Triethyl Tin-Induced Cerebral Edema: Implications for Determination of Cerebral Blood Flow in Edematous Tissue

Abstract

The interrelationships between cerebral edema, intracranial pressure (ICP), and cerebral blood flow (CBF) were studied in acute and chronic triethyl tin sulfate-treated rats. Prior to pentobarbital anesthesia behavioral observations were made. ICP and rCBF were measured under steady-state conditions and brain water content was determined by vacuum drying of the right cerebral hemisphere. Control and chronic animals were neurologically normal and had normal brain electrical activity. There were two distinct acute groups: acute low pressure (ALP) alert but tetraparetic; and acute high pressure (AHP) deeply stuporous, minimal pain response, gross EEG slowing. ICP was significantly elevated only in AHP animals. Hemispheric CBF was significantly reduced in AHP and in chronic animals. The interaction of increased pressure and edema (AHP) produced the greatest decrease in CBF, although deep white flows were significantly affected in all experimental groups. Chronic animals had significantly lower flow in four of seven regions compared to ALP animals despite no significant difference in ICP. Water content was significantly increased in all experimental groups with the greatest increase in the chronic animals. The marked increase in brain water content produced by triethyl tin intoxication can reduce CBF independent of ICP. However, CBF is not reduced below the critical level of O2 required by the brain, and function remains normal, until a significant increase in ICP occurs. Therefore, triethyl tin cerebral edema does not disturb brain function as long as CBF is adequate to supply the brain’s nutrient needs. Our studies also suggest that in white matter edema the measured reduction in CBF may reflect only an increase in white matter volume without any real interference with CBF in the microcirculation. If this conclusion is correct, then the actual flow through a vascular bed in edematous brain using any diffusable isotope can be determined only if the volume increase in the tissue supplied by that vascular bed can be calculated.