2014
DOI: 10.1038/jcbfm.2014.197
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Delayed Reperfusion Deficits after Experimental Stroke Account for Increased Pathophysiology

Abstract: Cerebral blood flow and oxygenation in the first few hours after reperfusion following ischemic stroke are critical for therapeutic interventions but are not well understood. We investigate changes in oxyhemoglobin (HbO2) concentration in the cortex during and after ischemic stroke, using multispectral optical imaging in anesthetized mice, a remote filament to induce either 30 minute middle cerebral artery occlusion (MCAo), sham surgery or anesthesia alone. Immunohistochemistry establishes cortical injury and … Show more

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Cited by 39 publications
(41 citation statements)
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“…38 This is again consistent with the mild ischemic damage present in our subjects, given that this phenomenon is seen following prolonged severe ischemia and is a marker of proceeding infarction involving secondary no-reflow from endothelial damage, inflammation and pericyte constriction. 4,36 The presence of SNL rather than infarction with 45 min tMCAo in Sprague-Dawley rats also agrees with current literature that almost consistently reports infarcts with 60 min occlusion and pure SNL with 30 min occlusion. 16 Although given the notorious difficulties with the thread occlusion model 39 incomplete MCAo could be raised as a possible explanation to our finding, adequate occlusion of the origin of the MCA was likely achieved firstly because the postmortem data showed striatal damage, and secondly because MCAo induced extensive fUS signal reductions (Figure 2(a)) that were marked in each rat (Table 1).…”
Section: Immunofluorescencesupporting
confidence: 89%
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“…38 This is again consistent with the mild ischemic damage present in our subjects, given that this phenomenon is seen following prolonged severe ischemia and is a marker of proceeding infarction involving secondary no-reflow from endothelial damage, inflammation and pericyte constriction. 4,36 The presence of SNL rather than infarction with 45 min tMCAo in Sprague-Dawley rats also agrees with current literature that almost consistently reports infarcts with 60 min occlusion and pure SNL with 30 min occlusion. 16 Although given the notorious difficulties with the thread occlusion model 39 incomplete MCAo could be raised as a possible explanation to our finding, adequate occlusion of the origin of the MCA was likely achieved firstly because the postmortem data showed striatal damage, and secondly because MCAo induced extensive fUS signal reductions (Figure 2(a)) that were marked in each rat (Table 1).…”
Section: Immunofluorescencesupporting
confidence: 89%
“…Again, animal placement for safe thread pushing up impeded concomitant imaging, although a model variant allowing to push the thread without moving over the animal has been recently reported. 36 Note that these limitations do not necessarily apply to MCAo models where access to the MCA is lateral or from above the skull, such as with distal occlusion. Assessing the perfusion changes immediately after occlusion and following them in real-time over the duration of the latter and after reperfusion will likely afford new insights into the mechanisms of ischemic brain damage.…”
Section: Fus Imagingmentioning
confidence: 99%
“…The MCAo model is also characterized by increased pathophysiology due to delayed reperfusion deficits. 61…”
Section: Discussionmentioning
confidence: 99%
“…A major issue in rtPA therapeutic use is the short half-life (4-8 min) in the circulation due to autolysis and the influences of inhibitors, enzymes, and antibodies in blood [3]. The poor affinity of rtPA toward thrombus also reduces its thrombolysis efficacy and might cause ischemia reperfusion injury to the neuron beyond the thrombolysis window [4]. Other limitations of rtPA for clinical use include the short window time for treatment (usually within 3 h) and the risk of hemorrhagic side effects [5].…”
Section: Introductionmentioning
confidence: 99%