischemic damage in both WKY and ffSHRSP rats but increased infarct volume only in WKY rats. There was only limited evidence of oxidative stress in hyperglycemic animals. Acute hyperglycemia, at clinically relevant levels, exacerbates early ischemic damage in both normal and metabolic syndrome rats. Management of hyperglycemia may have greatest benefit when performed in the acute phase after stroke in the absence or presence of comorbidities.

scholarly journals The influence of gender on ‘tissue at risk’ in acute stroke: A diffusion-weighted magnetic resonance imaging study in a rat model of focal cerebral ischaemia

2015 ◽  
Vol 36 (2) ◽  
pp. 381-386 ◽  
Author(s):  
Tracey A Baskerville ◽  
I Mhairi Macrae ◽  
William M Holmes ◽  
Christopher McCabe
Keyword(s):  
Diffusion Coefficient ◽  
Apparent Diffusion Coefficient ◽  
Middle Cerebral Artery ◽  
Middle Cerebral Artery Occlusion ◽  
Cerebral Artery ◽  
Artery Occlusion ◽  
Ischaemic Injury ◽  
Diffusion Weighted ◽  
Apparent Diffusion ◽  
Cerebral Artery Occlusion

This is the first study to assess the influence of sex on the evolution of ischaemic injury and penumbra. Permanent middle cerebral artery occlusion was induced in male (n = 9) and female (n = 10) Sprague-Dawley rats. Diffusion-weighted imaging was acquired over 4 h and infarct determined from T2 images at 24 h post-permanent middle cerebral artery occlusion. Penumbra was determined retrospectively from serial apparent diffusion coefficient lesions and T2-defined infarct. Apparent diffusion coefficient lesion volume was significantly smaller in females from 0.5 to 4 h post permanent middle cerebral artery occlusion as was infarct volume. Penumbral volume, and its loss over time, was not significantly different despite the sex difference in acute and final lesion volumes.

scholarly journals Infarct Volume Before Hemicraniectomy in Large Middle Cerebral Artery Infarcts Poorly Predicts Catastrophic Outcome

Stroke ◽  
2020 ◽  
Vol 51 (8) ◽  
pp. 2404-2410
Author(s):  
Barbara Casolla ◽  
Gregory Kuchcinski ◽  
Maéva Kyheng ◽  
Riyad Hanafi ◽  
Jean-Paul Lejeune ◽  
...  
Keyword(s):  
Magnetic Resonance Imaging ◽  
Diffusion Coefficient ◽  
Apparent Diffusion Coefficient ◽  
Middle Cerebral Artery ◽  
Cerebral Artery ◽  
Diffusion Weighted Imaging ◽  
Infarct Volume ◽  
Resonance Imaging ◽  
Diffusion Weighted ◽  
Apparent Diffusion

Background and Purpose: Infarct volumes predict malignant infarcts in patients undergoing decompressive hemicraniectomy (DH) for large middle cerebral artery territory infarcts. The aim of the study was to determine the optimal magnetic resonance imaging infarct volume threshold that predicts a catastrophic outcome at 1 year (modified Rankin Scale score of 5 or death). Methods: We included consecutive patients who underwent DH for large middle cerebral artery infarcts. We analyzed infarct volumes before DH with semi-automated methods on b1000 diffusion-weighted imaging sequences and apparent diffusion coefficient maps. We studied infarct volume thresholds for prediction of catastrophic outcomes, and analyzed sensitivity, specificity, and the area under the curve, a value ≥0.70 indicating an acceptable prediction. Results: Of 173 patients (109 men, 63%; median age 53 years), 42 (24.3%) had catastrophic outcomes. Magnetic resonance imaging b1000 diffusion-weighted imaging and apparent diffusion coefficient infarct volumes were associated to the occurrence of 1-year catastrophic outcome (adjusted odds ratio, 9.17 [95% CI, 2.00–42.04] and odds ratio, 4.18 [95% CI, 1.33–13.19], respectively, per 1 log increase). The optimal volume cutoff of were 211 mL on b1000 diffusion-weighted imaging and 181 mL on apparent diffusion coefficient maps. The 2 methods showed similar sensitivities and specificities and overlapping area under the curve of 0.64 (95% CI, 0.54–0.74). Conclusions: In patients with large middle cerebral artery infarcts, optimal magnetic resonance imaging infarct volume thresholds showed poor accuracy and low specificity to predict 1-year catastrophic outcome, with different b1000 diffusion-weighted imaging and apparent diffusion coefficient thresholds. In the setting of DH, optimal infarct volumes alone should not be used to deny DH, irrespectively of the method used.

