title: Impaired cerebral autoregulation 24 h after induction of transient unilateral focal ischaemia in the rat.
abstract: Cerebral blood flow (CBF) and cerebral autoregulation have been investigated 24 h after transient focal ischaemia in the rat. Cerebral blood flow was measured autoradiographically before and during a moderate hypotensive challenge, to test autoregulatory responses, using two CBF tracers, (99m)Tc-d,l-hexamethylproyleneamine oxide and 14C-iodoantipyrine. Prior to induced hypotension, 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 pressure reduced to 60 mmHg by increasing halothane concentration) did not compromise grey matter autoregulation in the contralateral hemisphere; CBF data were not significantly different at normotension and during hypotension. However, in the ipsilateral hemisphere, a significant volume of cortex adjacent to the infarct, which exhibited normal flow at normotension, became oligaemic 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 mm3, P = 0.003). Moderate hypotension induced a significant reduction in CBF in both ipsilateral and contralateral subcortical white matter (P < 0.01). In peri-infarct caudate tissue, CBF was not significantly affected by hypotension. In conclusion, a significant volume of histologically normal cortex within the middle cerebral artery territory was found to have essentially normal levels of CBF but impaired autoregulatory function at 24 h post-ischaemia.
authors.affiliation: Wellcome Surgical Institute and Hugh Fraser Neuroscience Laboratories, University of Glasgow, Garscube Estate, Glasgow G61 1QH, UK.
authors.forename: D G
authors.initials: DG
authors.lastname: MacGregor
authors.forename: H V
authors.initials: HV
authors.lastname: Carswell
authors.forename: D I
authors.initials: DI
authors.lastname: Graham
authors.forename: J
authors.initials: J
authors.lastname: McCulloch
authors.forename: I M
authors.initials: IM
authors.lastname: Macrae
mesh_terms: D000818:Animals; D000983:Antipyrine / Q000031:analogs & derivatives; D001794:Blood Pressure; D001921:Brain / Q000098:blood supply / Q000473:pathology*; D002250:Carbon Radioisotopes; D002531:Cerebellum / Q000098:blood supply; D002540:Cerebral Cortex / Q000098:blood supply; D002544:Cerebral Infarction / Q000473:pathology / Q000503:physiopathology; D002560:Cerebrovascular Circulation / Q000502:physiology*; D006706:Homeostasis; D002546:Ischemic Attack, Transient / Q000473:pathology / Q000503:physiopathology*; D008297:Male; D051381:Rats; D011916:Rats, Inbred F344; D012039:Regional Blood Flow; D019690:Technetium Tc 99m Exametazime; D013997:Time Factors
chemical_list: D002250:Carbon Radioisotopes; D019690:Technetium Tc 99m Exametazime; D000983:Antipyrine; C008135:iodoantipyrine