TY - JOUR
T1 - One session of remote ischemic preconditioning does not improve vascular function in acute normobaric and chronic hypobaric hypoxia
AU - Rieger, Mathew G.
AU - Hoiland, Ryan L.
AU - Tremblay, Joshua C.
AU - Stembridge, Mike
AU - Bain, Anthony R.
AU - Flück, Daniela
AU - Subedi, Prajan
AU - Anholm, James D.
AU - Ainslie, Philip N.
PY - 2017/9/1
Y1 - 2017/9/1
N2 - New Findings: What is the central question of this study? It is suggested that remote ischemic preconditioning (RIPC) might offer protection against ischaemia–reperfusion injuries, but the utility of RIPC in high-altitude settings remains unclear. What is the main finding and its importance? We found that RIPC offers no vascular protection relative to pulmonary artery pressure or peripheral endothelial function during acute, normobaric hypoxia and at high altitude in young, healthy adults. However, peripheral chemosensitivity was heightened 24 h after RIPC at high altitude. Application of repeated short-duration bouts of ischaemia to the limbs, termed remote ischemic preconditioning (RIPC), is a novel technique that might have protective effects on vascular function during hypoxic exposures. In separate parallel-design studies, at sea level (SL; n = 16) and after 8–12 days at high altitude (HA; n = 12; White Mountain, 3800 m), participants underwent either a sham protocol or one session of four bouts of 5 min of dual-thigh-cuff occlusion with 5 min recovery. Brachial artery flow-mediated dilatation (FMD; ultrasound), pulmonary artery systolic pressure (PASP; echocardiography) and internal carotid artery (ICA) flow (ultrasound) were measured at SL in normoxia and isocapnic hypoxia (end-tidal ((τVO2)) maintained at 50 mmHg) and during normal breathing at HA. The hypoxic ventilatory response (HVR) was measured at each location. All measures at SL and HA were obtained at baseline (BL) and at 1, 24 and 48 h post-RIPC or sham. At SL, RIPC produced no changes in FMD, PASP, ICA flow, end-tidal gases or HVR in normoxia or hypoxia. At HA, although HVR increased 24 h post-RIPC compared with BL [2.05 ± 1.4 versus 3.21 ± 1.2 l min−1 (% arterial O2 saturation)−1, P < 0.01], there were no significant differences in FMD, PASP, ICA flow and resting end-tidal gases. Accordingly, a single session of RIPC is insufficient to evoke changes in peripheral, pulmonary and cerebral vascular function in healthy adults. Although chemosensitivity might increase after RIPC at HA, this did not confer any vascular changes. The utility of a single RIPC session seems unremarkable during acute and chronic hypoxia.
AB - New Findings: What is the central question of this study? It is suggested that remote ischemic preconditioning (RIPC) might offer protection against ischaemia–reperfusion injuries, but the utility of RIPC in high-altitude settings remains unclear. What is the main finding and its importance? We found that RIPC offers no vascular protection relative to pulmonary artery pressure or peripheral endothelial function during acute, normobaric hypoxia and at high altitude in young, healthy adults. However, peripheral chemosensitivity was heightened 24 h after RIPC at high altitude. Application of repeated short-duration bouts of ischaemia to the limbs, termed remote ischemic preconditioning (RIPC), is a novel technique that might have protective effects on vascular function during hypoxic exposures. In separate parallel-design studies, at sea level (SL; n = 16) and after 8–12 days at high altitude (HA; n = 12; White Mountain, 3800 m), participants underwent either a sham protocol or one session of four bouts of 5 min of dual-thigh-cuff occlusion with 5 min recovery. Brachial artery flow-mediated dilatation (FMD; ultrasound), pulmonary artery systolic pressure (PASP; echocardiography) and internal carotid artery (ICA) flow (ultrasound) were measured at SL in normoxia and isocapnic hypoxia (end-tidal ((τVO2)) maintained at 50 mmHg) and during normal breathing at HA. The hypoxic ventilatory response (HVR) was measured at each location. All measures at SL and HA were obtained at baseline (BL) and at 1, 24 and 48 h post-RIPC or sham. At SL, RIPC produced no changes in FMD, PASP, ICA flow, end-tidal gases or HVR in normoxia or hypoxia. At HA, although HVR increased 24 h post-RIPC compared with BL [2.05 ± 1.4 versus 3.21 ± 1.2 l min−1 (% arterial O2 saturation)−1, P < 0.01], there were no significant differences in FMD, PASP, ICA flow and resting end-tidal gases. Accordingly, a single session of RIPC is insufficient to evoke changes in peripheral, pulmonary and cerebral vascular function in healthy adults. Although chemosensitivity might increase after RIPC at HA, this did not confer any vascular changes. The utility of a single RIPC session seems unremarkable during acute and chronic hypoxia.
KW - artery pressure
KW - cerebral blood flow
KW - chemosensitivity
KW - vascular function
U2 - 10.1113/EP086441
DO - 10.1113/EP086441
M3 - Article
C2 - 28699679
AN - SCOPUS:85028543288
SN - 0958-0670
VL - 102
SP - 1143
EP - 1157
JO - Experimental Physiology
JF - Experimental Physiology
IS - 9
ER -