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(Stroke. 1996;27:1405-1410.)
© 1996 American Heart Association, Inc.

Articles

Acute Changes in Intracranial Pressure and Pressure-Volume Index After Forebrain Ischemia in Normoglycemic and Hyperglycemic Rats

Yuji Morimoto, MD, PhD; Yoshiko Morimoto, MD; David S. Warner, MD Robert D. Pearlstein, PhD

the Departments of Anesthesiology (Y.M., Y.M., D.S.W.) and Surgery (R.D.P.), Duke University Medical Center, Durham, NC.

Correspondence to David S. Warner, MD, Department of Anesthesiology, Box 3094, Duke University Medical Center, Durham, NC 27710. E-mail warne002@mc.duke.edu.

Background and Purpose Hyperglycemia enhances the deleterious effect of 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 edema on postischemic cerebral perfusion dynamics, we measured acute changes in intracranial pressure (ICP), specific gravity, and the pressure-volume index (PVI) after forebrain ischemia in normoglycemic and hyperglycemic rats.

Methods Rats underwent 15 minutes of forebrain ischemia and 90 minutes of reperfusion. ICP and mean arterial pressure were continuously monitored. Before ischemia, rats received either saline or glucose intravenously. Ninety minutes after ischemia, the specific gravity 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 (11 mm Hg) occurred within 15 to 20 minutes after ischemia in both groups. Between 25 and 80 minutes after ischemia, ICP was significantly but only slightly greater in hyperglycemic than in normoglycemic rats. Cerebral perfusion pressure was similar between groups and remained greater than 100 mm Hg. Specific gravity was also similar for both groups but was less than normal values. The PVI in hyperglycemic rats was lower than in normoglycemic rats, indicating reduced compliance.

Conclusions These findings indicate that hyperglycemia-augmented intraischemic tissue acidosis does not contribute to worsened outcome by means of compromised cerebral perfusion pressure during the early stages of recovery. Nevertheless, evidence was found for decreased cerebral compliance, indicating an effect of hyperglycemia on intracranial volume compartments other than cortical parenchyma.

Editorial Comment

J. Paul Muizelaar, MD, PhD, Guest Editor

Department of Neurosurgery, Wayne State University, Detroit, Mich

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