Is all perfusion-weighted magnetic resonance imaging for stroke equal? Thetemporal evolution of multiple hemodynamic parameters after focal ischemiain rats correlated with evidence of infarction

Citation
G. Zaharchuk et al., Is all perfusion-weighted magnetic resonance imaging for stroke equal? Thetemporal evolution of multiple hemodynamic parameters after focal ischemiain rats correlated with evidence of infarction, J CEREBR B, 20(9), 2000, pp. 1341-1351
Citations number
58
Categorie Soggetti
Neurosciences & Behavoir
Journal title
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM
ISSN journal
0271678X → ACNP
Volume
20
Issue
9
Year of publication
2000
Pages
1341 - 1351
Database
ISI
SICI code
0271-678X(200009)20:9<1341:IAPMRI>2.0.ZU;2-T
Abstract
Although perfusion-weighted imaging techniques are increasingly used to stu dy stroke, no particular hemodynamic variable has emerged as a standard mar ker for accumulated ischemic damage. To better characterize the hemodynamic signature of infarction, the authors have assessed the severity and tempor al evolution of ischemic hemodynamics in a middle cerebral artery occlusion model in the rat. Cerebral blood flow (CBF) and total and microvascular ce rebral blood volume (CBV) changes were measured with arterial spin labeling and steady-state susceptibility contrast magnetic resonance imaging (MRI), respectively, and analyzed in regions corresponding to infarcted and spare d ipsilateral tissue, based on 2,3,5-triphenyltetrazolium chloride histolog y sections after 24 hours ischemia. Spin echo susceptibility contrast was u sed to measure microvascular-weighted CBV, which had a maximum sensitivity for vessels with radii between 4 and 30 mu m. Serial measurements between 1 and 3 hours after occlusion showed no change in CBF (22 +/- 20% of contral ateral, mean +/- SD) or in total CBV (78 +/- 13% of contralateral) in regio ns destined to infarct. However, microvascular CBV progressively declined f rom 72 +/- 5% to 64 +/- 11% (P < 0.01) during this same period. Microvascul ar CBV changes with time were entirely due to decreases in subcortical infa rcted zones (from 73 +/- 9% to 57+/-14%, P < 0.001) without changes in the cortical infarcted territory. The hemodynamic variables showed differences in magnitude and temporal response, and these changes varied based on histo logic outcome and brain architecture. Such factors should be considered whe n designing imaging studies for human stroke.