scholarly journals Penumbra Detection using PWI/DWI Mismatch MRI in a Rat Stroke Model with and without Comorbidity: Comparison of Methods

2012 ◽  
Vol 32 (9) ◽  
pp. 1765-1777 ◽  
Author(s):  
Emma Reid ◽  
Delyth Graham ◽  
M Rosario Lopez-Gonzalez ◽  
William M Holmes ◽  
I Mhairi Macrae ◽  
...  
Keyword(s):  
Artery Occlusion ◽  
Anatomical Location ◽  
Lesion Volume ◽  
Spatial Assessment ◽  
Spontaneously Hypertensive ◽  
Diffusion Weighted ◽  
Volumetric Assessment ◽  
Apparent Diffusion ◽  
Wistar Kyoto ◽  
Cerebral Artery Occlusion

Perfusion-diffusion (perfusion-weighted imaging (PWI)/diffusion-weighted imaging (DWI)) mismatch is used to identify penumbra in acute stroke. However, limitations in penumbra detection with mismatch are recognized, with a lack of consensus on thresholds, quantification and validation of mismatch. We determined perfusion and diffusion thresholds from final infarct in the clinically relevant spontaneously hypertensive stroke-prone (SHRSP) rat and its normotensive control strain, Wistar-Kyoto (WKY) and compared three methods for penumbra calculation. After permanent middle cerebral artery occlusion (MCAO) (WKY n=12, SHRSP n=15), diffusion-weighted (DWI) and perfusion-weighted (PWI) images were obtained for 4 hours post stroke and final infarct determined at 24 hours on T2 scans. The PWI/DWI mismatch was calculated from volumetric assessment (perfusion deficit volume minus apparent diffusion coefficient (ADC)-defined lesion volume) or spatial assessment of mismatch area on each coronal slice. The ADC-derived lesion growth provided the third, retrospective measure of penumbra. At 1 hour after MCAO, volumetric mismatch detected smaller volumes of penumbra in both strains (SHRSP: 31±50 mm3, WKY: 22±59 mm3, mean±s.d.) compared with spatial assessment (SHRSP: 36±15 mm3, WKY: 43±43 mm3) and ADC lesion expansion (SHRSP: 41±45 mm3, WKY: 65±41 mm3), although these differences were not statistically significant. Spatial assessment appears most informative, using both diffusion and perfusion data, eliminating the influence of negative mismatch and allowing the anatomical location of penumbra to be assessed at given time points after stroke.

scholarly journals Prediction of secondary ischemic lesions with diffusion-weighted imaging after transient middle cerebral artery occlusion in rats

Stroke ◽  
2001 ◽  
Vol 32 (suppl_1) ◽  
pp. 352-352
Author(s):  
Fuhai Li ◽  
Matthew D Silva ◽  
Xiangjun Meng ◽  
Christopher H Sotak ◽  
Marc Fisher
Keyword(s):  
Middle Cerebral Artery ◽  
Middle Cerebral Artery Occlusion ◽  
Cerebral Artery ◽  
Diffusion Weighted Imaging ◽  
Artery Occlusion ◽  
Lesion Volume ◽  
Diffusion Weighted ◽  
Adc Values ◽  
Cerebral Artery Occlusion ◽  
Initial Lesions

P75 Background and Purpose: Previous studies demonstrated that secondary ischemic lesions documented by diffusion-weighted imaging might be smaller than, larger than or similar to initial lesions that occur during ischemia. The purpose of this study was to investigate if the size of secondary lesions can be predicted. Methods: Twelve rats underwent 30 minutes of transient middle cerebral artery occlusion with the intraluminal suture method. Diffusion- and perfusion-weighted images were performed just before reperfusion, 90 minutes and 24 hours after reperfusion. The ischemic lesion size was calculated by tracing visual abnormalities on the apparent diffusion coefficient (ADC) maps. Cerebral blood flow index (CBF i ) ratio was calculated by dividing the ipsilateral CBF i by the contralateral CBF i . Based on difference between initial and secondary lesion volume, rats were assigned to reperfusion-benefit group (n=6) where secondary lesions were smaller than initial lesions (less than 85% of initial lesions) and reperfusion-nonbenefit group (n=6) where secondary lesions were similar to or larger than initial lesions (more than 85% of initial lesions). Results: At 90 minutes after reperfusion, the initial ischemic lesions almost disappeared in both groups. At 24 hours, secondary lesions were 54±11% (mean±SD) of the initial lesions in the reperfusion-benefit group and 100±14% of the initial lesions in the reperfusion-nonbenefit group (p<0.001). There was no difference in ADC values (47±2×10 -5 mm 2 /s vs 46±5×10 -5 mm 2 /s, p=0.7) and CBF i ratio (0.62±0.06 vs 0.67±0.04, p=0.2) between the two groups before reperfusion. However, the initial lesion volume was significantly smaller in the reperfusion-benefit group than in the reperfusion-nonbenefit group (125±54 mm 3 vs 195±36 mm 3 , p=0.037). Conclusions: Changes of ADC values and CBF before reperfusion are unable to predict if initial ischemic lesions will eventually shrink or not after reperfusion. Smaller size of initial lesions may suggest that secondary lesions will be smaller than initial lesions.

