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▪ Abstract  The relationship between flow in the arteries, particularly the wall shear stresses, and the sites where atherosclerosis develops has motivated much of the research on arterial flow in recent decades. It is now well accepted that it is sites where shear stresses are low, or change rapidly in time or space, that are most vulnerable. These conditions are likely to prevail at places where the vessel is curved; bifurcates; has a junction, a side branch, or other sudden change in flow geometry; and when the flow is unsteady. These flows, often but not always involving flow separation or secondary motions, are also the most difficult ones in fluid mechanics to analyze or compute. In this article we review the modeling studies and experiments on steady and unsteady, two-and three-dimensional flows in arteries, and in arterial geometries most relevant in the context of atherosclerosis. These include studies of normal vessels—to identify, on the basis of the fluid mechanics, lesion foci—and stenotic vessels, to model and measure flow in vessels after the lesions have evolved into plaques sufficiently large to significantly modify the flow. We also discuss recent work that elucidates many of the pathways by which mechanical forces, primarily the wall shear stresses, are transduced to effect changes in the arterial wall at the cellular, subcellular, and genetic level.

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The current study examined whether a postretrieval drug memory could be disrupted by the beta-adrenoceptor antagonist propranolol, administered following reactivation in a cocaine-mediated conditioned place preference paradigm. Following cocaine conditioning, rats were given a test of conditioned place preference, followed immediately by intraperitoneal administration of propranolol or saline. Rats that received propranolol following the preference test showed no preference for the cocaine-paired floor during a subsequent test, while vehicle-treated rats continued to express a preference for the cocaine-paired floor. These deficits in behavior were specific to retrieval of the cocaine-mediated memory, suggesting that postretrieval propranolol induced an impairment of drug-seeking behavior that is consistent with the disruption of a reconsolidation phase following retrieval.