Object: In ischemic stroke, the ischemic crisis activates a cascade of traumatic events that are potentiated by reperfusion and eventually lead to neuronal degeneration. The primary aim of this study was to investigate a procedure that could minimize this damage by interfering with the interactions between reestablished blood flow and ischemically damaged tissue, as well as by improving regional microcirculation.
Methods: Using a novel hollow filament, the authors flushed the ischemic territory with heparinized saline before vascular reperfusion after occlusion of the middle cerebral artery (MCA). The results demonstrate a statistically significant (p < 0.001) reduction in infarct volume (75%; from 45.3 +/- 3.6% to 11.4 +/- 1.7%, determined with Nissl staining) in rats in which a 2-hour MCA occlusion was followed by a 48-hour reperfusion. Infarction and neuronal degeneration were confirmed using silver staining, which revealed a significantly larger infarct (36.3%, p < 0.05) than that detected with Nissl staining. The long-term neuroprotection of the prereperfusion flushing was also evaluated. This was determined by a series of motor behavior tasks (foot placing, parallel bar traversing, rope and ladder climbing) performed up to 28 days after reperfusion. Motor deficits were found to be significantly ameliorated in animals that underwent the flushing procedure (p < 0.001). In addition, neurological outcome was also improved significantly (p < 0.001) in the same animals.
Conclusions: These results indicate that interaction between reperfusion and the metabolically and biochemically compromised tissue could be interrupted by the prereperfusion flushing procedure, which could lead to a reduction in brain injury from stroke. Mechanical reopening of the cerebral occlusion with local flushing and isolated reperfusion of the regionally injured brain might offer new treatment options for patients with stroke.
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http://dx.doi.org/10.3171/jns.2002.96.2.0310 | DOI Listing |
Background And Aims: Sterile inflammation is a major clinical concern during ischemia-reperfusion injury (IRI) triggered by traumatic events, including stroke, myocardial infarction, and solid organ transplantation. Despite high-mobility group box 1 (HMGB1) clearly being involved in sterile inflammation, its role is controversial because of a paucity of patient-focused research.
Approach And Results: Here, we examined the role of HMGB1 oxidation states in human IRI following liver transplantation.
Ann Transplant
December 2019
Department of Anesthesia and Perioperative Medicine, Medical University of South Carolina, Charleston, SC, USA.
Clin Transplant
February 2012
Lowe Family Genomics Core, Johns Hopkins University, Baltimore, MD, USA.
Introduction: Molecular biomarkers validated previously in animal models are increasingly being studied in conjunction with traditional clinical endpoints in therapeutic trials.
Patient And Methods: We hypothesized that human kidneys would exhibit a brisk, gene-specific inflammatory response during ischemia reperfusion injury (IRI), which would be modified by anti-adhesive therapy. Forty deceased-donor kidneys were biopsied prior to implantation and ∼1 h after reperfusion during an intervention trial with the selectin antagonist YSPSL (recombinant P-selectin glycoprotein ligand Ig).
Neurosci Lett
November 2004
Department of Neurological Surgery, Wayne State University School of Medicine, Lande Medical Research Building, Room 48, 550 E. Canfield, Detroit, MI 48201, USA.
The aim in this study was to investigate whether our experimental model for stroke therapy, flushing the ischemic territory with saline prior to reperfusion, could ameliorate disruption of microvascular integrity by reducing matrix metalloproteinase (MMP) expression during reperfusion. Stroke in Sprague Dawley rats (n = 42) was induced by a 2-h right middle cerebral artery (MCA) occlusion using a novel intraluminal hollow filament. Prior to reperfusion, 24 of the ischemic rats received 6ml isotonic saline at 37 degrees C infused into the ischemic area through the filament.
View Article and Find Full Text PDFNeurosci Lett
December 2003
Department of Neurological Surgery, Lande Medical Research Building, Room 48, 550 East Canfield, Detroit, MI 48201, USA.
The aim in this study was to investigate if our new experimental model for stroke therapy, flushing the ischemic territory with saline prior to reperfusion, could reduce overexpression of inflammatory mediators during reperfusion. Stroke in Sprague-Dawley rats (n=24) was induced by a 2-h middle cerebral artery occlusion using a novel intraluminal hollow filament. Prior to reperfusion, 12 of the ischemic rats received 6 ml isotonic saline at 37 degrees C infused into the ischemic area through the filament.
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