scholarly journals Differential Effects of 17β-Estradiol upon Stroke Damage in Stroke Prone and Normotensive Rats

2004 ◽  
Vol 24 (3) ◽  
pp. 298-304 ◽  
Author(s):  
Hilary V Carswell ◽  
Deborah Bingham ◽  
Kirsty Wallace ◽  
M Nilsen ◽  
David I Graham ◽  
...  
Keyword(s):  
Brain Damage ◽  
Infarct Volume ◽  
Artery Occlusion ◽  
Negative Effects ◽  
Spontaneously Hypertensive ◽  
Endogenous Estrogen ◽  
17Β Estradiol ◽  
Wistar Kyoto Rat ◽  
Wistar Kyoto ◽  
Cerebral Artery Occlusion

We previously reported that during pro-estrus (high endogenous estrogen levels), brain damage after middle cerebral artery occlusion (MCAO) was reduced in stroke-prone spontaneously hypertensive rats (SHRSP) but not in normotensive Wistar Kyoto rat (WKY). In the present study, we examined the effect of exogenous estrogen on brain damage after MCAO in SHRSP and WKY. A 17β-estradiol (0.025mg or 0.25mg, 21 day release) or matching placebo pellet was implanted into ovariectomized WKY and SHRSP (3 to 4 months old) who then underwent distal diathermy-induced MCAO 2 weeks later. Plasma 17β-estradiol levels for placebo and 17β-estradiol groups were as follows: WKY 0.025 mg 16.4 ± 8.5 (pg/mL, mean ± SD) and 25.85 ± 12.6; WKY 0.25 mg 18.2 ± 9.0 and 69.8 ± 27.4; SHRSP 0.25 mg 20.7 ± 8.8 and 81.0 ± 16.9. In SHRSP, infarct volumes at 24 hours after MCAO were similar in placebo and 17β-estradiol groups: SHRSP 0.025 mg 126.7 ± 15.3 mm3 (n = 6) and 114.0 ± 14.1 mm3 (n = 8) (not significant); SHRSP 0.25 mg 113.5 ± 22.3 mm3 (n = 8) and 129.7 ± 26.2 mm3 (n = 7) (not significant), respectively. In WKY, 17β-estradiol significantly increased infarct volume by 65% with 0.025mg dose [36.1 ± 20.7 mm3 (n = 8) and 59.7 ± 19.3 mm3 (n = 8) ( P = 0.033, unpaired t-test)] and by 96% with 0.25 mg dose [55.9 ± 36.4 mm3 (n = 8) and 109.7 ± 6.7 mm3 (n = 4) ( P = 0.017)]. Thus, 17β-estradiol increased stroke damage in normotensive rats with no significant effect in stroke-prone rats. Despite being contrary to our hypothesis, our findings add substance to the recently reported negative effects of 17β-estradiol in clinical studies.

scholarly journals Investigation of Estrogen Status and Increased Stroke Sensitivity on Cerebral Blood Flow after a Focal Ischemic Insult

2000 ◽  
Vol 20 (6) ◽  
pp. 931-936 ◽  
Author(s):  
Hilary V. O. Carswell ◽  
Niall H. Anderson ◽  
James J. Morton ◽  
James McCulloch ◽  
Anna F. Dominiczak ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Internal Control ◽  
Artery Occlusion ◽  
Cumulative Distribution ◽  
Distribution Analysis ◽  
Spontaneously Hypertensive ◽  
Endogenous Estrogen ◽  
Wistar Kyoto ◽  
Cerebral Artery Occlusion

