HYPERCHOLESTEROLEMIA AND HUMAN SKIN BLOOD FLOW

这个子项目是许多研究子项目中利用 资源由NIH/NCRR资助的中心拨款提供。子项目和 调查员(PI)可能从NIH的另一个来源获得了主要资金， 并因此可以在其他清晰的条目中表示。列出的机构是 该中心不一定是调查人员的机构。 高胆固醇血症是动脉粥样硬化的危险因素。内皮一氧化氮(NO)的丧失，促进血管扩张(VD)，保护血管系统，伴随着氧化应激的增加，与全身血管功能障碍有关。可能的机制1)增加血管精氨酸酶活性和2)内皮型一氧化氮合酶(ENOS)“解偶联”导致氧化应激。我们将体内(皮内微透析)和体外实验(皮肤活检)配对，研究高胆固醇血症(HC)的发病机制，并与年龄匹配的非高胆固醇血症(NC)进行比较。我们研究了羟甲基戊二醛(HMG)辅酶A还原酶抑制剂降低胆固醇。

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Hypercholesterolemia is a risk factor for atherosclerosis. Loss of endothelial nitric oxide (NO) which protects the vasculature through promoting vasodilation (VD) coupled with increased oxidative stress is associated with systemic vascular dysfunction. Possible mechanisms 1) increased vascular arginase activity and 2) endothelial nitric oxide synthase (eNOS) "uncoupling" contributing to oxidative stress. We pair in vivo (intradermal microdialysis) and in vitro experiments (skin biopsy) examining mechanisms in hypercholesterolemics (HC) and comparing with age-matched non-hypercholesterolemics (NC). We investigate reducing cholesterol with a hydroxymethylglutaryl (HMG) CoA reductase inhibitor.