TY - JOUR
T1 - Prolonged Low Flow Reduces Reactive Hyperemia and Augments Low Flow Mediated Constriction in the Brachial Artery Independent of the Menstrual Cycle
AU - Rakobowchuk, Mark
AU - Parsloe, Emily R.
AU - Gibbins, Sarah E.
AU - Harris, Emma
AU - Birch, Karen M.
PY - 2013/2/5
Y1 - 2013/2/5
N2 - Non-invasive forearm ischemia-reperfusion injury and low flow induced vascular dysfunction models provide methods to evaluate vascular function. The role of oestrogen, an endogenous anti-oxidant on recovery from ischemia-reperfusion injury has not been evaluated nor has the impact of prolonged low flow on vascular function been established. Eight healthy women (33±10 yr) attended the lab during the follicular, ovulatory and mid-luteal phases of their menstrual cycles. After 30 minutes of rest, brachial artery vascular function was assessed by ultrasound measurements of diameter changes during 5 minutes of forearm ischemia and 3 minutes after. Subsequently, a 20-minute forearm ischemia period was completed. Further, vascular function assessments were completed 15, 30 and 45 minutes into recovery. Flow-mediated dilation, low-flow-mediated constriction, and reactive hyperaemia proximal to the area of ischemia were determined. Flow-mediated dilation was reduced at 15 minutes of recovery but recovered at 30 and 45 minutes (PRE: 7.1±1.0%, POST15:4.5±0.6%, POST30:5. 5±0.7% POST45:5.9±0.4%, p<0.01). Conversely, low-flow mediated constriction increased (PRE: -1.3±0.4%, POST15: -3.3±0.6%, POST30: -2.5±0.5% POST45: -1.5±0.12%, p<0.01). Reactive hyperaemia was reduced throughout recovery (p<0.05). Data were unaffected by menstrual phase. Prolonged low flow altered vascular function and may relate as much to increased vasoconstriction as with decreased vasodilation. Reductions in anterograde shear and greater retrograde shear likely modulate the brachial artery response, but the reduced total shear also plays an important role. The data suggest substantial alterations in vascular function proximal to areas of ischemia with potential clinical implications following reperfusion.
AB - Non-invasive forearm ischemia-reperfusion injury and low flow induced vascular dysfunction models provide methods to evaluate vascular function. The role of oestrogen, an endogenous anti-oxidant on recovery from ischemia-reperfusion injury has not been evaluated nor has the impact of prolonged low flow on vascular function been established. Eight healthy women (33±10 yr) attended the lab during the follicular, ovulatory and mid-luteal phases of their menstrual cycles. After 30 minutes of rest, brachial artery vascular function was assessed by ultrasound measurements of diameter changes during 5 minutes of forearm ischemia and 3 minutes after. Subsequently, a 20-minute forearm ischemia period was completed. Further, vascular function assessments were completed 15, 30 and 45 minutes into recovery. Flow-mediated dilation, low-flow-mediated constriction, and reactive hyperaemia proximal to the area of ischemia were determined. Flow-mediated dilation was reduced at 15 minutes of recovery but recovered at 30 and 45 minutes (PRE: 7.1±1.0%, POST15:4.5±0.6%, POST30:5. 5±0.7% POST45:5.9±0.4%, p<0.01). Conversely, low-flow mediated constriction increased (PRE: -1.3±0.4%, POST15: -3.3±0.6%, POST30: -2.5±0.5% POST45: -1.5±0.12%, p<0.01). Reactive hyperaemia was reduced throughout recovery (p<0.05). Data were unaffected by menstrual phase. Prolonged low flow altered vascular function and may relate as much to increased vasoconstriction as with decreased vasodilation. Reductions in anterograde shear and greater retrograde shear likely modulate the brachial artery response, but the reduced total shear also plays an important role. The data suggest substantial alterations in vascular function proximal to areas of ischemia with potential clinical implications following reperfusion.
UR - http://www.scopus.com/inward/record.url?scp=84873507666&partnerID=8YFLogxK
UR - http://journals.plos.org/plosone/
U2 - 10.1371/journal.pone.0055385
DO - 10.1371/journal.pone.0055385
M3 - Article
C2 - 23393572
AN - SCOPUS:84873507666
VL - 8
JO - PLoS One
JF - PLoS One
SN - 1932-6203
IS - 2
M1 - e55385
ER -