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Stroke, Vol 12, 211-217, Copyright © 1981 by American Heart Association

ARTICLES

Blood flow and regulation of blood flow in experimental peritumoral edema

KA Hossman and M Bloink

In 27 pentobarbital-anesthetized cats cerebral blood flow and regulation of cerebral blood flow was measured one to 3 weeks following stereotactical xenotransplantation of a rat glioma clone into the internal capsula. Tumor growth was accompanied by severe vasogenic peritumoral edema in the white matter of the tumor-bearing hemisphere. White matter water content in the vicinity of the tumor increased from 69.1 +/- 0.9 to 0.5 +/- 0.7 ml/100 g wet weight (means +/- SE) which corresponds to an increase in tissue volume of about 60%. Intracranial pressure after 3 weeks was 12 +/- 2.6 mm Hg. Blood flow in the peritumoral white matter decreased from 32.2 +/- 5.6 to 18.6 +/- 1.9 ml/100/g/min but it did not change in the peritumoral grey matter or the opposite hemisphere. The decrease in blood flow was due to the volume expansion of the swollen edematous tissue and not to a compression of the microcirculation because neither flow nor vascular resistance changed when referred to dry rather than to wet weight of the edematous tissue. Flow regulation in the peritumoral edematous white matter was disturbed. CO2 reactivity of blood flow was 5.4% mm Hg change in aPCO2 (non-edematous contralateral white matter 6.4%/mm Hg), and the autoregulatory capacity between 40 and 170 mm Hg was 0.7%/mm Hg (non-edematous white matter 1.0% mm Hg). It is concluded that in the absence of significant intracranial hypertension, even severe degrees of vasogenic peritumoral edema do not interfere with blood flow and flow regulation. This is in contrast to the cytotoxic type of edema, and indicates that microcirculatory compression by edema, when present, is the consequence of pericapillary glial hydrops and not of an accumulation of extravasated edema fluid.

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