HYPERCHOLESTEROLEMIA AND HUMAN SKIN BLOOD FLOW

高胆固醇血症和人体皮肤血流

• 批准号: 7951330
• 负责人: LACY HOLOWATZ
• 金额: $ 4.02万
• 依托单位: PENNSYLVANIA STATE UNIV HERSHEY MED CTR
• 依托单位国家: 美国
• 财政年份: 2009
• 资助国家: 美国
• 起止时间: 2009-04-01 至 2010-03-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7951330
• 关键词: Age; Atherosclerosis; Biopsy; Blood Vessels; Blood flow; Cholesterol; Clinical Research; Computer Retrieval of Information on Scientific Projects Database; Coupled; Functional disorder; Funding; Grant; Human; Hydroxymethylglutaryl-CoA Reductase Inhibitors; In Vitro; Institution; Microdialysis; Nitric Oxide; Oxidative Stress; Research; Research Personnel; Resources; Risk Factors; Skin; Source; United States National Institutes of Health; Vasodilation; arginase; human NOS3 protein; hypercholesterolemia; in vivo; research study

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.

这个子项目是许多研究子项目中的一个 由NIH/NCRR资助的中心赠款提供的资源。子项目和 研究者（PI）可能从另一个NIH来源获得了主要资金， 因此可以在其他CRISP条目中表示。所列机构为 研究中心，而研究中心不一定是研究者所在的机构。 高胆固醇血症是动脉粥样硬化的危险因素。 通过促进血管舒张（VD）保护脉管系统的内皮一氧化氮（NO）的损失与增加的氧化应激相结合，与全身性血管功能障碍相关。 可能的机制1）增加血管平滑肌细胞的活性和2）内皮型一氧化氮合酶（eNOS）的“解偶联”有助于氧化应激。 我们在体内（皮内微透析）和体外实验（皮肤活检）检查机制，高胆固醇血症（HC）和年龄匹配的非高胆固醇血症（NC）进行比较。 我们研究用羟甲基戊二酰（HMG）CoA还原酶抑制剂降低胆固醇。