Article date: 1992/3/1
PubMed ID: 1542903
Journal name: Stroke (ISSN: 0039-2499)
These data suggest that the rapid transition to cortical hypoperfusion after forebrain ischemia may be triggered locally by a neuronal mechanism but that this mechanism does not underlie the initial hyperemia.
We assessed local cortical blood flow continuously by laser Doppler flowmetry to permit observation of any rapid flow changes after forebrain ischemia induced by four-vessel occlusion for 20 minutes in rats. To investigate the role of local cortical neurons in the regulation of any blood flow fluctuations, five rats received intracortical microinjections of a neurotoxin (10 micrograms ibotenic acid in 1 microliter; 1.5-mm-depth parietal cortex) 24 hours before ischemia to induce selective and localized neuronal depletion in an area corresponding to the sample volume of the laser Doppler probe (1 mm3). Local cerebral blood flow was measured within the injection site and at an adjacent control site.
Ischemia was followed by marked hyperemia (235 +/- 23% of control, n = 7), followed by secondary hypoperfusion (45 +/- 3% of control, n = 7). The transition from hyperemia to hypoperfusion occurred not gradually but precipitously (maximal slope of flow decay: 66 +/- 6%/min; n = 7). In ibotenic acid-injected rats, hyperemia was preserved at the injection site, but the sudden decline of blood flow was abolished (maximal slope of flow decay: 5 +/- 3%/min compared with 53 +/- 8%/min at the control site; n = 5, p less than 0.001) and no significant hypoperfusion developed (103 +/- 20% of control at 60 minutes).
Author List: Frerichs K U, Sirén A L, Feuerstein G Z, Hallenbeck J M
Publication Types: Journal Article; Research Support, U.S. Gov't, P.H.S.
Substances mentioned in the article: Ibotenic Acid;
Mesh terms: Animals; Blood Pressure; Brain/pathology; Brain Ischemia/pathology; Cerebrovascular Circulation; Ibotenic Acid/pharmacology; Lasers; Male; Neurons/drug effects; Rats; Rats, Inbred Strains; Ultrasonography;