Dg. Macgregor et al., Impaired cerebral autoregulation 24 h after induction of transient unilateral focal ischaemia in the rat, EUR J NEURO, 12(1), 2000, pp. 58-66
Cerebral blood flow (CBF) and cerebral autoregulation have been investigate
d 24 h after transient focal ischaemia in the rat. Cerebral blood flow was
measured autoradiographically before and during a moderate hypotensive chal
lenge, to test autoregulatory responses, using two CBF tracers, Tc-99m-d,l-
hexamethylproyleneamine oxide and C-14-iodoantipyrine, Prior to induced hyp
otension, CBF was significantly reduced within areas of infarction; cortex
(28 +/- 20 compared with 109 +/- 23 mL/100 g/min contralateral to ischaemic
focus, P= 0.001) and caudate (57 +/- 31 compared with 141 +/- 32 mL/100 g/
min contralaterally, P= 0.005). The hypotensive challenge (mean arterial pr
essure reduced to 60 mmHg by increasing halothane concentration) did not co
mpromise grey matter autoregulation in the contralateral hemisphere; CBF da
ta were not significantly different at normotension and during hypotension.
However, in the ipsilateral hemisphere, a significant volume of cortex adj
acent to the infarct, which exhibited normal flow at normotension, became o
ligaemic during the hypotensive challenge (e.g. frontal parietal cortex 109
+/- 15% to 65 +/- 15% Of cerebellar flow, P<0.01). This resulted in a 2.5-
fold increase in the volume of cortex which fell below 50% cerebellar flow
(39 +/- 34 to 97 +/- 46 mm(3), P=0.003), Moderate hypotension induced a sig
nificant reduction in CBF in both ipsilateral and contralateral subcortical
white matter (P<0.01). In peri-infarct caudate tissue, CBF was not signifi
cantly affected by hypotension. In conclusion, a significant volume of hist
ologically normal cortex within the middle cerebral artery territory was fo
und to have essentially normal levels of CBF but impaired autoregulatory fu
nction at 24 h post-ischaemia.