title: Noninvasive near infrared spectroscopy monitoring of regional cerebral blood oxygenation changes during peri-infarct depolarizations in focal cerebral ischemia in the rat.
abstract: Intermittent peri-infarct depolarizations (PID), which spread from the vicinity of the infarction over the cortex, have been reported in focal ischemia. These depolarizations resemble cortical spreading depression except that they damage the cortex and enlarge the infarct volume possibly because of compromised oxygen delivery. The main purpose of this study was to evaluate the noninvasive technique of near-infrared spectroscopy (NIRS) for the identification of PID and to evaluate its capability for further pathophysiological studies. We used male barbiturate-anesthetized Wistar rats (n = 10) in which middle cerebral artery occlusion had been performed with a surgical thread. Middle cerebral artery occlusion resulted in a drop in parietally measured regional cerebral blood flow (laser Doppler flowmetry) to 31 +/- 8% of baseline flow. Six +/- 4 minutes after the induction of focal ischemia, 5 +/- 2 direct current deflections were recorded during a one-hour measurement period which may be regarded as PID. Measuring regional cerebral blood oxygenation changes with a NIRO 500 revealed dynamic concentration changes in the three chromophores oxyhemoglobin [HbO2], deoxyhemoglobin [Hb], and the oxidized form of cytochrome aa3 [CytO] during PID. Typically, an initial slight decrease of [HbO2] (-6.1 +/- 1.7 arbitrary units [AU] and an increase of [Hb] (+11.5 +/- 7.7 AU) were followed by an increase of [HbO2] (+10.8 +/- 4.7 AU) and a decrease of [Hb] (-4.7 +/- 5.5 AU); [CytO] decreased during the depolarizations (-2.0 +/- 1.2 AU). We conclude that NIRS can detect typical PID-associated changes in blood oxygenation. We hypothesize that during the course of PID, unlike "normal" spreading depression, hypoxygenation precedes hyperoxygenation of the microcirculation in a given cortex volume as the depolarization wave propagates through hemodynamically compromised to intact tissue. This would accord with the known damaging effect of PID. The NIRS "fingerprint" of PID encourages the search for PID during early stroke in patients.
authors.affiliation: Charité Hospital, Department of Neurology, Humboldt-University Berlin, Germany.
authors.forename: T
authors.initials: T
authors.lastname: Wolf
authors.forename: U
authors.initials: U
authors.lastname: Lindauer
authors.forename: U
authors.initials: U
authors.lastname: Reuter
authors.forename: T
authors.initials: T
authors.lastname: Back
authors.forename: A
authors.initials: A
authors.lastname: Villringer
authors.forename: K
authors.initials: K
authors.lastname: Einhäupl
authors.forename: U
authors.initials: U
authors.lastname: Dirnagl
mesh_terms: D000818:Animals; D002545:Brain Ischemia / Q000097:blood* / Q000503:physiopathology; D002544:Cerebral Infarction / Q000097:blood* / Q000503:physiopathology; D002560:Cerebrovascular Circulation; D004594:Electrophysiology; D008297:Male; D010100:Oxygen / Q000378:metabolism*; D051381:Rats; D017208:Rats, Wistar; D019265:Spectroscopy, Near-Infrared
chemical_list: D010100:Oxygen