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Serial MRI After Transient Focal Cerebral Ischemia in Rats: Dynamics of Tissue Injury, Blood-Brain Barrier Damage, and Edema Formation
Abstract
Background and Purpose —With the advent of thrombolytic therapy for acute stroke, reperfusion-associated mechanisms of tissue injury have assumed greater importance. In this experimental study, we used several MRI techniques to monitor the dynamics of secondary ischemic damage, blood-brain barrier (BBB) disturbances, and the development of vasogenic edema during the reperfusion phase after focal cerebral ischemia in rats. Methods —Nineteen Sprague-Dawley rats were subjected to transient middle cerebral artery occlusion of 30 minutes, 60 minutes, or 2.5 hours with the suture occlusion model. MRI, including diffusion-weighted imaging (DWI), T2-weighted imaging, perfusion-weighted imaging, and T1-weighted imaging, was performed 5 to 15 minutes before reperfusion, as well as 0.5, 1.5, and 2.5 hours and 1, 2, and 7 days after withdrawal of the suture. Final infarct size was determined histologically at 7 days. Results —In the 30-minute ischemia group (and partially also after 60 minutes), DWI abnormalities reversed transiently during the early reperfusion period but recurred after 1 day, probably due to secondary ischemic damage. After 2.5 hours of ischemia, DWI abnormalities no longer reversed, and signal intensity on both DWI and T2-weighted images increased rapidly in the previously ischemic region due to BBB damage (enhancement on postcontrast T1-weighted images) and edema formation. Early BBB damage during reperfusion was found to be predictive of relatively pronounced edema at subacute time points and was probably related to the increased mortality rates in this experimental group (3 of 7). Conclusions —Reperfusion after short periods of ischemia (30 to 60 minutes) appears to be mainly complicated by secondary ischemic damage as shown by the delayed recurrence of the DWI lesions, whereas BBB damage associated with vasogenic edema becomes a dominant factor with longer occlusion times (2.5 hours).
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Citations
Cites
Tissue Plasminogen Activator for Acute Ischemic Stroke
(1995) · New England Journal of Medicine · doi:10.1056/nejm199512143332401 · Cited by 11,654
Cited by
Blood–brain barrier, reperfusion injury, and hemorrhagic transformation in acute ischemic stroke
Khatri, R., McKinney, A. M., Swenson, B., & Janardhan, V. (2012) · Neurology · doi:10.1212/wnl.0b013e3182697e70 · Cited by 478
Shi, Y., Zhang, L., Pu, H., Mao, L., Hu, X., Jiang, X., Xu, N., Stetler, R. A., Zhang, F., Liu, X., et al. (2016) · Nature Communications · doi:10.1038/ncomms10523 · Cited by 431
CCL2 disrupts the adherens junction: implications for neuroinflammation
Roberts, T. K., Eugenin, E. A., Lopez, L., Romero, I. A., Weksler, B. B., Couraud, P.-O., & Berman, J. W. (2012) · Laboratory Investigation · doi:10.1038/labinvest.2012.80 · Cited by 115
Acute Vascular Disruption and Aquaporin 4 Loss After Stroke
Friedman, B., Schachtrup, C., Tsai, P. S., Shih, A. Y., Akassoglou, K., Kleinfeld, D., & Lyden, P. D. (2009) · Stroke · doi:10.1161/strokeaha.108.523720 · Cited by 71
Rewell, S. S. J., Churilov, L., Sidon, T. K., Aleksoska, E., Cox, S. F., Macleod, M. R., & Howells, D. W. (2017) · PLOS ONE · doi:10.1371/journal.pone.0171688 · Cited by 54
Blood brain barrier inflammation and potential therapeutic role of phytochemicals
Welcome, M. O. (2020) · PharmaNutrition · doi:10.1016/j.phanu.2020.100177 · Cited by 22
Cai, N., Xu, B., Li, X., Qin, Y., Li, M., Chen, K., Xu, J., & Wang, H. (2022) · European Journal of Pharmacology · doi:10.1016/j.ejphar.2022.175027 · Cited by 13
Metadata
- Authors
- Neumann-Haefelin, T., Kastrup, A., de Crespigny, A., Yenari, M. A., Ringer, T., Sun, G. H., & Moseley, M. E.
- Venue
- Stroke
- Published
- 2000-08
- Volume
- 31
- Issue
- 8
- Pages
- 1965-1973
- ISSN
- 0039-2499 (ISSN-L)
- 1524-4628
- OpenAlex
- W1655344346
- Cited by
- 347
- References
- 1
- FWCI
- 14.17
- Type
- journal article
- Language
- en
- Open access
- closed
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