Integrative function of microcirculation and skeletal muscle function in peripheral artery disease

Advisor Information

Song-Young Park

Location

MBSC Dodge Room 302A - G

Presentation Type

Oral Presentation

Start Date

4-3-2022 2:00 PM

End Date

4-3-2022 3:15 PM

Abstract

Peripheral artery disease (PAD) is an atherosclerotic disease that impairs lower-extremity circulatory function. Attenuated skeletal muscle mitochondrial function and oxygen utility capacity have been reported in the ischemic limbs; however, the underlying mechanisms are not well-understood. We investigated the impacts of chronic ischemia on skeletal muscle arteriole vasodilatory function and its contribution to skeletal muscle mitochondrial function and microvascular oxygen delivery and utilization capacity (TOI) in PAD. Skeletal muscle and arteriole samples from patients with PAD (n=18, 68.4±10.2 years) and age-matched controls (CON, n=11, 64.6±9.3 years) were harvested. Endothelial-dependent and endothelial-independent vasodilatory function was assessed by flow, acetylcholine (ACh), and sodium nitroprusside (SNP), and skeletal muscle mitochondrial function was measured by high-resolution respirometry. TOI was assessed by near-infrared spectroscopy in-vivo. Endothelial-dependent vasodilation was attenuated in PAD in response to ACh (10-3M, CON: 71.1±7%, PAD: 45.5±6%, PP-3M, CON: 101.5±4%, PAD: 91.6±5%, P=0.12). Complex I + II state 3 respiration was lower in PAD (CON: 26.1±2.1, PAD: 7.8±1.4 pmol∙s-1∙mg-1, P-1, Pr=0.6 and r=0.5, respectively, Pr=0.5 and r=0.6, respectively, P

This document is currently not available here.

COinS
 
Mar 4th, 2:00 PM Mar 4th, 3:15 PM

Integrative function of microcirculation and skeletal muscle function in peripheral artery disease

MBSC Dodge Room 302A - G

Peripheral artery disease (PAD) is an atherosclerotic disease that impairs lower-extremity circulatory function. Attenuated skeletal muscle mitochondrial function and oxygen utility capacity have been reported in the ischemic limbs; however, the underlying mechanisms are not well-understood. We investigated the impacts of chronic ischemia on skeletal muscle arteriole vasodilatory function and its contribution to skeletal muscle mitochondrial function and microvascular oxygen delivery and utilization capacity (TOI) in PAD. Skeletal muscle and arteriole samples from patients with PAD (n=18, 68.4±10.2 years) and age-matched controls (CON, n=11, 64.6±9.3 years) were harvested. Endothelial-dependent and endothelial-independent vasodilatory function was assessed by flow, acetylcholine (ACh), and sodium nitroprusside (SNP), and skeletal muscle mitochondrial function was measured by high-resolution respirometry. TOI was assessed by near-infrared spectroscopy in-vivo. Endothelial-dependent vasodilation was attenuated in PAD in response to ACh (10-3M, CON: 71.1±7%, PAD: 45.5±6%, PP-3M, CON: 101.5±4%, PAD: 91.6±5%, P=0.12). Complex I + II state 3 respiration was lower in PAD (CON: 26.1±2.1, PAD: 7.8±1.4 pmol∙s-1∙mg-1, P-1, Pr=0.6 and r=0.5, respectively, Pr=0.5 and r=0.6, respectively, P