An assessment of the extent and distribution of experimentally induced cerebral atheroembolic vascular occlusions and infarcts.

Certain types of stroke, TIAs and Amaurosis Fugax can result from atheroembolism from the Carotid bifurcation. This study was undertaken to establish qualitative and quantitative baseline criteria in an animal model for future studies evaluating the effectiveness of thrombolytic and cholesterol emulsifying agents which could eliminate or reduce experimentally induced occlusive atheroembolic lesions. Sixteen male NZW rabbit received sublethal intracarotid injections of human atheroma. After 24 hours the animals were sacrificed, having their brains fixed by cardiac perfusion. Each left hemisphere was coronally sliced anteroposteriorly at 3 mm intervals, and paraffin or methacrylate sections were taken from each slice and stained with H & E or Toluidine Blue. Samples from infarcted tissue were processed for TEM observation. Each section was projected onto the digitizing tablet of a Microplan II image analysis system. The perimeter length, area and maximum diameter were measured for each infarct. The regional distribution of each infarct per section level was recorded on stereotaxic atlas diagrams. The vascular lesions were characteristic of cerebral atheroembolic occlusions. The infarcts were distributed primarily in the cortical and subcortical regions, and were largest in the distribution territory of the Middle Cerebral artery. The morphometric parameters of the infarcts were highly variable at all slice levels.