INFLUENCE OF HYPOGLYCEMIC COMA ON BRAIN WATER AND OSMOLALITY

To study the effects of pronounced hypoglycemia on brain osmolality an d brain edema formation, fasted rats were rendered hypoglycemic by inj ection of insulin, and subjected to 30 min of hypoglycemic coma. Recov ery was accomplished by glucose administration. The change in water co ntent in different brain regions was measured as a change in specific gravity after 30 min of hypoglycemic coma, or 30, 60, and 180 min afte r glucose administration. Plasma and brain tissue osmolality were meas ured in separate animals. The results show a significant decrease in s pecific gravity (increase in water content) in all structures measured (caudoputamen, neocortex, hippocampus, and cerebellum) at the end of the period of coma, as well as after 30 min and 60 min of recovery. At 180 min of recovery, brain water was normalized. The edema affected a ll structures to the same degree regardless of their vulnerability to hypoglycemic damage. Brain tissue osmolality showed a tendency to decr ease with decreasing tissue glucose content. The decrease was signific ant (P<0.01) at 30 min of isoelectric coma. In the recovery phase, nor mal brain osmolality was restored within 30 min. Measurements of blood -brain barrier (BBB) permeability after 30 min of hypoglycemic coma sh owed no extravasation of Evan's blue, though a small but significant i ncrease in the permeability for aminoisobutyric acid (AIB) in caudoput amen and in cerebellum was found. To analyze the importance of tissue acidosis for formation of edema, hypoglycemic animals were made acidot ic by increasing the CO2 concentration in inspired air to produce an a rterial plasma pH of 6.8-6.9. In these animals the edema was of a simi lar degree to the normocapnic animals, and the permeability for AIB wa s normal. We conclude that osmolytic mechanisms are not the primary ca use of the selective neuronal vulnerability in hypoglycemic coma. Furt hermore, the BBB is largely intact during a hypoglycemic insult.