Recently the authors have shown that female stroke-prone spontaneously hypertensive rats (SHRSPs) in proestrus (high endogenous estrogen), sustain more than 20% smaller infarcts after middle cerebral artery occlusion (MCAO) compared with SHRSPs in metestrus (low endogenous estrogen). Because estrogen has vasodilator properties, the authors investigated whether the estrous state influences cerebral blood flow (CBF) after MCAO. CBF was measured 2.5 hours after a distal MCAO by [14C]iodo-antipyrine autoradiography in conscious SHRSPs either in metestrus or in proestrus. There were no significant differences in CBF when analyzed either at predetermined anatomic regions or by cumulative distribution analysis of areas with flow <25 mL/100 g/min. As a positive internal control, the authors compared results in SHRSPs with those in their normotensive reference strain, Wistar Kyoto rat. SHRSPs displayed more severe and widespread ischemia than Wistar Kyoto rats. Thus, the absence of demonstrable CBF differences between estrous states appears to be unrelated to the CBF measurement paradigm. In conclusion, the smaller infarct size afforded in proestrus in SHRSPs is unlikely to be due to an influence on CBF.

scholarly journals Brain Injury and Cerebrovascular Fibrin Deposition Correlate with Reduced Antithrombotic Brain Capillary Functions in a Hypertensive Stroke Model

2000 ◽  
Vol 20 (6) ◽  
pp. 998-1009 ◽  
Author(s):  
Takashi Ninomia ◽  
Liang Wang ◽  
S. Ram Kumar ◽  
Anthony Kim ◽  
Berislav V. Zlokovic
Keyword(s):  
Spontaneously Hypertensive Rats ◽  
Artery Occlusion ◽  
Fibrin Deposition ◽  
Hypertensive Rats ◽  
Brain Capillary ◽  
Spontaneously Hypertensive ◽  
Wistar Kyoto ◽  
Hemostasis Factors ◽  
Cerebral Artery Occlusion ◽  
Brain Microcirculation

Hemostasis factors may influence the pathophysiology of stroke. The role of brain hemostasis in ischemic hypertensive brain injury is not known. We studied ischemic injury in spontaneously hypertensive rats in relation to cerebrovascular fibrin deposition and activity of different hemostasis factors in brain microcirculation. In spontaneously hypertensive rats subjected to transient middle cerebral artery occlusion versus normotensive Wistar-Kyoto (W-K) rats, infarct and edema volumes were increased by 6.1-fold ( P < 0.001) and 5.8-fold ( P < 0.001), respectively, the cerebral blood flow (CBF) reduced during middle cerebral artery occlusion (MCAO) by 55% ( P < 0.01), motor neurologic score increased by 6.9-fold ( P < 0.01), and cerebrovascular fibrin deposition increased by 6.8-fold ( P < 0.01). Under basal conditions, brain capillary protein C activation and tissue plasminogen activator activity were reduced in spontaneously hypertensive rats compared with Wistar-Kyoto rats by 11.8-fold ( P < 0.001) and 5.1-fold ( P < 0.001), respectively, and the plasminogen activator inhibitor-1 antigen and tissue factor activity were increased by 154-fold ( P < 0.00001) and 74% ( P < 0.01), respectively. We suggest that hypertension reduces antithrombotic mechanisms in brain microcirculation, which may enhance cerebrovascular fibrin deposition and microvascular obstructions during transient focal cerebral ischemia, which results in greater neuronal injury.

scholarly journals Spironolactone reduces cerebral infarct size and EGF-receptor mRNA in stroke-prone rats

2001 ◽  
Vol 281 (3) ◽  
pp. R944-R950 ◽  
Author(s):  
Anne M. Dorrance ◽  
Heather L. Osborn ◽  
Roger Grekin ◽  
R. Clinton Webb
Keyword(s):  
Egf Receptor ◽  
Artery Occlusion ◽  
Cerebral Vasculature ◽  
Cerebral Infarcts ◽  
Spontaneously Hypertensive ◽  
Smooth Muscle Proliferation ◽  
Epidermal Growth ◽  
Wistar Kyoto ◽  
Cerebral Artery Occlusion

