Katherine L Shields1, Ryan M Broxterman2,3, Catherine L Jarrett2,3, Angela V Bisconti2,3,4, Soung Hun Park1, Russell S Richardson1,2,3. 1. Department of Nutrition and Integrative Physiology, University of Utah, Salt Lake City, UT, USA. 2. Geriatric Research, Education, and Clinical Center, Veterans Affairs Medical Center, Salt Lake City, UT, USA. 3. Department of Internal Medicine, University of Utah, Salt Lake City, UT, USA. 4. Department of Biomedical Sciences for Health, University of Milan, Milan, MI, Italy.
Abstract
NEW FINDINGS: What is the central question of this study? What is the distribution of the hyperaemic response to passive leg movement (PLM) in the common (CFA), deep (DFA) and superficial (SFA) femoral arteries? What is the impact of lower leg cuff-induced blood flow occlusion on this response? What is the main finding and its importance? Of the total blood that passed through the CFA, the majority was directed to the DFA and this was unaffected by cuffing. As a small fraction does pass through the SFA to the lower leg, cuffing during PLM should be considered to emphasize the thigh-specific hyperaemia. ABSTRACT: It has yet to be quantified how passive leg movement (PLM)-induced hyperaemia, an index of vascular function, is distributed beyond the common femoral artery (CFA), into the deep femoral (DFA) and the superficial femoral (SFA) arteries, which supply blood to the thigh and lower leg, respectively. Furthermore, the impact of cuffing the lower leg, a common practice, especially with drug infusions during PLM, on the hyperaemic response is, also, unknown. Therefore, PLM was performed with and without cuff-induced blood flow (BF) occlusion to the lower leg in 10 healthy subjects, with BF assessed by Doppler ultrasound. In terms of BF distribution during PLM, of the 380 ± 191 ml of blood that passed through the CFA, 69 ± 8% was directed to the DFA, while only 31 ± 8% passed through the SFA. Cuff occlusion of the lower leg significantly attenuated the PLM-induced hyperaemia through the SFA (∼30%), which was reflected by a fall in BF through the CFA (∼20%), but not through the DFA. Additionally, cuff occlusion significantly attenuated the PLM-induced peak change in BF (BFΔpeak ) in the SFA (324 ± 159 to 214 ± 114 ml min-1 ), which was, again, reflected in the CFA (1019 ± 438 to 833 ± 476 ml min-1 ), but not in the DFA. Thus, the PLM-induced hyperaemia predominantly passes through the DFA and this was unaltered by cuffing. However, as a small fraction of the PLM-induced hyperaemia does pass through the SFA to the lower leg, cuffing the lower leg during PLM should be considered to emphasize thigh-specific hyperaemia in the PLM assessment of vascular function.
NEW FINDINGS: What is the central question of this study? What is the distribution of the hyperaemic response to passive leg movement (PLM) in the common (CFA), deep (DFA) and superficial (SFA) femoral arteries? What is the impact of lower leg cuff-induced blood flow occlusion on this response? What is the main finding and its importance? Of the total blood that passed through the CFA, the majority was directed to the DFA and this was unaffected by cuffing. As a small fraction does pass through the SFA to the lower leg, cuffing during PLM should be considered to emphasize the thigh-specific hyperaemia. ABSTRACT: It has yet to be quantified how passive leg movement (PLM)-induced hyperaemia, an index of vascular function, is distributed beyond the common femoral artery (CFA), into the deep femoral (DFA) and the superficial femoral (SFA) arteries, which supply blood to the thigh and lower leg, respectively. Furthermore, the impact of cuffing the lower leg, a common practice, especially with drug infusions during PLM, on the hyperaemic response is, also, unknown. Therefore, PLM was performed with and without cuff-induced blood flow (BF) occlusion to the lower leg in 10 healthy subjects, with BF assessed by Doppler ultrasound. In terms of BF distribution during PLM, of the 380 ± 191 ml of blood that passed through the CFA, 69 ± 8% was directed to the DFA, while only 31 ± 8% passed through the SFA. Cuff occlusion of the lower leg significantly attenuated the PLM-induced hyperaemia through the SFA (∼30%), which was reflected by a fall in BF through the CFA (∼20%), but not through the DFA. Additionally, cuff occlusion significantly attenuated the PLM-induced peak change in BF (BFΔpeak ) in the SFA (324 ± 159 to 214 ± 114 ml min-1 ), which was, again, reflected in the CFA (1019 ± 438 to 833 ± 476 ml min-1 ), but not in the DFA. Thus, the PLM-induced hyperaemia predominantly passes through the DFA and this was unaltered by cuffing. However, as a small fraction of the PLM-induced hyperaemia does pass through the SFA to the lower leg, cuffing the lower leg during PLM should be considered to emphasize thigh-specific hyperaemia in the PLM assessment of vascular function.
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