Cortical Tissue Pressure Gradients in Early Ischemic Brain Edema

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.

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

Journal of Cerebral Blood Flow & Metabolism ◽

10.1038/jcbfm.1986.100 ◽

1986 ◽

Vol 6 (5) ◽

pp. 546-552 ◽

Cited By ~ 24

Author(s):

Shizuo Hatashita ◽

Julian T. Hoff

Keyword(s):

Hydrostatic Pressure ◽

Pressure Gradient ◽

Water Content ◽

Brain Edema ◽

Intraluminal Pressure ◽

Tissue Pressure ◽

Ischemic Brain ◽

Hydrostatic Pressure Gradient ◽

Arterial Blood ◽

Ischemic Brain Edema

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.

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