Pj. Luthert et J. Greenwood, SELECTIVE CLOSURE OF THE VASCULAR BED OF AN EXPERIMENTAL GLIOMA MODELDURING IN-SITU SALINE PERFUSION, Neuropathology and applied neurobiology, 20(5), 1994, pp. 448-453
Flow through the vasculature of an experimental rat glioma has been in
vestigated during in situ perfusion of the brain, via the ascending ao
rta, with a simple saline solution. Using such a system, it has been s
hown previously that the blood-brain barrier will remain intact with a
n adequate cerebral perfusate flow rate for at least 10 min, providing
that the metabolic inhibitor 2,4-dinitrophenol is present. Cerebral p
erfusate flow rate was measured in both tumour and non-tumour areas us
ing [C-14] iodoantipyrine. The perfusion pump rate was set between 4.8
and 84 ml/min in different animals and the mean flow rate for cerebra
l hemisphere remote from the tumour was 1.03 +/- 0.67 ml/min/g (mean /- sd; n = 17) whereas that for intracerebral tumour was considerably
lower at 0.060 +/- 0.11 ml/min/g (mean +/- sd; n = 17). Linear regress
ion of tumour now on cerebrum now showed a highly significant correlat
ion (r = 0.88). Light and electron microscope examination of the tumou
r vessels revealed no luminal obstruction or perivascular oedema to ex
plain the low flow. We suggest that perfusion with a low viscosity med
ium, at now rates that result in a low intraluminal pressure, probably
causes glioma vessels to close preferentially because they require a
higher intraluminal pressure to remain patent than do normal cerebral
vessels.