In response to the changes in arteriolar tone that accompany hypercholesterolemia, red blood cell velocity is reduced. This leads to erythrocyte aggregation and stasis in smaller microvessels. Humans with elevated blood cholesterol levels are said to exhibit reduced capillary perfusion, which likely reflects a diminished red blood cell velocity in capillaries. Recent work suggests that NO-dependent pathways contribute to the impaired capillary perfusion during hypercholesterolemia. There is evidence that leukocyte accumulation in downstream venules may also contribute to the impaired capillary perfusion during hypercholes-terolemia, possibly through the release of inflammatory mediators.
Administration of oxLDL to otherwise normal animals promotes the degradation of the endothelial glycocalyx in capillaries. Platelets adhere to the endothelial cells of these damaged capillaries. The glycocalyx breakdown and resultant platelet adhesion can be inhibited by superoxide dis-mutase (SOD) and catalase. It remains unclear whether diet-induced hypercholesterolemia induces a similar injury response in capillaries. However, it has been shown that hypercholesterolemia exacerbates the capillary leak that occurs in response to acute inflammatory stimuli, such as ischemia-reperfusion (I/R). This likely reflects impaired endothelial junction integrity and occurs in a neutrophil-dependent manner, suggesting that leukocytes adherent within venules may release inflammatory mediators such as ROS that worsen the response to other stimuli.
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