title: Local cerebral blood flow during the first hour following acute ligation of multiple arterioles in rat whisker barrel cortex.
abstract: The objectives are to measure the early time-course of the flows of blood, red cells, and plasma in brain tissue destined to infarct following arterial occlusion. The flux of fluorescent red blood cells (fRBCs) through venules and the arteriovenous transit times (AVTT) of fluorescein-labeled plasma albumin were periodically monitored in anesthetized adult Wistar rats before and up to 60 min after permanent ligations of several small branches of the middle cerebral artery. Of note, fRBC is a function of venular erythrocyte flow and volume, whereas AVTT is a function of plasma flow and volume in visible arteriole-capillary-venule units. In another group of anesthetized rats, local cerebral blood flow (ICBF) was measured 1 h after permanent arterial occlusion by [14C]iodoantipyrine (IAP) autoradiography. With this model of focal ischemia, the lesion is highly reproducible and involves part of the whisker barrel cortex. Infarction of this area was observed in 12 of 13 rats. From 10 to 60 min after arterial occlusion, AVTT was nearly four times longer in the ischemic barrel cortex than at the same site before ligations, and fRBC flux was 25%. Neither parameter changed appreciably over this time. After 60 min of ischemia, ICBF on the ipsilateral barrel cortex was 18% of that on the contralateral side and 15% of the sham control value for the same area of the barrel cortex. Since whole blood flow in the ischemic barrel cortex was < 20% of normal at 60 min and AVTT and fRBC flux were essentially constant from 10 to 60 min, the rates of plasma and red cell flows were similarly depressed during the first hour of arteriolar occlusion. In conclusion, such lowering of red cell, plasma, and blood flows produced consistent infarctions in the barrel cortex.
authors.affiliation: Department of Cell Biology and Physiology, Washington University School of Medicine, St. Louis, Missouri 63110, USA.
authors.forename: L
authors.initials: L
authors.lastname: Wei
authors.forename: K
authors.initials: K
authors.lastname: Craven
authors.forename: J
authors.initials: J
authors.lastname: Erinjeri
authors.forename: G E
authors.initials: GE
authors.lastname: Liang
authors.forename: D
authors.initials: D
authors.lastname: Bereczki
authors.forename: C M
authors.initials: CM
authors.lastname: Rovainen
authors.forename: T A
authors.initials: TA
authors.lastname: Woolsey
authors.forename: J D
authors.initials: JD
authors.lastname: Fenstermacher
mesh_terms: D000208:Acute Disease; D000758:Anesthesia; D000818:Animals; D000894:Anti-Inflammatory Agents, Non-Steroidal; D000983:Antipyrine / Q000031:analogs & derivatives; D001157:Arterial Occlusive Diseases / Q000503:physiopathology*; D001160:Arterioles / Q000502:physiology; D001345:Autoradiography; D002545:Brain Ischemia / Q000503:physiopathology*; D002250:Carbon Radioisotopes; D002536:Cerebral Arteries / Q000502:physiology; D002550:Cerebral Veins / Q000502:physiology; D002560:Cerebrovascular Circulation / Q000502:physiology*; D002561:Cerebrovascular Disorders / Q000503:physiopathology; D004396:Coloring Agents; D004912:Erythrocytes / Q000166:cytology / Q000502:physiology; D005260:Female; D019793:Fluorescein; D005456:Fluorescent Dyes; D008026:Ligation; D008297:Male; D008928:Mitochondria / Q000201:enzymology; D009562:Nissl Bodies / Q000737:chemistry / Q000502:physiology; D010088:Oxidoreductases / Q000378:metabolism; D010640:Phenothiazines; D051381:Rats; D017208:Rats, Wistar; D013003:Somatosensory Cortex / Q000098:blood supply* / Q000503:physiopathology; D014738:Vibrissae / Q000502:physiology*
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D002250:Carbon Radioisotopes; D004396:Coloring Agents; D005456:Fluorescent Dyes; D010640:Phenothiazines; D010088:Oxidoreductases; D000983:Antipyrine; D019793:Fluorescein; C008135:iodoantipyrine; C009469:thionine