title: Complementary use of T2-weighted and postcontrast T1- and T2*-weighted imaging to distinguish sites of reversible and irreversible brain damage in focal ischemic lesions in the rat brain.
abstract: The evolution of a photochemically induced cortical infarct was monitored using T2-, postcontrast (GdDOTA) T1-, and postcontrast (DyDTPA-BMA) T2*-weighted NMR imaging techniques. Data acquired with these different NMR imaging types were compared, both qualitatively and quantitatively. The T2*-weighted NMR images after spordiamide injection (DyDTPA-BMA) were perfusion-weighted images that allowed the differentiation between several infarct-related areas in terms of different degrees of perfusion deficiency. No quantitative information on cerebral blood flow (CBF) was obtained. A clear distinction was made between areas with a complete lack of CBF located in the core of the lesion and temporary CBF insufficiencies in the rim surrounding this core. Concomitant observations on T2-weighted and postcontrast T1-weighted images revealed the same temporary rim characterized by an increased water content, and an intact blood-brain barrier (BBB), as well as by reduced perfusion. This rim appeared within the first hours after infarct induction, reached a maximum 24 h later, and lasted between 3-5 days, when its size gradually decreased until complete disappearance. These observations suggest the existence of an area at risk. Only on postcontrast T1-weighted images, the core of the lesion remained visible during the whole experimental period (10 days) and reflected in all likelihood the irreversibly damaged ischemic central core. The combined application of different NMR imaging techniques when studying focal cerebral infarctions in the rat brain allowed us to distinguish, in terms of NMR characteristics, zones of reversible from irreversible brain damage and to estimate the severity of the damage. This might offer an appropriate experimental setup for the screening of cerebroprotective compounds.
authors.affiliation: Department of Medicine, University of Antwerp, Belgium.
authors.forename: D
authors.initials: D
authors.lastname: Lanens
authors.forename: M
authors.initials: M
authors.lastname: Spanoghe
authors.forename: J
authors.initials: J
authors.lastname: Van Audekerke
authors.forename: A
authors.initials: A
authors.lastname: Oksendal
authors.forename: A
authors.initials: A
authors.lastname: Van der Linden
authors.forename: R
authors.initials: R
authors.lastname: Dommisse
mesh_terms: D000818:Animals; D001921:Brain / Q000473:pathology*; D002545:Brain Ischemia / Q000175:diagnosis*; D002544:Cerebral Infarction / Q000175:diagnosis*; D002560:Cerebrovascular Circulation / Q000502:physiology; D003287:Contrast Media; D004419:Dysprosium; D005682:Gadolinium; D006571:Heterocyclic Compounds; D007091:Image Processing, Computer-Assisted; D008279:Magnetic Resonance Imaging / Q000379:methods*; D008297:Male; D009942:Organometallic Compounds; D004369:Pentetic Acid / Q000031:analogs & derivatives; D051381:Rats; D017208:Rats, Wistar; D013997:Time Factors
chemical_list: D003287:Contrast Media; D006571:Heterocyclic Compounds; D009942:Organometallic Compounds; C061756:sprodiamide; D004419:Dysprosium; D004369:Pentetic Acid; C050823:gadolinium 1,4,7,10-tetraazacyclododecane-N,N',N'',N'''-tetraacetate; D005682:Gadolinium