This Article Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Bolander, H. G. Articles by Olsson, Y. Search for Related Content PubMed PubMed Citation Articles by Bolander, H. G. Articles by Olsson, Y.

Stroke, Vol 20, 930-937, Copyright © 1989 by American Heart Association

ARTICLES

Regional cerebral blood flow and histopathologic changes after middle cerebral artery occlusion in rats

HG Bolander, L Persson, L Hillered, R d'Argy, U Ponten and Y Olsson
Department of Neurosurgery, Uppsala University, Sweden.

Changes in regional cerebral blood flow were correlated with the distribution of histopathologic signs of brain injury in 35 rats after middle cerebral artery occlusion. Rats were allowed to survive for periods of up to 4 weeks after the operation, and we focused particular interest on the time course of blood flow changes from the initial ischemic events to the late stage of infarction. Regional blood flow was measured using [14C]iodoantipyrine and a quantitative autoradiographic technique. Blood flow in regions with histologic signs of infarction (i.e., the lateral caudoputamen and adjacent neocortex) was below 0.238 ml/g/min, corresponding to 15% of normal values for those regions. In perifocal regions without infarction such as the medial caudoputamen and globus pallidus, cerebral blood flow was also reduced, but it never declined below 20% of its normal value. The decrease in cerebral blood flow was most marked during the first hours after occlusion. Thereafter, cerebral blood flow values gradually normalized, and at 4 weeks there were no significant differences compared with the contralateral side. The border between cortical regions with hypoperfusion and normal cerebral blood flow was rather sharp in the coronal plane, but in the sagittal plane there was a more gradual transitional region. The region with hypoperfusion, observed in the sagittal plane, was most widespread in the acute stage, and normalization of flow occurred particularly from anterior and posterior cortical regions toward the ischemic focus. The possibility for penumbral conditions in the cortex thus exists, particularly in the anterior and posterior borders of the infarction, and remains for several hours after the initial insult.(ABSTRACT TRUNCATED AT 250 WORDS)

This article has been cited by other articles:

				Y. Zhang, L. Wang, J. Li, and X.-L. Wang 2-(1-Hydroxypentyl)-benzoate Increases Cerebral Blood Flow and Reduces Infarct Volume in Rats Model of Transient Focal Cerebral Ischemia J. Pharmacol. Exp. Ther., June 1, 2006; 317(3): 973 - 979. [Abstract] [Full Text] [PDF]

				N. R. Sibson, A. M. Blamire, V. H. Perry, J. Gauldie, P. Styles, and D. C. Anthony TNF-{alpha} reduces cerebral blood volume and disrupts tissue homeostasis via an endothelin- and TNFR2-dependent pathway Brain, November 1, 2002; 125(11): 2446 - 2459. [Abstract] [Full Text] [PDF]

				P. Lipton Ischemic Cell Death in Brain Neurons Physiol Rev, October 1, 1999; 79(4): 1431 - 1568. [Abstract] [Full Text] [PDF]

				H. Bolay, T. Dalkara, and J. H. Garcia Mechanisms of Motor Dysfunction After Transient MCA Occlusion: Persistent Transmission Failure in Cortical Synapses Is a Major Determinant • Editorial Comment Stroke, September 1, 1998; 29(9): 1988 - 1994. [Abstract] [Full Text] [PDF]

				N. R. Sibson, A. Dhankhar, G. F. Mason, K. L. Behar, D. L. Rothman, and R. G. Shulman In vivo 13C NMR measurements of cerebral glutamine synthesis as evidence for glutamate-glutamine cycling PNAS, March 18, 1997; 94(6): 2699 - 2704. [Abstract] [Full Text] [PDF]

				Y. Kim, R. Busto, W. D. Dietrich, S. Kraydieh, M. D. Ginsberg, and W. I. Rosenblum Delayed Postischemic Hyperthermia in Awake Rats Worsens the Histopathological Outcome of Transient Focal Cerebral Ischemia Stroke, December 1, 1996; 27(12): 2274 - 2281. [Abstract] [Full Text]