Stroke, Vol 22, 225-232, Copyright © 1991 by American Heart Association
N Futrell
To provide further evidence that the multiple cerebral infarcts found in
rats following photochemical damage to the carotid artery are caused by
emboli and to eliminate the systemic hypotension and heating of the blood
reported with the previous photochemical embolic stroke model (rose bengal
and a green laser), I have modified the photochemical technique. Brain
pathology was studied in 18 Wistar rats following carotid artery
irradiation with a red laser (632 nm) at powers ranging from 100 to 800
mW/cm2 for 10 or 20 minutes following the injection of the photosensitizing
dye Photofrin II. Multiple cerebral arterioles were occluded by platelet
aggregates containing frequent erythrocytes and leukocytes, identical to
the thrombotic material in the carotid artery but different from the
platelet aggregates seen in the carotid artery and the brain in the rose
bengal model. Eighty infarcts were distributed randomly throughout the
brain ipsilateral to the nonocclusive carotid thrombus. Significant heating
(0.5 degree C or more) of the blood occurred only with laser powers higher
(1,600 mW/cm2) or laser irradiations longer (25 minutes) than those used in
the improved model of embolic stroke. This model mimics one mechanism of
stroke in humans and provides a means to study systematically the
morphological evolution of small cerebral infarcts.
ARTICLES
An improved photochemical model of embolic cerebral infarction in rats
Department of Neurology, Henry Ford Hospital, Detroit, Mich. 48202-2689.
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