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Trial Lecture – time and place
See Trial Lecture.
Adjudication committee
- First opponent: Professor Maria Hopman, Radboud University, Netherlands
- Second opponent: Associate Professor Klas Österberg, University of Gothenburg, Sweden
- Third member and chair of the evaluation committee: Associate Professor Tone Kristin Bergersen, University of Oslo
Chair of the Defence
Professor Mathis Korseberg Stokke, University of Oslo
Principal Supervisor
Professor II Jonny Hisdal, University of Oslo
Summary
This thesis, within the field of vascular physiology, examines the mechanisms contributing to acute haemodynamic change during intermittent negative pressure (INP) - an emerging therapeutic strategy for vascular disease. While prior work has demonstrated perfusion changes in both conduit arteries and the microcirculation, the underlying mechanisms remain incompletely defined. Herein, we characterise the haemodynamic responses to INP and sustained negative pressure (SNP), and identify their physiological drivers.
Across four studies in healthy participants, negative pressure was applied to the lower leg while participants were seated or supine. Arterial and venous pressures were measured invasively, and blood flow was assessed using Doppler ultrasound and laser Doppler fluxometry. Topical anaesthesia was used to block local neurally mediated vasoconstrictor mechanisms in the skin and distinguish between the myogenic response and the venoarteriolar reflex.
INP increased the arteriovenous pressure gradient, particularly in the supine posture, producing transient acceleration in blood flow and shear rate. This was followed by a decline in conduit artery blood flow and skin perfusion. In the skin, this decline was blunted when local vasoconstrictor mechanisms were blocked, confirming the role of locally mediated vasoconstriction during negative pressure.
These findings show that changes in lower limb blood flow and shear rate during INP are driven by both mechanical and vascular responses: an initial acceleration from pressure gradient augmentation, followed by local vasoconstriction. The effects are more pronounced in the supine posture, highlighting the interplay between posture, pressure, and vascular control. These mechanisms may influence the positive clinical effects of INP through the patterns of blood flow that are elicited.
Additional information
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