Pathophysiologic Aspects of Ischemic Edema

Abstract

1. Within 5 min of interference with the arterial blood supply, a recognizable water uptake, as measured by specific gravity of the brain tissue, can be observed. This abnormal water uptake, based on the swelling of cellular elements of the affected brain parenchyma, progresses further with the continuation of ischemia. 2. The onset of necrotic changes in the brain parenchyma (with the exclusion of blood vessels) produces a drastic further reduction in specific gravity, presumably due to the osmotic effect of products of lysosomal digestion, as well as to fatty transformation of the necrotic tissue. 3. Release of the arterial occlusion and reestablishment of the circulation markedly accelerate the reduction in specific gravity of brain tissue which has been exposed to prolonged ischemia (3 or 6 h). Following 1 h of occlusion, a pronounced drop in specific gravity occurs after some delay and in relation to the development of necrotic changes. 4. Opening of the blood-brain barrier (BBB) to serum proteins in the post-ischemic periods, as evaluated by the behavior of Evans blue tracer, is of a transitory nature. This opening, which appears to be due to a greatly increased pinocytotic passage of proteins across the endothelial layer, seems to be independent of necrotic changes in the parenchyma or of an increase in the cerebral blood flow (CBF). 5. Ischemic brain edema can be regarded as predominantly of the cytotoxic type, starting with an intracellular accumulation of water, and later intensifying markedly due to osmotic movement of water into necrotic areas of the brain parenchyma. Opening of the BBB to proteins, which occurs after some delay according to the principles of the “maturation” phenomenon, introduces in addition a vasogenic component into the ischemic pathology.