Pathophysiologic Aspects of Ischemic Edema

147

The relationship between increase in water content in ischemic brain and levels of regional blood flow has been studied in 11 primates. Flows were recorded using the method of hydrogen (2-minute) clearance, from a total of 128 electrodes in cortex and white matter, and a gradation of ischemia was produced by middle cerebral occlusion transorbitally. The flows were reduced in the area of densest ischemia from control levels of 12.0 +/- 12.0 ml/100g/min to 7.0 +/- 5.4 ml/100g/min, with lesser decreases over the remainder of the ischemic hemisphere. Water content was measured in cortex and white matter, in regions topographically related to those of flow measurements, by densitometric assessment using precalibrated kerosene/bromobenzine columns. The average water content of cortex in regions remote from ischemia was 797.4 +/- 5.8 mg/gm and in white matter 708.5 +/- 8.2 mg/gm. Significant increases in water content (comparing corresponding regions of the two hemispheres) of up to 11.4 +/- 7.5 mg/gm were demonstrated in the most ischemic cortical areas. A gradient of water increase was evident in the ischemic hemisphere, increases water content being greatest in the opercular zone and least in the parasagittal area. Significant differences in white matter water content between the 2 hemispheres were demonstrated only in the most densely ischemic areas in the current experiments where ischemia was limited to 93 +/- 20 mins in the 11 animals without reperfusion. The relationship between ischemic density and water content increase showed that significant increases in water content occurred in regions where terminal flows had been below 20 ml/100g/min, indicating that accumulation of water in ischemic brain begins at flow values comparable to those associated with the failure of synaptic transmission, higher than those associated with failure of the ionic pump of the cell. Possible pathophysiological mechanisms are discussed.

Section: Time Factor In Development Of Regional Water Increases In Comentioning

confidence: 78%

Ischemic brain edema following middle cerebral artery occlusion in baboons: relationship between regional cerebral water content and blood flow at 1 to 2 hours.

Symon¹,

Branston²,

Chikovani³

1979

147

“…There is, however, a degree in selection of their material as only those with severe neurological signs were selected for further histology. Fugimoto et al 19 have assessed flow by autoradiography. Although their paper does not publish the actual results of the flow measurements, it does show marked changes in the ipsilateral hemisphere, particularly the subcortical grey matter, with a suggestion that the contralateral thalamus may also be affected.…”

Section: Discussionmentioning

confidence: 99%

Cerebral blood flow and edema following carotid occlusion in the gerbil.

Crockard¹,

Iannotti²,

A³

et al. 1980

146

SUMMARY A technique for measuring focal cerebral blood flow (CBF) and brain specific gravity (SG) in gerbils is described; CO S reactivity and autoregulation were tested. The mean CBF was 29.5 ± 4.5 ml/100 gm/min and brain SG 1.0500 ±0.0004. Unilateral carotid occlusion resulted in a reduction of flow to 12.8 ± 5.8 ml/100 gm/min in the ipsilateral hemisphere with little change in the contralaterai hemisphere; there was also a decrease in brain SG. One hour after occlusion, brain edema, as judged by decreased SG, developed at CBF less than 20 ml/100 gm/min and reached maximal levels at 7 ± 2 ml/100 gm/min. The amount of edema appeared to be related chiefly to the residual post-occlusion flow. With bilateral occlusion, CBF was close to zero and there was no change in SG, indicating that in the "no flow" situation, there is no edema.

“…15 - 49 We have shown in a previous study that distinct electrophysiological phases of depression, epileptiform activity, and subsequent loss of intensity are associated with laminar necrosis of the underlying cortex. 13 Epileptiform activity per se can cause intracellular edema in neonatal rat cortex.…”

mentioning

confidence: 98%

Time course of intracellular edema and epileptiform activity following prenatal cerebral ischemia in sheep.

Williams

Gunn

Gluckman

1991

171

The role of edema in the pathogenesis of hypoxic-ischemic injury in the immature brain is controversial. We studied 15 chronically instrumented fetal sheep following transient cerebral ischemia, to estimate changes in extracellular space using an impedance technique, to quantify the electroencephalogram with real-time spectral analysis, and to assess histologic outcome 3 days after the insult These measurements were made in the parasagittal cortex. There was a rapid loss of extracellular space from 5±2 minutes after the onset of ischemia. Following 10 minutes of ischemia (n=7) the intracellular edema peaked but then quickly resolved (6±4 minutes), and mild selective ncuronal loss was seen. In contrast, the swelling was biphasic after 30-40 minutes of ischemia (n=8). The early edema resolved slowly (28±12 minutes) but incompletely, and secondary swelling began at 7±2 hours and peaked at 28±6 hours. The early swelling was the more severe. Postinsult epileptiform activity began at 8±2 hours and peaked at 10 ±3 hours; later there was laminar necrosis of the underlying cortex. The secondary decrease of extracellular space indicates that a progressive loss of membrane function started with the onset of postischemic epileptiform activity. The increased metabolic load of the epileptiform activity may have worsened this delayed deterioration. (Stroke 1991,22:516-521)