One session of remote ischemic preconditioning does not improve vascular function in acute normobaric and chronic hypobaric hypoxia

Application of repeated short duration bouts of ischemia to the limbs, termed remote ischemic preconditioning (RIPC), is a novel technique that may 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, 3800m), participants underwent either a sham protocol or one session of 4x5 minutes of dual-thigh cuff occlusion with 5-minutes recovery. Brachial artery flow-mediated dilation (FMD; ultrasound), pulmonary artery systolic pressure (PASP; echocardiography), and internal carotid artery flow (ICA; ultrasound) were measured at SL in normoxia and isocapnic hypoxia [end-tidal PO (PETO ) maintained to 50mmHg], 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), 1 hour, 24 hours, and 48 hours 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 hours post RIPC compared to BL (2.05{plus minus}1.4 vs. 3.21{plus minus}1.2 L•min-1•%SaO2-1, p<0.01), there were no significant differences in FMD, PASP, ICA flow, 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 may increase following RIPC at HA, this did not confer any vascular changes. The utility of a single RIPC session seems unremarkable during acute and chronic hypoxia

The effect of beta-blockade on the transient increase in coronary vascular resistance resulting from haemorrhage.

Abrupt reduction in aortic blood pressure by haemorrhage in the anaesthetized dog has previously been used to assess the effect of elastic recoil and myogenic properties of the coronary vascular wall on diastolic coronary resistance. Using such assessments this study examines whether beta-blockade influences the magnitude of the effect of the vessel wall on coronary resistance. In two groups of dogs abrupt reduction in aortic blood pressure caused by haemorrhage resulted in an initial increase in diastolic coronary resistance, followed by its decline to the control value. In the first group with intact vagi, beta-blockade resulted in a greater initial increase in resistance and attenuation of its subsequent decline. Vagotomy in the second group did not abolish the effect of beta-blockade on diastolic coronary resistance. The findings suggest that during abrupt reduction in perfusion pressure, beta-blockade and reduction in heart rate and coronary blood flow resulted in a greater elastic recoil of the coronary vascular wall associated with an initial increase in diastolic coronary resistance and attenuation of myogenic properties related to return of diastolic coronary resistance to the control level