The impact of ischaemic preconditioning on cerebrovascular function in healthy individuals.

Introduction: Remote ischaemic preconditioning (RIPC) refers to non-lethal repeated bouts of ischaemia followed by reperfusion applied to a vascular bed, tissue or organ rendering protection to future ischaemic events. RIPC has been reported to enhance functional recovery from heart attacks and strokes, as well as improve conduit artery and microvessel function. Remarkably, very few human studies have examined the impact of RIPC on cerebral blood flow (CBF) or cerebrovascular function. The overall aim of this thesis was to assess, in healthy individuals, the impact of bilateral arm RIPC or SHAM on resting CBF, cerebrovascular reactivity, cerebral autoregulation, and autoregulation during hypercapnia. Methods: Nine healthy participants (age 32.6±11.1 yrs; BMI 25.9±4.4 kg/m2) underwent two laboratory visits; RIPC and SHAM. RIPC consisted of 4 x 5 min periods of cuff inflation (to 200 mmHg) around the upper arm, with cuff inflation alternated between arms every 5 mins. SHAM consisted of the same protocol, but with cuff inflation to a pressure of 10 mmHg. CBF was measured using transcranial Doppler ultrasonography. Cerebral autoregulation was assessed using the squat to stand technique (5 second squat-5 second stand) while cerebral CO2 reactivity was assessed via a period of hypercapnia involving inhalation of 5% CO2. Finally, cerebral autoregulation was again assessed during hypercapnia. Results: CBF was not affected during either RIPC or SHAM (P>0.05). RIPC did not significantly affect cerebral autoregulation or CO2 reactivity, compared to SHAM (P>0.05). Hypercapnia reduced transfer function phase (39 to 16) radians during autoregulation, with no difference between the IPC and Sham conditions. Conclusion: These data indicate that an acute bout of bilateral RIPC does not affect CBF, cerebral autoregulation or cerebral reactivity. Additionally, an acute bout of RIPC does not attenuate the impairment to cerebrovascular function caused by hypercapnia.

Name dc:type.qualificationname

mphil

Level dc:type.qualificationlevel

masters

Grantor dc:publisher.institution

Liverpool John Moores University

Year dc:date.issued

2016

Author dc:creator

• Maxwell, J

Contributors dc:contributor

• Jones, H
• Thijssen, D
• Carter, H

• RC1200 Sports Medicine

DOI dc:identifier.doi

https://doi.org/10.24377/LJMU.t.00004656

OAI identifier oai:identifier

oai:researchonline.ljmu.ac.uk:4656