Remodeling of the cerebral vasculature contributes to the pathogenesis of cerebral ischemia. Remodeling is caused by increased smooth muscle proliferation and may be due to an increase in the responsiveness of vascular cells to epidermal growth factor (EGF). Aldosterone is a risk factor for stroke, and the literature suggests it may play a role in increasing the expression of the receptor for EGF (EGFR). We hypothesized that mRNA for the EGF-stimulated pathway would be elevated in the vasculature of stroke-prone spontaneously hypertensive rats (SHRSP) and that this and experimental ischemic cerebral infract size would be reduced by aldosterone inhibition with spironolactone. We found that spironolactone treatment reduced the size of cerebral infarcts after middle cerebral artery occlusion in SHRSP (51.69 ± 3.60 vs. 22.00 ± 6.69% of hemisphere-infarcted SHRSP vs. SHRSP + spironolactone P < 0.05). Expression of EGF and EGFR mRNA was higher in cerebral vessels and aorta from adult SHRSP compared with Wistar-Kyoto rats. Only the expression of EGFR mRNA was elevated in the young SHRSP. Spironolactone reduced the EGFR mRNA expression in the aorta (1.09 ± 0.25 vs. 0.56 ± 0.11 phosphorimage units SHRSP vs. SHRSP + spironolactone P < 0.05) but had no effect on EGF mRNA. In vitro incubation of aorta with aldosterone ± spironolactone produced similar results, suggesting a direct effect of aldosterone. Thus spironolactone may reduce the size of cerebral infarcts via a reduction in the expression of the EGFR mRNA, leading to reduced remodeling.

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 Acute Focal Ischemia-Induced Alterations in MAP2 Immunostaining: Description of Temporal Changes and Utilization as a Marker for Volumetric Assessment of Acute Brain Injury

1996 ◽  
Vol 16 (1) ◽  
pp. 170-174 ◽  
Author(s):  
Deborah A. Dawson ◽  
John M. Hallenbeck
Keyword(s):  
Brain Injury ◽  
Focal Ischemia ◽  
Artery Occlusion ◽  
Acute Brain Injury ◽  
Lesion Volume ◽  
Rapid Reduction ◽  
Ischemic Lesion ◽  
Volumetric Assessment ◽  
Cerebral Artery Occlusion ◽  
Over Time

The utility of microtubule-associated protein 2 (MAP2) immunostaining as a marker of acute focal ischemic injury was investigated. Permanent middle cerebral artery occlusion (MCAO) elicited a rapid reduction in MAP2 immunostaining that was visible 1 h post-MCAO and that increased in intensity and area encompassed over time. The ischemic lesion borders were well defined by loss of MAP2 immunostaining, but alterations in staining within the lesion were more heterogeneous. Lesion volume increased significantly from 1 to 4 h post-MCAO (from 63.8 ± 10.8 to 111.3 ± 19.0 mm3, mean ± SD). Thus, MAP2 immunostaining is a sensitive, quantifiable indicator of acute brain injury following focal ischemia.

scholarly journals Neuroprotective mechanisms of erythropoietin in a rat stroke model

2020 ◽  
Vol 11 (1) ◽  
pp. 48-59
Author(s):  
Martin Juenemann ◽  
Tobias Braun ◽  
Nadine Schleicher ◽  
Mesut Yeniguen ◽  
Patrick Schramm ◽  
...  
Keyword(s):  
Blood Flow ◽  
Infarct Size ◽  
Cerebral Edema ◽  
Infarct Volume ◽  
Artery Occlusion ◽  
Lesion Volume ◽  
Ischemic Lesion ◽  
Human Erythropoietin ◽  
Male Wistar Rats ◽  
Cerebral Artery Occlusion

AbstractObjectiveThis study was designed to investigate the indirect neuroprotective properties of recombinant human erythropoietin (rhEPO) pretreatment in a rat model of transient middle cerebral artery occlusion (MCAO).MethodsOne hundred and ten male Wistar rats were randomly assigned to four groups receiving either 5,000 IU/kg rhEPO intravenously or saline 15 minutes prior to MCAO and bilateral craniectomy or sham craniectomy. Bilateral craniectomy aimed at elimination of the space-consuming effect of postischemic edema. Diagnostic workup included neurological examination, assessment of infarct size and cerebral edema by magnetic resonance imaging, wet–dry technique, and quantification of hemispheric and local cerebral blood flow (CBF) by flat-panel volumetric computed tomography.ResultsIn the absence of craniectomy, EPO pretreatment led to a significant reduction in infarct volume (34.83 ± 9.84% vs. 25.28 ± 7.03%; p = 0.022) and midline shift (0.114 ± 0.023 cm vs. 0.083 ± 0.027 cm; p = 0.013). We observed a significant increase in regional CBF in cortical areas of the ischemic infarct (72.29 ± 24.00% vs. 105.53 ± 33.10%; p = 0.043) but not the whole hemispheres. Infarct size-independent parameters could not demonstrate a statistically significant reduction in cerebral edema with EPO treatment.ConclusionsSingle-dose pretreatment with rhEPO 5,000 IU/kg significantly reduces ischemic lesion volume and increases local CBF in penumbral areas of ischemia 24 h after transient MCAO in rats. Data suggest indirect neuroprotection from edema and the resultant pressure-reducing and blood flow-increasing effects mediated by EPO.

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