Time course of cerebral blood flow and histological outcome after focal cerebral ischemia in rats.

Abstract

Background and Purpose:The relation between time-dependent changes in cerebral blood flow and the appearance of infarction after focal cerebral ischemia is still a matter for debate. The aim of this study was to measure perfusion after simultaneous occlusions of the left middle cerebral artery and ipsilateral common carotid artery in rats and correlate it with the timing and distribution of histological changes.Methods: We studied histological and cerebral blood flow changes 5 minutes and 4, 24, and 48 hours after the onset of focal ischemia. Blood flow was determined autoradiographically using [ >4 C]iodoantipyrine. A coronal template subdivided into regions of interest was applied to the autoradiographs and the histological data.Results: In some regions of the nonoccluded hemisphere, cerebral blood flow 5 minutes after occlusion fell below 50% of normal. Many ischemic structures showed stable blood flow for 48 hours after occlusion, confirming that in this model reperfusion is minimal. Infarction occurred eventually in all areas in which blood flow at 5 minutes fell below 10% of that in control rats, but infarction appeared earlier in regions in which blood flow at 5 minutes was below 5% of that in control rats. When blood flow at 5 minutes rose above 12% of that in control rats, the occurrence of infarction became unpredictable.Conclusions: Despite the general dependence of infarction on perfusion levels, blood flow was not a reliable indicator of those regions committed to infarction. (Stroke 1992;23:1138-1144)

Cortical Negative DC Deflections following Middle Cerebral Artery Occlusion and KCl-Induced Spreading Depression: Effect on Blood Flow, Tissue Oxygenation, and Electroencephalogram

“…Histopathological studies in focal ischemic rats demonstrated growth of infarction from 4 to 24 h postocclusion, although blood flow was stable in most ischemic structures (Hakim et al, 1992). This is in line with our finding of a progressive deterio ration of the EEG power spectrum and suggests that penumbral tissue suffers an increasing mis match between metabolic demands and substrate supply.…”

Dynamics of Cerebral Tissue Injury and Perfusion After Temporary Hypoxia-Ischemia in the Rat

“…1 Both primary and secondary injury do not develop uniformly in the brain; the severity and progression of damage show considerable regional differences. This region-specific response has been reported predominantly in transient global ischemia models [2][3][4] but has also been recognized in experimental focal ischemia 5,6 and after cardiorespiratory arrests in humans. 7 Certain brain areas, such as the hippocampal CA1 region, are extremely susceptible to a reduction in the supply of oxygen and glucose and inevitably become damaged.…”

Protection Against Ischemia and Improvement of Cerebral Blood Flow in Genetically Hypertensive Rats by Chronic Pretreatment With an Angiotensin II AT 1 Antagonist

“…We measured CBF in cortical and subcortical areas of interest 17 in awake animals treated with 0.3 mg/kg per day candesartan, 0.1 mg/kg per day nicardipine, or vehicle for 28 days, 3 hours after MCA occlusion, by a modified quantitative autoradiographic technique using 4-iodo-[N-methyl- 14 C]antipyrine. 18 We quantified local tissue concentrations of 14 C by autoradiography.…”