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The uptake of trypan blue and [131I]human serum albumin (HSA) has been studied in the dog's abdominal aorta between 1 and 42 days after removal of an experimental stenosis (approximately 90%) applied 1 week previously. Previous work has shown that when the stenosis was present during circulation of these markers, their uptake was increased immediately proximal to the stenosis decreasing to normal by the renal artery level. Distal to the stenosis uptake was reduced apart from small areas of high uptake probably due to turbulent jet impacts. Within the stenosed section the uptake was normal. In this present study it was found that, after removal of the stenosis, proximal uptake initially remained elevated, returning to normal after approximately 15 days whilst the distal uptake returned to normal after approximately 10 days. In the previously stenosed section uptake was increased markedly following the release of the stenosis but returned to normal within approximately 20 days. The relationship of these findings to alterations in the local haemodynamic state and to possible changes in endothelial morphology are discussed.

The influence of abdominal aortic stenosis on the uptake of the protein-binding trypan blue dye and 131I human serum albumin (HSA) has been studied. The major change was a region of high uptake proximal to the stenosis, returning to normal by the level of the renal arteries. There was reduced uptake distal to the stenosis, apart from occasional small areas of high uptake probably due to turbulence. The increase in uptake immediately proximal to the stenosis was dependent on the severity and duration of the stenosis. Removal of the stenosis immediately before the injection of dye and 131I-HSA still resulted in elevated uptake in the proximal region. Some haemodynamic modifications resulting from a stenosis are described. It is suggested that the most satisfactory haemodynamic explanation of the observed uptake change is a proximal increase in oscillatory pressure/strain. The relevance of these findings to atherosclerotic development at and above arterial junctions is discussed.