scholarly journals Role of a Hydrostatic Pressure Gradient in the Formation of Early Ischemic Brain Edema

1986 ◽  
Vol 6 (5) ◽  
pp. 546-552 ◽  
Author(s):  
Shizuo Hatashita ◽  
Julian T. Hoff

We studied whether a hydrostatic pressure gradient between arterial blood and brain tissue plays a role in the formation of early ischemic cerebral edema after middle cerebral artery (MCA) occlusion in cats. Tissue pressure, regional CBF, and water content were measured from the cortex in the core and the peripheral zone of brain normally perfused by the MCA. Intraluminal arterial pressure was altered at intervals by inflation of an aortic balloon to vary the blood–tissue pressure gradient in the ischemic zone. Brain water content in the ischemic core, where flow fell to 5.5 ml/100 g/min, increased within 1 h of occlusion. After occlusion tissue pressure rose from 7.95 ± 0.72 mm Hg at 1 h to 13.16 ± 1.13 mm Hg at 3 h. When intraluminal pressure was increased, water content increased further, but only at 1 h after occlusion. In the periphery where flow was 18.9 ml/100 g/min during normotension. neither water content nor tissue pressure rose within 3 h of occlusion. Increased intraluminal pressure was accompanied by increased water content only at 3 h. This study indicates that a hydrostatic pressure gradient is an important element in the development of ischemic brain edema, exerting its major effect during the initial phase of the edema process.

1986 ◽  
Vol 6 (1) ◽  
pp. 1-7 ◽  
Author(s):  
Shizuo Hatashita ◽  
Julian T. Hoff

We examined the role of ischemic brain edema, tissue pressure gradients, and regional CBF (rCBF) in adjacent regions of cerebral cortex in cats with middle cerebral artery (MCA) occlusion (MCAO). Tissue pressure, rCBF, and water content were measured from gray matter in the central core and the peripheral margin of the MCA territory over 6 h after MCAO. Ventricular fluid pressure and CSF pressure were recorded. Tissue pressure in the ischemic core, with a flow of ∼5 ml/100 g/min, increased more than that in the periphery where flow was ∼19 ml/100 g/min. Tissue pressure rose progressively to 14.8 ± 1.0 mm Hg in the core over 6 h after MCAO, establishing a significant pressure gradient between that tissue and the lateral ventricle nearby or the subarachnoid space in the middle fossa within the first 3 h. The increase in tissue pressure was linearly related to the amount of edema fluid that developed until the edema reached a severe degree. This study shows that a hydrostatic tissue pressure gradient within ischemic cortex is associated with ischemic brain edema. The magnitude of the gradient that develops is related to the severity of ischemic edema in that tissue.


1981 ◽  
Vol 9 (3) ◽  
pp. 273-282 ◽  
Author(s):  
Kyuya Kogure ◽  
Raul Busto ◽  
Peritz Scheinberg

1988 ◽  
Vol 8 (4) ◽  
pp. 552-559 ◽  
Author(s):  
Shizuo Hatashita ◽  
Julian T. Hoff ◽  
Shahriar M. Salamat

The relationship of the osmotic pressure gradient between blood and brain, and the development of ischemic brain edema was studied. Focal cerebral ischemia was produced by left middle cerebral artery occlusion in rats. Brain osmolality was determined with a vapor pressure osmometer, brain water content by wet–dry weight, and tissue sodium and potassium contents by flame photometry. Permeability of the BBB was tested by Evans blue. Measurements were made from the ischemic cortex within 14 days of occlusion. Brain osmolality increased from 311 ± 2 to 329 ± 2 mOsm/kg by 6 h after occlusion. Serum osmolality did not change significantly. The osmotic gradient between blood and brain peaked at ∼26 mOsm/kg. Brain osmolality then decreased to 310 ± 2 mOsm/kg by 12 h after occlusion and remained at about that same level. Water content increased progressively within 1 day of occlusion, then gradually decreased by 14 days. Brain tissue sodium plus potassium content did not increase within 6 h of occlusion, and Evans blue extravasation was not seen within that time. These findings indicate that an osmotic pressure gradient contributes to the formation of edema only during the early stage of cerebral ischemia. Furthermore, the increase in brain osmolality is not related to tissue electrolyte change or BBB disruption to protein.


Brain Edema ◽  
1985 ◽  
pp. 360-366 ◽  
Author(s):  
S. Inao ◽  
H. Kuchiwaki ◽  
N. Hirai ◽  
S. Takada ◽  
N. Kageyama ◽  
...  

Stroke ◽  
1986 ◽  
Vol 17 (6) ◽  
pp. 1149-1152 ◽  
Author(s):  
Y Horikawa ◽  
S Naruse ◽  
C Tanaka ◽  
K Hirakawa ◽  
H Nishikawa

Stroke ◽  
1980 ◽  
Vol 11 (6) ◽  
pp. 593-601 ◽  
Author(s):  
F J Schuier ◽  
K A Hossmann

Stroke ◽  
1987 ◽  
Vol 18 (1) ◽  
pp. 150-157 ◽  
Author(s):  
W D Lo ◽  
A L Betz ◽  
G P Schielke ◽  
J T Hoff

2014 ◽  
Vol 127 ◽  
pp. 5-9 ◽  
Author(s):  
Wen-Wen Wang ◽  
Cheng-long Xie ◽  
Li-Li Zhou ◽  
Guo-Sheng Wang

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