Alterations in behavior, brain electrical activity, cerebral blood flow, and intracranial pressure produced by triethyl tin sulfate induced cerebral edema.

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 regional CBF 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. There were two distinct acute groups: (1) acute low pressure (ALP) animals - alert but tetraperetic, and (2) acute high pressure (AHP) animals - deeply stuporous, with minimal pain response and gross EEG slowing. ICP was significantly elevated only in AHP animals. Hemispheric CBF was significantly reduced in AHP and 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. In the absence of any significant increase in ICP, cerebral edema appears to cause a significant reduction in cerebral blood flow and this reduction corresponds with the magnitude and location of the edema.

Cerebral blood flow in the monkey after focal cryogenic injury.

“…10 ' " The mechanism by which blood flow falls around injured brain cannot be discerned from this investigation. The role, if any, of vasospasm produced by biogenic amines released from injured tissue, 14 increasing tissue pressure, 12 -13 or traumatic edema 14 remains to be defined.…”

Brain Water Content: a Misunderstood Measurement?

“…The water content has been expressed as % brain water, determined from the difference in wet and dry weights (i.e. the water weight) divided by the wet weight (1–3). As described below, this is unfortunate as it can lead to a misinterpretation of the impact of ‘small’ changes in % brain water.…”

Role of vasopressin and its antagonism in stroke related edema

“…A staple of today's stroke management is the evaluation of ICP and maintenance of cerebral perfusion pressure. Early studies on cerebral edema regarded swelling of the brain as a relatively benign process in isolation and instead focused on reduction in blood flow after development of edema as the primary cause of cellular dysfunction (Marshall et al, ; O'Brien, ). We have since discovered that the pathogenesis of cerebral edema is inextricable from many of the damaging responses to stroke, including inflammation (Taya et al, ), dysregulation of electrolytes (Yang et al, ), and neurotransmitter homeostasis, all of which are known to worsen patient outcomes after stroke (Gotoh et al, ; Minamisawa et al, ; Kochanek and Hallenbeck, ; Rane et al, ; Castellanos et al, ).…”