Mg. Muhonen et al., MECHANISM OF REDISTRIBUTION OF CEREBRAL BLOOD-FLOW DURING HYPERCARBIAAND SEIZURES, The American journal of physiology, 266(5), 1994, pp. 80002074-80002081
After occlusion of an artery to the brain, hypercarbia and seizures ma
y produce a paradoxical reduction in cerebral blood flow to the region
supplied by collateral vessels. We measured pressure in an occluded b
ranch of the middle cerebral artery and measured regional cerebral blo
od flow (rCBF) to collateral-dependent cerebrum in dogs (n = 25) to ex
amine hemodynamic mechanisms that account for the reduction in flow. D
uring hypercarbia (arterial Pco(2) = 70 +/- 5 mmHg), rCBF to collatera
l-dependent cerebrum, measured with microspheres and identified using
the shadow flow technique, decreased from 95 +/- 6 (mean +/- SE) to 71
+/- 9 ml.100 g(-1).min(-1) (P < 0.05), while flow to normal brain inc
reased from 105 +/- 9 to 281 +/- 15 ml.100 g(-1).min(-1) (P < 0.05). P
ressure in a branch of the middle cerebral artery decreased during hyp
ercarbia from 50 +/- 6 to 25 +/- 3 mmHg (P < 0.05), concurrent-with a
significant increase in resistance of collateral vessels. Small vessel
resistance was the same in collateral-dependent and normal brain. Dur
ing bicuculline-induced seizures, with blood pressure maintained at co
ntrol levels by withdrawal of blood, rCBF decreased in collateral-depe
ndent cerebrum from 128 +/- 16 to 67 +/- 11 ml.100 g(-1).min(-1) (P <
0.05), and flow to normal brain increased from 169 +/- 14 to 418 +/- 1
7 ml.100 g(-1).min(-1) (P < 0.05). Small vessel resistance decreased i
n both regions, but the decrease was much greater in normal cerebrum.
Changes in cerebral artery pressure and resistance of collateral vesse
ls during seizure were similar to those during hypercarbia. Thus, afte
r occlusion of an artery, redistribution of cerebral blood flow away f
rom collateral-dependent cerebrum during hypercarbia and seizures is t
he result of 1) an increase in resistance of collateral vessels and 2)
a large decrease in perfusion pressure to collateral-dependent cerebr
um and a greater decrease in small vessel resistance in normal cerebru
m than in collateral-dependent cerebrum.