Stroke, Vol 11, 593-601, Copyright © 1980 by American Heart Association
FJ Schuier and KA Hossmann
In cats, the early development of ischemic brain edema was studied 1 to 4
hours after transorbital occlusion of the left middle cerebral artery
(MCA). Two groups of animals were compared: those in which blood flow in
the territory of the MCA decreased below the threshold of 10--15 ml/100
g/min (critical ischemia) and those in which it remained above this level
(non-critical ischemia). In animals with critical ischemia, water content
in the cortex of the MCA territory increased from 80.7 +/- 0.4 to 83.0 +/-
0.3 vol. % (means +/- SE) within 4 h. Edema was associated with an increase
in tissue osmolality by 16--22 mosm/kg w.w., and a rise of sodium from 262
+/- 9 to 454 +/- 13 meq/kg d.w. and a decrease of potassium from 442 +/- 20
to 305 +/- 32 meq/kg d.w. The sodium/potassium ratio rose from 0.60 +/-
0.03 to 1.55 +/- 0.17. The water and electrolyte disturbances were
accompanied by a major shift of extracellular fluid into the intracellular
compartment, as evidenced by the increase in cortical impedance from 282 to
660 ohm/cm within 2 h. According to the Maxwell equation, this reflects a
narrowing of the extracellular space from 19.8 to 11.4%. Brain volume was
continuously monitored using an induction transducer; swelling began within
a few minutes of vascular occlusion, and it continued throughout the 4 h
observation period. During this time the blood-brain barrier remained
intact as evidenced by the absence of Evans blue staining. Edema was
associated with disturbances of the energy producing metabolism, but there
was no strict correlation with either lactate or the concentration of high
energy phosphates. In animals without critical ischemia, i.e. in which
blood flow remained above 10--15 ml/100 g/min, edema was absent despite a
distinct deterioration of the energy state of the brain. Edema was also
absent in the border zone, in the territory of the posterior cerebral
artery and in the contralateral hemisphere of animals with both critical
and non-critical ischemia. It is concluded that the early ischemic brain
edema following middle cerebral artery occlusion is of the cytotoxic type,
that it develops at a flow rate below 10--15 ml/100 g/min, and that it is
not strictly correlated with the energy state of the brain.
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