Project Details


Large tissue net ionic shifts are associated with cerebral edema after
middle cerebral artery occlusion (MCAo). The net ionic shifts correlate
highly with water concentration changes with regression slopes of 150-160
mu moles/ml, close to plasma ionic concentrations, suggesting that ionic
shifts caused edema since participation of other osmotic agents would
reduce the slope. The causes of the net ionic shift are not known. We
will test the hypotheses that (a) net ionic shifts result from differences
in extracellular Na and K gradients driving Na entry and K loss and (b)
glial K uptake causes different in the Na and K gradients. Extracellular
Na and K will be measured with ion-selective microelectrodes after MCAo
and compared with tissue ionic and water shifts. Albumen and IgG passage
across the blood brain barrier, regional blood flow, blood pressure, and
plasma ionic levels will be monitored. Ionic shifts will be investigated
in rat cortical freeze lesions. Freezing disrupts glial cells, prevent K
uptake, and thereby should reduce net ionic shift and edema. The effects
of systemic furosemide, mannitol, and/or methylprednisolone on
extracellular and tissue ionic shifts will be studied in the rat MCAo and
cortical freeze models. Neurophysiological and morphological changes will
be correlated with ionic shifts. These studies will clarify ionic
mechanisms in edema, relate tissue ionic shifts to tissue damage, and
establish rational bases for treating ionic edema in stroke.
Effective start/end date1/1/9011/30/93


  • National Institute of Neurological Disorders and Stroke


  • Physiology


Explore the research topics touched on by this project. These labels are generated based on the underlying awards/grants. Together they form a unique fingerprint.