scholarly journals Exacerbation of Ischemic Brain Damage by Localized Striatal Injection of Interleukin-1β in the Rat

1998 ◽  
Vol 18 (8) ◽  
pp. 833-839 ◽  
Author(s):  
R. Paul Stroemer ◽  
Nancy J. Rothwell
Keyword(s):  
Body Temperature ◽  
Middle Cerebral Artery ◽  
Middle Cerebral Artery Occlusion ◽  
Brain Damage ◽  
Infarct Volume ◽  
Artery Occlusion ◽  
Ischemic Damage ◽  
Ischemic Brain ◽  
Site Of Action ◽  
Cerebral Artery Occlusion

Interleukin-1β (IL-1β) has been implicated in ischemic brain damage. The site of action of IL-1β in such damage is not known, but we have demonstrated previously that injection of the interleukin-1 receptor antagonist (IL-1ra) in the striatum but not the cortex of rats inhibits damage caused by permanent middle cerebral artery occlusion. The present study investigated the site of action of IL-1β on ischemic damage by examining the effects of intracerebroventricular, striatal, or cortical injection of recombinant IL-1β at the onset of permanent middle cerebral artery occlusion in the rat. Intracerebroventricular injection of IL-1β (2.5 ng) significantly increased infarct volume in the striatum (35%, P < 0.0001) and in the cortex (44%, P < 0.0001) compared with vehicle treatment. Direct injection of IL-1β into the striatum also increased infarct volume in both the striatum (36%, P < 0.0001) and the cortex (38%, P < 0.0001), whereas injection of IL-1β into the cortex failed to affect infarct volume in either the striatum or the cortex. Cortical injection of a higher dose of IL-1β (20 ng) also failed to affect ischemic damage in either the striatum or the cortex. Injection of IL-1β into the striatum contralateral to the infarction had no effect on striatal damage in the ischemic hemisphere, but did increase cortical damage by 18% ( P < 0.0001). In separate groups of animals, IL-1β (2.5 ng) was injected into either the striatum or the cortex, and body temperature was recorded continuously in conscious free-moving animals by remote telemetry. Injection of IL-1β at either site failed to influence body temperature, suggesting that exacerbation of brain damage by striatal injection of IL-1β is not caused by effects on body temperature. These results imply that IL-1β exacerbates ischemic damage by specific actions in the striatum where it can influence damage at distant sites in the cortex.

MitoKATP opener, diazoxide, reduces neuronal damage after middle cerebral artery occlusion in the rat

2002 ◽  
Vol 283 (3) ◽  
pp. H1005-H1011 ◽  
Author(s):  
Katsuyoshi Shimizu ◽  
Zsombor Lacza ◽  
Nishadi Rajapakse ◽  
Takashi Horiguchi ◽  
James Snipes ◽  
...  
Keyword(s):  
Middle Cerebral Artery ◽  
Middle Cerebral Artery Occlusion ◽  
Cerebral Artery ◽  
Ischemia Reperfusion Injury ◽  
Neuronal Damage ◽  
Infarct Volume ◽  
Ischemia Reperfusion ◽  
Artery Occlusion ◽  
Sham Treatment ◽  
Cerebral Artery Occlusion

We investigated effects of diazoxide, a selective opener of mitochondrial ATP-sensitive K+ (mitoKATP) channels, against brain damage after middle cerebral artery occlusion (MCAO) in male Wistar rats. Diazoxide (0.4 or 2 mM in 30 μl saline) or saline (sham) was infused into the right lateral ventricle 15 min before MCAO. Neurological score was improved 24 h later in the animals treated with 2 mM diazoxide (13.8 ± 0.7, n = 13) compared with sham treatment (9.5 ± 0.2, n = 6, P < 0.01). The total percent infarct volume (MCAO vs. contralateral side) of sham treatment animals was 43.6 ± 3.6% ( n = 12). Treatment with 2 mM diazoxide reduced the infarct volume to 20.9 ± 4.8% ( n = 13, P < 0.05). Effects of diazoxide were prominent in the cerebral cortex. The protective effect of diazoxide was completely prevented by the pretreatment with 5-hydroxydecanoate (100 mM in 10 μl saline), a selective blocker of mitoKATP channels ( n = 6). These results indicate that selective opening of the mitoKATP channel has neuroprotective effects against ischemia-reperfusion injury in the rat brain.

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