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Pathogenesis of Hemorrhagic Infarction of the BrainII. Protective Effect of Low Molecular Weight Dextran
CREIGHTON HARDIN, MD;
THOMAS H. HENDREN, MD;
AMIN A. FARIS, MD;
CHARLES M. POSER, MD
Arch Neurol. 1963;9(5):473-476.
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Introduction
In a previous article on the experimental investigation of the pathogenic mechanism of hemorrhagic infarction of the brain1 we were able to demonstrate in dogs that the combination of systemic hypertension and an adequate collateral circulation appeared to be essential in producing hemorrhagic infarction within an ischemic area resulting from surgical occlusion of the middle cerebral artery.
A recent report by Cyrus and his collaborators2 concerning the apparent protective effect of intravenous low molecular weight dextran* (LMWD) led us to in vestigate the use of this material under the experimental conditions described for the production of hemorrhagic infarction.
Materials and Method
Fourteen mongrel dogs weighing between 10-14 kg were used in this experiment. Systemic hypertension was induced by making a surgical coarctation of the thoracic aorta 2 cm above the diaphragm, reducing the lumen of the aorta to approximately 20% of normal. Craniotomy was performed two to
. . . [Full Text PDF of this Article]
Author Affiliations
KANSAS CITY, KAN
From the Department of Surgery and the Section of Neurology, Department of Medicine, University of Kansas Medical Center.
Footnotes
Submitted for publication June 24, 1963; accepted Aug 15.
Associate Professor of Surgery (Dr. Hardin); Resident in Surgery (Dr. Hendren); Chief Resident in Neurology (Dr. Faris); Associate Professor of Medicine (Neurology) (Dr. Poser).
Supplied as Rheomacrodex by Pharmacia Laboratory, Inc., New York.
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