Abstract 18245: Palmitic Acid-induced Endothelial Dysfunction in Human Leptomeningeal and Adipose Arterioles

• DOI: 10.1161/circ.132.suppl_3.18245
• Publication Date: 2021-07-03T04:10:04Z
• Authors: Seth Truran; Nina Karamanova; Geidy Serrano; Daniel Franco; Camelia Burciu; Thomas Beach; Alex Roher; Raymond Q Migrino
• Keywords: Dilator; Endothelial Dysfunction

Introduction: Epidemiologic data show strong link between cardiovascular risk factors and dementia-related illnesses (DRI) such as Alzheimer’s disease (AD) with evidence that the earliest changes in AD involve vascular dysfunction. The mechanisms behind impairment DRI remain poorly understood, lack of a human model to study them impedes progress towards cure. Aim: aim is determine effects acute exposure palmitic acid (PA), saturated fatty implicated atherosclerosis, on endothelium-dependent smooth muscle dependent function leptomeningeal arterioles (LMA) peripheral adipose tissue (AA). Methods: LMA from cadavers brain donors (post-mortem interval 3.3±0.4 hours; 2 mild cognitive impairment, 1 Parkinson's disease, Lewy body dementia) abdominal subcutaneous AA living subjects no undergoing routine surgery were isolated, cannulated pressurized. Following preconstriction endothelin-1, baseline (control) dilation response acetylcholine papaverine was measured. Arterioles then exposed hour PA (150 μM) second Results: (see Figure) decreased dilator both (PA-induced change 10-4M: -28.1±6.8 % for -33.8±7.4% AA, p<0.05 versus control). There significant reduction papaverine. control not different AA. Conclusions: Acute induced endothelial dysfunction suggesting potential mechanism could contribute AD. Similarity suggests which easier obtain, may be novel surrogate microvascular function.