ACUTE CHANGES IN INTRACRANIAL-PRESSURE AND PRESSURE-VOLUME INDEX AFTER FOREBRAIN ISCHEMIA IN NORMOGLYCEMIC AND HYPERGLYCEMIC RATS

Background and Purpose Hyperglycemia enhances the deleterious effect o f global cerebral ischemia. One possible explanation is that increased anaerobic glycolysis leads to exaggeration of intracellular acidosis and increased postischemic edema. To examine the importance of this ed ema on postischemic cerebral perfusion dynamics, we measured acute cha nges in intracranial pressure (ICP), specific gravity, and the pressur e-volume index (PVI) after forebrain ischemia in normoglycemic and hyp erglycemic rats. Methods Rats underwent 15 minutes of forebrain ischem ia and 90 minutes of reperfusion. ICP and mean arterial pressure were continuously monitored. Before ischemia, rats received either saline o r glucose intravenously. Ninety minutes after ischemia, the specific g ravity of the neocortex was measured. In a second experiment, the PVI was measured at 20 and 60 minutes after ischemia. Results Preischemic ICP (mean+/-SD) was 7+/-1 mm Hg in both groups. A peak ICP (approximat e to 11 mm Hg) occurred within 15 to 20 minutes after ischemia in both groups. Between 25 and 80 minutes after ischemia, ICP was significant ly but only slightly greater in hyperglycemic than in normoglycemic ra ts. Cerebral perfusion pressure was similar between groups and remaine d greater than 100 mm Hg. Specific gravity was also similar for both g roups but was less than normal values. The PVI in hyperglycemic rats w as lower than in normoglycemic rats, indicating reduced compliance. Co nclusions These findings indicate that hyperglycemia-augmented intrais chemic tissue acidosis does not contribute to worsened outcome by mean s of compromised cerebral perfusion pressure during the early stages o f recovery. Nevertheless, evidence was found for decreased cerebral co mpliance, indicating an effect of hyperglycemia on intracranial volume compartments other than cortical parenchyma.